Multiple Sclerosis

D R . P O O J A PA T E L ( P T )
M P T N E U R O.
Multiple sclerosis (MS) is an autoimmune
disease characterized by inflammation,
selective demyelination, and gliosis.
It is a chronic inflammatory demyelinating
disease of the brain and spinal cord.

Affects largely young adults between the ages

of 20 and 40
Dr. Jean Charcot described the symptoms in
by its clinical and pathological characteristics

Paralysis and cardinal symptoms of :

 Tremors
 Scanning speech
 Nystagmus
They were termed as “charcots triad”
 Epidemiology

 8,000 – 10,000 new cases are diagnosed annually

 Affects nearly 500,000 individuals in the U.S.
 Occurs most frequently between ages 15 - 50
 Female: male ratio = 2:1
 Ethnic differences
 White population more affected
 African population at half the risk
 Asian and native American at low risk
 Etiology

Unknown
Auto-immune nature
Risk of MS is increased in persons with an
affected family member. Major
histocompatibility complex (MHC)
Induced by viral or other infectious agents
 Herpes virus, chlamydial pneumonia
Increased IgG in CSF
More risk in smokers and Vit D deficiency
Pathophysiology
 MS is a Demyelinating Disease

Blood vessel Inflammation

Myelin – provides
insulation to nerve
processes (axons)
Blood vessel
Inflammation

Blood vessel
Inflammation
Immune response triggered by T-lymphocytes,
macrophages and Igs

Autoimmune cytotoxic effects in the CNS

Failure of BBB

Myelin sensitized T-lymphocytes enter and

attack myelin
 DEMYELINATION: slow transmission,
conduction block

Local inflammation, odema  mass effect

Affects conductivity of nerve fibre

After inflammation subsides some fluctuation
in function is present
During early stages, oligodendrocytes survive
and can produce remyelination

This process is often incomplete and becomes

chronic

Eventually oligodendrocytes get involved and

myelin repair cannot occur
 Demyelinated areas become filled with
fibrous astrocytes and undergo GLIOSIS

Glial scars

Primary affection is white matter

Grey matter involved in later stages
Certain areas are most frequently involved

 Optic nerves
 Periventricular white matter
 Spinal cord ( corticospinal tracts, posterior
white columns)
 Cerebellar peduncles
 Disease course
It is highly variable and unpredictable
Differs from person-person and over time

It has various types

1. Benign MS
2. Malignant MS ( Marburg’s disease)
 Benign MS

Patient remains fully functional after 15 years

of onset in all neurological systems
Only 20% cases
 Malignant MS

Rapid progression
Significant disability or death within
relatively short time after onset
Rare
4 major disease courses (clinical sub-types)

1. Relapsing-remitting MS (RRMS): 85%

2. Primary Progressive MS (PPMS): 10%
3. Secondary Progressive MS (SPMS)
4. Progressive-relapsing MS (PRMS): 5%
 Relapsing-remitting Secondary-progressive

Disability
Disability

Time Time

Primary-progressive Progressive-relapsing

Disability
Disability

Time Time
 1. RRMS

Characterized by relapse with full recovery

and some remaining neurological S/S residual
deficit upon recovery
Periods b/w relapse are characterized by
LACK of disease progression
 2. PPMS

Progression from onset

Without plateaus or remission

Or occasional plateaus and temporary minor

improvements
Usually after 40years
Permanent neurological disability
10% cases
 3. SPMS

Progressive disease from onset

Initially relapsing remitting course
Followed by progressive

80% of RRMS go on to develop SPMS

 4. PRMS

Progressive disease
Without acute relapses
Or may have some recovery
Commonly seen after 40years

Intervals b/w relapse are marked by

continous disease progression
 Exacerbating factors

MS relapses (exacerbation) are defined by

new and recurrent symptoms that last atleast
24 hrs

And are unrelated to other etiology

Avoiding these factors ensures patients

optimal function
1) Viral/bacterial infection
2) Disease of major organ system
3) Stressful events
4) Reaction to heat (uthoff’s symptom)
5) Psuedoexacerbation

 Psuedo-attacks resolve by 24hrs

 CLINICAL MANIFESTATIONS

They are variable

Early symptoms typically include

 Minor visual disturbances
 Paraesthesias
 Fatigability

Onset of symptoms can develop rapidly over

a course of minutes or hours or over period of
weeks and months
1. Sensory changes
2. Pain
3. Visual changes
4. Motor dysfunction
5. Cognitive symptoms
6. Emotional symptoms
7. Bladder/bowel
8. Speech and swallowing dysfunction
9. Sexual symptoms
10. Cardiovascular dysautonomia
 1. Sensory changes

Complete loss of any sensation is rare

Focal deficit in limited area
Altered sensation are more common:
 Paresthesia (pins and needles sensation)
 Numbness of face, body or extremities

 Disturbances in position sense

 LE vibratory sense impairment
 2. Pain

80% patients complain of pain

Chronic pain
Paroxysmal pain (sudden and spontaneous)

Pain described as :
 Intense
 Sharp
 Shooting
 Electric-shock like
 burning
Common types:
 Trigeminal neuralgia
 Paroxysmal limb pain
 Headache

Lhermitte’s sign
 TRIGEMINAL NEURALGIA

Demyelination of sensroy division of 5th CN

Innervating face, cheeks and jaw
Eating, shaving or touching the face
aggravates the symptoms
Can trigger painful episods
 LHERMITTE’S SIGN

Sign of posterior
column damage
Flexion of neck
produces electric
shock-like sensation
running down the
spine and into the LE
 PAROXYSMAL LIMB PAIN

Abnormal burning, aching

Most common in MS
Worse at night and after exercise
Aggravated by temperature elevation
“Hyperpathia”: hypersensitivity to minor
sensory stimuli
 HEADACHE

More frequent
Migrane or tension type

NEUROPATHIC PAIN

Due to demyelinating lesion in spinothalamic

tract or sensory roots
More common in patients with minimum
disability
Described as burning pain similar to disc
herniation
 MUSCULOSKELETAL PAIN

Associated with muscle and ligament strain

Developed due to
 mechanical stress
 Abnormal postures
 Immobility
 Weak muscles
 Spasticity
 Tonic spasms

Anxiety and fear can worsen the pain

 3. Visual symptoms

80% patients have visual involvement

Involvement of Optic nerve produces:
 Altered visual acuity
 Blindness (rare)
 OPTIC NEURITIS

Inflammation of optic nerve

Ice-pick like pain behind the eye
Associated with blurring or greying of
vision or blindness in one eye
A scotoma may occur in the centre of the
visual field
Neuritis can occur in both eyes, its self
limiting
Improves within 4-12 weeks
Affects the light reflex too
 MARCUS GUNN PUPIL

Develops after optic neuritis

Light reflex is inhibited
Shining a bright light into healthy eye will
produce reflex contraction in both eyes
But if light is shown in affected eye, a
paradoxical widening of one or both pupils
occur
NYSTAGMUS
Eye movements are disturbed
Lesion of cerebellum or central vestibular
pathways
Involuntary cyclic movement of eyeballs
(horizontal or vertical)

Develops when patient looks to side or moves

the head
INTERNUCLEAR OPHTHALMOPLEGIA (INO)

Incomplete eye adduction

Lateral gaze palsy
On affected side
Nystagmus on opposite side
Due to demyelination of pontine medial
longitudinal fasciculus
ADDITIONAL IMPAIRMENTS
Conjugate gaze and control of eye
movements is affected due to brainstem
lesion of 3,4,6 CN or MLF
Diplopia can occur due to lack of co-
ordinated eye muscles

These impairments are primary cause of

disability
Lead to impaired balance and movement
 3. Motor Dysfucntion

a) WEAKNESS
Patients with corticospinal lesions
demonstrate feature of UMNL
 Spasticity
 Brisk DTR
 Involuntary flexor and extensor spasm
 Clonus
 Babinski sign
Movements are slow,stiff and weak
Loss of orderly recruitment and
Reduced firing rate modulation of motor
neurons
Reduce muscle strength, power and
endurance
Impaired synergistic relationship
Cerebellar lesions:
Asthenia / generalised muscle weakness
With ataxia
Muscle weakness secondary to inactivity

Mild paresis total paralysis

 b) FATIGUE
Def given by a panel on fatigue of MS council
for Clinical Practice Guidelines
“a subjective lack of physical and/or mental
energy that is perceived by the individual or
caregiver to interfere with usual and desired
activities”
It is a daily event experienced by 75-95%
individuals
50-60% say it is one of the most troubling
factors
Comes abruptly, without warning (like flu)
Fatigue is unrelated to disease severity
It is due to CENTRAL ACTIVATION FAILTURE
(central fatigue) and
Failure in excitation-contraction coupling
Precipitating factors: exersion, heat and
humidity, depression, sleep dis., low self esteem,
mood dis., medical condition or secondary
impairments and side effect of medicine
Environment mastery
c) SPASTICITY
80%
Mild  severe depending on the progression
U/E and L/E muscles
DTR, clonus, synergy, decreased ROM

Causes pain, contractures, abnormal

posturing, lack of skin integrity
Fatigue, functional mobility, ADL
Exacerbating factors: same
Disabling in advances stages
d) BALANCE AND CORDINATION
Ataxia
Postural and intension tremors
Hypotonia
Truncal weakness
“dysmetria, dysynergia, dysdiadochokinesia”
Ataxia of trunk and extremities
Postural tremor: shaking, back and forth
 During sitting, standing when the body is
supported against gravity
 Intension tremor: involuntary rhythmic
shaking during purposeful movements

Different in severity
More severe = more disability
(fine/quivering)  (gross/shaking)
Seen during
 Eating
 Speaking
 Writing
 Walking, etc

Exacerbated by stress, excitement, anxiety,

“all adrenalin releasing conditions”
Sensory ataxia
Dizziness
lesion in archicerebellum or central
vestibular pathways
Difficulty in balance, nausea, vertigo
Worsen by head movements
Paroxysmal attacks
Followed by hyperventilation
e) AMBULATION AND MOBILITY
Due to
 Weakness
 Fatigue
 Spasticity
 Impaired sensation
 Visual problems
 Ataxia
Staggering
Uneven steps
Poor foot placement
Uncoordinated limb movements
Frequent loss of balance
4. Speech and Swallowing Dysfunction

Due to
 Muscle weakness
 Spasticity
 Ataxia
 Tremor

Dysarthria
Dysphonia
Dysphagia
slurred, poorly articulated speech,
Low volume
Unnatural emphasis
Slow rate

Changes in vocal quality

Harshness, hoarshness
Breathiness or hypernasal sound
Poor co-ordination of tongue and oral muscles

Difficulty in chewing and maintaining lip-seal

Inability to swallow, spit or cough
Serious complication: aspiration pneumonia

Poor co-ordination of breath control and

posture contributes to speech and feeding
difficulties
 5. Cognitive and Affective changes

COGNITIVE IMPAIRMENTS
50% of patients
Mild  moderate
Only 10% find it disabling
Depends on the area affected and distribution
of demyelination rather than severity
Attention (divided, alternating)
Concentration
Slow processing
Impaired recent memory
Impaired executive functions (concept
formation, abstract processing, problem
solving, planning and sequencing)
Focal frontal lobe lesions can produce
cognitive inflexibility
Global dementia is rare
Major factor in determining QoL, working
status, etc
DEPRESSION
50% Experience a major depressive
episode
Depressive symptoms include
 Feeling of hopelessness, despair
 Diminished interest in activities or
pleasure
 Changes in appetite, weight gain or loss
 Insomnia, lethargy
 Feeling of worthlessness
 Decreased concentration
 Frequent thought of suicide or death
It can occur due to
 Direct lesion of MS
 Drug induced (steroids, ACTH)
 Psychological reaction to stress of far-
reaching and unpredictable disease

Anxiety, anger, denial, aggression,

dependency
Social embarrassment (tremor, scanning
speech, incontinence) adds to the emotional
distress
AFFECTIVE CHANGES
10%
Changes in mood, feelings, expression and
control
Psuedobulbar affect (emotional liability,
emotional dysregulation syndrome)
 Sudden loss of emotional control on multiple
occasions that is typically unrelated to
external circumstance, depression or
underlying mood
 More disability with progression
Euphoria in advanced stages
Exaggerated state of well-being
Sense of optimism incongruent with patients
disability
More in advanced stage

Bipolar affective disorders (depression,

mania)
Diffused bilateral cerebral involvement
(prefrontal cortex and corticobulbar tracts)
 5. Autonomic Changes

CARDIOVASCULAR DYSAUTONOMIA
Caused by involvement of ANS
Problems with cardio-acceleration and
reduction in BP response during exercise
Attenuated or absent sweating response
BLADDER DYSFUNCTION
80%
Loss of volitional and synergistic control of
micturation reflex
Produced by demyelinating lesion of lateral
and posterior spinal tracts
Types:
1. Small spastic bladder
2. Big flaccid bladder
3. Dyssynergic bladder
Dyssynergic or conflicting bladder represents
a problem with co-ordination between
bladder contraction and spinchter relaxation
Urgency
Frequency
Hesitancy
Nocturia
Dribbling
Incontinence
Pyramidal tract involvement
Decreased functional mobility
Poor hygiene
Emotional distress

Emptying dysfunction
Large residual urine volume

UTI and kidney damage

BOWEL DYSFUNCTION
Constipation
Gastrocolic reflex dysfunction

Spasticity of PFM
Inactivity
Lack of fluid intake
Poor diet
Depression
Medicine side effects
Diarrhea and incontinence is less of a
problem
SEXUAL DYSFUNCTION
91% men 72% women
Women:
 Changes in sensation
 Vaginal dryness
 Trouble reaching orgasm
 Loss of libido
Men:
 Impotency
 Decreased sensation
 Inability to ejaculate
 Loss of libido

Psychological factors have a large impact

For the patient and the partner
 DIAGNOSIS

By a neurologist based on

HISTORY
CLINICAL FINDINGS
SUPPORTIVE CLINICAL TESTS
MRI
CSF examination
EP
 Imaging

Gd MRI
 For acute lesions
 6 weeks
 T2 bright spots

 Dark lesion: more severe damage

 MRI may not correlate to the symptoms
 CSF

Elevated total immunoglobulin

IgG bands (80-90%)
 Evoked Potentials

Abnormal EP in 90%
Visual
Somatosensory
Motor pathways
Slowed or
abnormal conduction
 PROGNOSIS

Only a small percentage of patients die as a

consequence
In most patients life expectancy is not
reduced

At/after 15years will require some assistive

device
20 years later, 50% require wheelchair
 Medical Management

 Disease Modifying Agents

 Synthetic Interferon beta
 Immunomodulater
 Slower the immune response
 Reduce swelling, odema, rapid proliferation
of T and B cells
 Corticosteroid
Management of relapses and symptoms
1. Spasticity
2. Pain
3. Fatigue
4. Tremor
5. Cognitive and emotional problems
6. Bladder and bowel problems
 Spasticity: muscle
relaxants
Baclofen
Dantrolene
BDZ
Intrathecal
administration of
baclofen
 Surgical intervention:
 Rhizotomy
 Neurectomy
 Tenotomy (for
contractures)
Pain:
BDZ
Phenytoin
Fatigue
Amantadine hydrochloride
Modafinil ( antiviral and dopamin agonist)
 Tremors
Intermittent Clonazepam

 Vertigo
Antinauseating drugs (meclizine)
Corticosteroids

 Sx
Thalamotomy
DBS
Cognitive emotional problems:
Donepezil (anti-alzheimers drug)

Antidepressant:
Fluoxetine
Zoloft
Helpful in fatigue as well
Councelling and support groups
Bladder and bowel problems
After urodynamic workup

For spastic bladder:

Anticholinergic drugs
Dietary limitation
More fluid intake
Reduction in alcohol and caffeine
Flaccid bladder:
Crede manuver
Catheterization

Dyssynergic bladder:
Alpha-adrenergic blocking agents
Anti-spasticity agents
Continuous/ indwelling catheter
To control infection:
Antibiotics

Constipation:
Dietary changes
Laxatives
Enemas
Stool softeners
 PHYSIOTHERAPY ASSESSMENT

Multiple areas of brain are affected

Hence careful examination is necessary
Neurological and functional impairment

Regular follow-up
 History

Will help to find:

 Severity of problems
 Stage of disease
 Age
 Phase of rehabilitation
 Other factors
 Test and Measures

Cognition
Affective and psychosocial function
Sensation
Cranial nerves
Visual acuity
Muscle performance
Fatigue (MFIS)
Temperature
Motor function
Posture
Balance gait and locomotion
Aerobic capacity and endurance
Skin integrity and condition
Functional status
Environment
General health
Disease-specific measures
GOALS
 TREATMENT

1. MANAGEMENT OF SENSORY DEFICITS

AND SKIN CARE
 Strategies to increase awareness of sensory
deficits
 Compensate for sensory loss
 Promote safety

 Availability of other intact sensations

 Proprioceptive loss: movement control
difficulty
 Increase other sensory awareness
Vision
Tapping
Verbal cueing
Biofeedback
Proprioceptive loading exercise
VISUAL LOSS
 Use of bright lights
 Contrast color use eg, marking the stairs,
doors
 Diplopia: patching of one eye
 Avoid using frequently due to adaptation

 Refferal
DEFICIT OF SUPERFICIAL SENSATION
 Possess a risk of skin damage
 Decubitus ulcer
 Excessive friction of skin
 Change is position
 Pressure relief
 Awareness
 Protection
 Care of desensitezed part, taught to
patient and family/caregiver
Skin should be kept clean and dry
Cleaned and dried promptly
Regular skin inspection (redness, bony
prominence)
Clothing should be breathable and comfortable
Seams, buttons, pockets shouldn’t press against
the skin
Regular pressure relief
Change position frequently, every 2hrs in bed and
15min when sitting in wheelchair
WC pushups and repositioning manuvers
PRD
Mainly matress
Cushions, boots, cuffs

Prevention is better than cure

Inspection
 2. MANAGEMENT OF PAIN

Depends on determination of the cause of

pain
Musculoskeletal pain
Joint mal-alignment
Muscle weakness
Regular stretching and exercise
Massage
Ultrasound
Posture correction

Lhermitt sign: soft collar to limit neck

flexion
Hydrotherapy/Pool therapy with
lukewarm water: dysaesthesia
Pressure stockings and gloves to relieve
pain (with neural warmth)
Stress management
Relaxation
Biofeedback
To reduce pain and anxiety
TENS
 3. EXERCISE TRAINING

 Strength and conditioning

 Cardiovascular conditioning
 Flexibility exercise
STRENGTH AND CONDITIONING
FITT
Scheduled on alternate days, usually in the
morning (reason?)
More neurological involvement  more
frequency of exercise
Submaximal intensities (50-70% MVC)
Resistance training
Circuit training may also be useful
Discountinous work, adequate rest
Slow progression

 Precaution:
 Sensory loss: use alternative machines
Fatigue, don’t work uptill exhaustion
Monitor “time-to-fatigue”
TEMPERATURE CONTROL (A.C., cooler,
sprays, fans, wraps, cold water to bath or
aquatic exercise)
Cognitive or memory impairments: written
diagrams/instructions
Functional training: closed chain exercise

Balance issues: more stable postures

(plantigrade, quadripod)
Group exercise: motivation, support
CARDIOVASCULAR CONDITIONING
Changes in HR, BP, VO2, RPE
RR increases
However HR and BP responses maybe
blunted secondary to cardiovascular
dysautonomia
Continous or discontinous protocol is used
Discontinous for symptomatic patients
Submaximal test (70-85% of HRmax)
SBP > 200mmHg
DBP > 110mmHg or
Hypotensive response

Precautions:
BP
Core temp
Fatigue
Overwork
Effect of medicine
Daily exercise of lower intensity
3 sessions/week (alternate days)
Cycling, walking, swimming, etc
Circuit training is best
30min/ session (3 session of 10min each)
Depression can affect adherence to the
program ( counseling is necessary)
Patient education is imp
Self monitoring, lifestyle modification, safety
consideration
Type of exercise can include cycling, walking,
swimming, or water aerobics.
Circuit training may prove best for optimizing
training.
Individuals with balance problems or sensory
loss will require non–weight-bearing
activities.
FLEXIBILITY EXERCISES
Stretching and ROM exercise
Counteract spasticity
Sedentary patients or wheelchair-ridden
patients are likely to develop tightness in
 Hip flexors, adductors, hamstring, gastroc
 Pectorals, lattissimus dorsi
Bed-ridden patients experience tightness of
 Hip/knee extensors
 Planterflexors

AROM/PROM performed daily

Tai chi
 4. MANAGEMENT OF FATIGUE

One of the most debilitating

Sleepiness, excessive tiredness
Sense of weakness suddenly and severely

Task for a therapist too

Whether to prescribe aerobic exercise or to
prevent overload
Energy Effectiveness Strategies (EES)
Maintain “activity diary”
1. Sleep
2. Daily activities by hour
3. “cost” of that activity

 Level of fatigue (F)

 Value/importance of that activity (V)
 Satisfaction percieved with the activity
(S)
Eg: fixing lunch
F=7, V=3, S=2
Aggravating factor: heat

Based on the information, therapist can

initiate training sessions, teaching ESS
Energy conservation refer to the adoption
of strategies that reduce overall energy
requirements of task and overall level of
fatigue
Modifying the task or the environment to
ensure successful completion of daily
activities

Eg, motorized scooter/powered wheelchair

for mobility
Activities that are difficult or have high
energy needs can be broken down into
components
Activity pacing refers to balancing of
activity with rest periods interspersed
throughout the day
For chronic fatigue:
Rest-activity ratios are developed
Periodic rest planned in advance
Time-outs with complete rest

Overall energy need can be improved

Prioritize
Limit certain activities and save that time
Planning, work simplification
OT, vocational rehab councellor
Weekly review
Environmental examination
Education
Recommendations
 5. MANAGEMENT OF SPASTICITY

It is functionally limiting and leads to various

secondary impairments like:
 Contractures
 Postural deformity
 Decubitus ulcers, etc
Management can be done by
Hydrotherapy, cryotherapy, theraputic
exercises, positioning or a combination of
any of the above
Antispasticity medication
Eg,

Icepacks, wraps, cool baths (short-term

effects)
Tendon reflex excititbility
Slowing conduction impulses or nerve and
muscles
Careful about autonomic response
Early ROM exercises
In the face of unremitting spasticity,
stretching techniques are indicated to
increases the extensibility of muscle tendon
unit and connective tissue
Intermitten static stretching minimum 30-60
sec hold
5-10 reps
Stretching with rhythmic rotation
PNF stretching (HRAC/CRAC)
Maintained stretch 30min-3hours
Tilt table
Wedge
Low load weights using skin traction
Serial cast
Air splints

Stretching as HEP
Prevent fast, ballistic stretching (why)
Common muscles:
 Quads
 Adductors
 Planterflxors

WC
 Hamstring
 Hip flexors
Active exercise at slow or self-selected speed
For expanding ROM
Emphasis on contracting the antagonist
muscle (reciprocal inhibition)
ES to antagonist muscle
Patients with abnormal co-contraction:
improve motor control (timing) and
biofeedback
Tai chi, yoga, aquatic exercise (relaxation)
Functional activities for on tone reduction
should focus on trunk or proximal segments
LE flexion with trunk rotation
LTR in side lying or hook lying to reduce
extensor tone
Hook lying with ball, gentle rocking
Quadrupad to side-sitting
Overall tone reduction: slow rocking,
relaxation technique
Patient with limited functional mobility:
Positioning out of abnormal, spastic posture

Mechanical positioning device

Resting splints, toe spreader
Ankle splint etc
6. MANAGEMENT OF BALANCE AND CO-ORDINATION
DEFICITS

To promote static postural control

Static holding in weight bearing, antigravity
postures (squatting, quadrupad, kneeling,
plantigrade and standing)

Progression:
 Varying BOS
 height of COG
 degree of freedom
Joint approximation through proximal
joints
Shoulder, hips, head and spine
Rhythmic stabilization (PNF)
Slow reversal

Dynamic postural control:

Weight shift or reaching (UE)
Or stepping (LE)
Sitting: resisted PNF chop pattern
Functional movements: bridging, sit-stand,
scooting, wall squats, etc
Pool exercise
Water provides graded resistance and
reduces ataxic movement
Improve strength, reduce fatigue, improve
endurance
Equilibrium and non-equilibrium exercises
Force platform training
 To reduce postural sway
 To control alignment
 Functional balance control
Vestibular training

Control of ataxic limb movements:

 Proprioceptive loading and light resistance
 Elastic resistance, weight cuffs
 Weighted boots, jacket, belt etc
 Be careful for fatigue
 Weighted canes or walkers for UE
External device like braces/splints can be
used to reduce ataxia

Frenkel’s exercises
 Supine, sitting and standing

Stress management as it can worsen the

symptoms
feedback
Repetition
 7. LOCOMOTOR TRAINING

Poor balance
Heaviness of limb
Weak dorsiflexors
Spasticity
Sensory loss
Ataxia
Weakness of quads, hip abductors
Weight bearing
Adequate weight transfer
Maintain normal gait pattern
Verbal, manual cueing
Body weight supported training

AFO
 Canes, walkers to compensate for
Strength
Balance
Sensory loss
Ataxia
Fatigue

Counseling: better than wall-walking or

furniture walking
For fatigue:
WC with large wheels

Powered WC
Should be feasible
Proper alignment
Medial knee block/pommel for adductor
spasticity
Reclining
Transfer board
Hydraulic lift
 8. FUNCTIONAL TRAINING

Problem solving
Appropriate decision making
Safe performance in home and community
Training functional mobility (eg. Bed mobility,
transfer, locomotion)
ADL training (dressing, personal hygiene,
toileting, and feeding)
By OT
Adaptive device prescription and
maintenance
Environmental modification
Energy conservation
Effective communication
 9. MANAGEMENT OF SPEECH AND SWALLOWING
DEFICITS

Shallow respiratory pattern

Recurrent infection
Respiratory muscle training
Manual contact, resistance, spirometry etc

For MS patients: improve trunk stability,

head control
Dysphagia:
Co-ordinate with speech language
pathologist and OT
Improve sitting position, head control and
oro-motor co-ordination

For good swallowing and to avoid

aspiration
Upright posture
Forward head
Chin parallel to table or slightly tucked in
Oro-motor exercise
Lip closure
Tongue movements
Jaw control

Stretch and resistance can be used to

strengthen week muscles
Swallowing reflex can be stimulated (GAG)
Icy beverages, sherbat, fruit slush
Begin with cold meals, take one small sip
No consecutive swallowing
Resistive sucking through straw
Thicker liquids  more resistance
Moist food > dry food are easier to manage
Semisolid and pureed food > solid
Avoid irritable foods like vineger
Crumbly foods like cake, cookies, cheese
etc
Focus on chewing not talking
Late in the day  thick liquids
Early  thin liquids

Power swallow:
Inhale  hold  swallow  exhale  swallow
again
Feeding tube in future
10. MANAGEMENT OF COGNITIVE DEFICITS

Major difficulty
Refer to neuropsychologist
Compensatory strategies:
 Memory aids and devices
 List of to-do things, daily events and
reminders
 Audiotapes
 Pill dispenser
 Alarm clock
Complex tasks can be broken up
Written direction

Additional strategies:
 Mental rehersal
 Requesting assistance
 Maximizing alertness
 Avoidance of difficult situation
 Mental exercises
Caregiver councelling
 Psychosocial issues

Patient and caregiver

Significant emotional and cognitive stress
Patient required initial acceptance and
flexibility
Depression and fatigue

Self efficacy
Stress reduction and coping strategies
 Patient & family/caregiver education

Positive affirming attitude

Strong collaborative relationship
Hope and encouragement with realism
Information
Prevention
Rehab
HEP
Assistive and adaptive devices
Community resources
Thank You