MULTIPLE SCLEROSIS
 measles
I. Definition
 Multiple Sclerosis (MS) is a chronic,
demyelinating disease of the CNS
characterized by inflammation,
segmental demyelination and gliosis
 Cardinal signs: Charcot’s triad
 Scanning speech
 Intention tremor
 Nystagmus
II. Epidemiology
 MC inflammatory demyelinating disease
of CNS
 Onset: 20-40 y/o
 Overall ratio: F > M (2:1)
 Rare in childhood and in adults >50 y/o
 Affects predominantly white population
High frequency: Temperate climates
 North Europe
 Scandinavia
 North US
Low frequency: Tropical climates
 Asia
 Africa
 South America
III. Etiology
 Exact etiology unknown (idiopathic)
 Genetic theory:
 family history of MS
 absence of KIR2DL3 gene
 mixed histocompatibility complex
(MHC/HLA-6) region of
chromosome 6
 Immunologic theory: autoreactive T cells
are activated by foreign microbes
causing overproduction of
proinflammatory histamine
 Viral theory: virus causing self-
perpetuating autoimmune process
 Some of the investigated viruses
include:
 Epstein-Barr virus
 canine distemper
 Chlamydia pneumonia
o Risk Factors:
 F>M
 20-40 y/o
 Temperate climates
 Vitamin D deficiency
 Smoking
IV. Basic Medical Sciences
 Neurons - structural and functional units
of the nervous system specialized for
rapid communication
 Parts:
 Cell body: also called perikaryon,
contains the nucleus, organelles
 Dendrites: convey action potential
towards cell body (soma)
 Axon: convey action potential away
from cell body
 Myelin sheath: covering of the axon
 Nodes of Ranvier: space between
two myelin sheaths; facilitates
saltatory conduction
 CNS Neuroglia:
 Oligodendrocytes: produce myelin
sheath in CNS
 Astrocytes: maintain BBB
 Microglia: removes cell waste
 Ependymal: assist in CSF circulation
PNS Neuroglia:
 Schwann cells: produce myelin
sheath in PNS
 Satellite cells: regulate
neurotransmitter levels in ganglia
V. Pathophysiology
 Hallmark: demyelinated plaques in
CNS as seen in MRI
 Immune response
Activation of immune cells (e.g., T cells,
CD4+ helper T cells, B cells) that cross the
BBB
Production of autoimmune cytotoxic
effects within the CNS
Phagocytic activity of macrophages
Demyelination (hallmark)
Neural transmission slows down and
causes nerves to fatigue rapidly
Conduction block occurs causing
disruption of function
Acute inflammatory event occurs further
interfering with conductivity
Inflammation gradually subsides and may
account for the clinical syndromes
Four pathological patterns of MS:
With repeated attacks, the anti-
inflammatory processes become less
effective and are unable to keep up
Oligodendrocytes survive the initial insult
Remyelination of the surviving naked axons,
producing shadow plaques
Oligodendrocytes become involved and myelin repair
cannot occur (PPMS exclusively associated with
disease of the oligodendrocytes)
Astrocyte infiltration
Gliosis
Glial scars (plaques)
The axon becomes interrupted and undergoes
neurodegeneration
Permanent neurological disability
 Early stages:
 Plaque locations: POB4Cs
o Periventricular white matter
o Optic Nerve
o Brainstem
o Cortex
o CST
o Cerebellum
o Cervical spinal cord (posterior
white column)
1. Pattern I – purely cell mediated where T
cells produce demyelination
2. Pattern II – the most common type,
similar to I, but appears to involve
additional intralesional
 immunoglobulins and activated
compliment (cell- and antibody
mediated)
3. Pattern III – apoptosis of
oligodendrocytes with selective loss of
myelin associated glycoprotein
4. Pattern IV – primary degeneration of
oligodendrocytes
 Clinical Types
1. Benign MS
 Mild
 patient remains fully
functional in all neurological
systems 15 years after onset
2. Malignant MS
 Aka Marburg’s disease
 More severe
 Rapid onset
 Continual progression
leading to
death/significant
disability within a
short time
 Four major clinical sub-types:
1. Relapsing-remitting MS (RRMS):
 MC type
 85% of patients w/ MS
 characterized by discrete attacks of
neurological deficits (relapse) w/
either full or partial recovery
(remission)
2. Primary-progressive MS (PPMS):
 10% of patients w/ MS
 Later onset (40 y/o) and equal
gender distribution
 characterized by disease
progression and steady functional
decline from onset
 moderate fluctuations w/o discrete
attacks
3. Secondary-Progressive MS (SPMS)
 characterized by initial relapsing-
remitting course, followed by
progression to steady and
irreversible decline with or without
continued acute attacks
 majority of patients with RRMS
progress to SPMS
4. Progressive-relapsing MS (PRMS)
 5% of patients w/ MS
 characterized by steady
deterioration in disease from onset
with occasional acute attacks
 intervals between attacks are
characterized by continuing disease
progression
VI. Clinical Manifestations
 In advanced stages, Charcot’s triad
may be seen
1. Sensory symptoms
o Paresthesia
o Hypoesthesia (numbness)
2. Pain
o Headache
o Optic neuritis
 - icepick sensation  Pseudo-exacerbation of neurologic
o Trigeminal neuritis (tic symptoms due to heat
douloureux)
– intense facial pain on VII. Diagnostic Tools & Imaging
one side of the face studies
o Lhermitte’s sign
– posterior column 1. MRI
damage o Greatest sensitivity
o Paroxysmal limb pain o FLAIR or T2-weighted
– MC type of pain imaging
 Worse at night and
o bright spots: new lesions
after exercise
with active inflammation
 Abnormal burning
(occur during the preceding
pain
6 weeks)
o black holes: represent long
3. Visual
o Diplopia (mx: patch term disease activity (e.g.,
unaffected eye) loss of myelin and axons,
o Nystagmus gliosis)
o Scotoma  *Darker lesions = extensive tissue
o Lateral gaze palsy damage
o Marcus Gunn pupil (usually
after optic neuritis) 2. Evoked potentials (EP)
o High sensitivity
4. Motor (Corticospinal tract > UMNL) o 90% of individuals with MS
demonstrate abnormal EP
 Paresis or paralysis o slowed conduction =
 Fatigue presence of demyelinating
 Spasticity lesions on visual, auditory,
 Ataxia and somatosensory
 Babinski sign pathways
 Hypertonia o Visual EP – helpful

5. Cognitive 3. Lumbar puncture w/ CSF Analysis

o elevated total
 Short-term memory immunoglobulin (IgG) in
 Decreased attention, concentration CSF
and executive function o Oligoclonal IgG bands
(greatest sensitivity)
6. Speech and swallowing
4. CT Scan (least sensitive)
 Dysarthria (scanning speech)
 Dysphonia (hoarseness) o Not effective in visualizing
 Dysphagia lesion of brainstem,
cerebellum, and optic nerve
7. Bowel and bladder

 Spastic bladder (failure to store) Diagnostic Criteria for MS (simplified)

 Flaccid bladder (failure to empty)
 Dyssynergic bladder
 Constipation hx of relapsing and
Possible MS possible remitting
8. Uthoff’s phenomenon signs
 (-) prior neurogenic - headaches photosensitivity
symptoms - paresis in limbs - arthritis
- memory loss - oral ulcers
1 site of involvement
- autoimmune - dry eyes
- CNS lesion - skin rashes
Sjogren’s - fatigue - joint swelling
Syndrome - (+) - persistent dry
2 documented attacks autoantibodies cough
with clinical evidence - MRI: - (+) peripheral
Probable MS of 1 lesion periventricular & neuropathy
subcortical
OR lesions

1 documented attack, - weakness - skin rashes

2 lesions Lyme - fatigue - joint pain
Disease - paresthesia - fever & chills
- cognitive - common in
dysfunction children
2 attacks separated by
- (+) blurred - treatable
Definite MS 1 month, 2 separate vision
lesions - fatigue - fever & chills
- headache - skin rashes
- memory loss - chronic
AIDS - dysphagia diarrhea
2017 McDonald Criteria for diagnosis of MS
- blurry vision - (+) oral
leukoplakia
- swollen
lymph glands

- fatigue - fever
- blurred vision - skin rashes
Sarcoidosis - headaches - night sweats
- depression - joint pain
- no cure - SOB
- (+)
granulomas
- weight loss

IX. Course and Prognosis

GOOD POOR
 Females  Males
 < 40 y/o  > 40 y/o
 Sensory  Motor symptom
VIII. Differential Diagnosis symptom at at onset
onset  Polysymptomatic
 One symptom  Progressive
R/I R/O at onset (PPMS or PRMS)
- autoimmune - migraines  RRMS
SLE - fatigue - skin rashes
  Neuro findings: Pyramidal and Interferon -anti- -flu-like
cerebellar signs with involvement in beta: Inflammatory symptoms
Betaseron (β- and regulates -fever
multiple sites is worse at 5 years,
1b) immune -myalgia
indicates more severe disability Extavia responses -injection-
Plegtidy -delays site
 MRI findings: Good prognosis if Avonex (β-1a) progression reactions
there’s low total lesion burden, low Rebif (β-1a)
active lesion formation and
Anti- -for spasticity -sedation
negligible myelin or axon loss
spasticity: -for -hypo-
Baclofen paroxysmal tension
Dantrium spasm -dizziness
X. Surgical Intervention Valium -causes -weak
Tegretol motor point ness
1. Rhizotomy Phenol block
 Selected nerve root is cut at the Dantrolene
point they emerge from the spinal sodium
cord
 For treating spasticity Anti- -regulates -sedation
 Glycerol rhizotomy – for acute pain cholinergic: bladder -blurred
relief of trigeminal neuralgia, poor Propantheline emptying vision
long-term pain relief Imipramine -dizziness
(Tofranil) -confusion
2. Deep Brain stimulation -inc HR
 Implanted electrodes interrupt
activity in the thalamus through Glatiramer -for fatigue -confusion
shock acetate: -*blocks -chest
 Treats muscle tremors Copaxone* immune cells discomfort
heading to -SOB
Amantadine myelin -orthostatic
3. Tenotomy
hypotension
 Cuts tight tendons to relieve tension
 Treats spasticity
Mitoxantrone -modify -nausea
relapsing & -diarrhea
4. Baclofen pump
Novantrone secondary -weakness
 Injecting baclofen pump near the
Immunex progressive -consti
spine
MS Pation
 Treats spasticity *special -headache
precautions
needed
XI. Pharmacological Intervention Clonazepam -for -sedation
Drugs Indication Risks Isoniazid cerebellar -unsteadi-
incoordina- Ness
Corticosteroid -Reduce the -GI
Tion -dizziness
severity and problems
(ataxia & -incoordi-
Prednisone duration of -fluid
intention nation
Methylpred- acute attacks retention
tremor)
nisolone - anti- -osteo-
inflammatory Porosis Natalizumab -immuno- -headache
and immune- -HTN (Tysabri) Suppressive -fatigue
suppressive -DM *IV/month -lower -diarrhea
relapse rate -nausea
  Timed Up and Go (TUG)

XIII. Problem List

XII. PT Applications
1. Sensory deficit
1. Standardized Ax and Evaluative tools 2. Visual problems
3. Pain
 Kurtzke’s Expanded Disability 4. Spasticity
Status Scale (EDSS) 5. Paresis
- quantifies disability in MS 6. Ataxia
- low score = good prognosis 7. Fatigue
- assign a severity score that ranges 8. Cognitive dysfunction
from 0-10 in increments of 0.5. 9. Speech problem
- each functional system is scored on 10. Feeding problem
a scale of 0 (no disability) to 5 or 6 11. Bowel and bladder dysfunction
(more severe disability) 12. Decreased cardiorespiratory
13. Psychosocial issues
 Modified Fatigue Impact scale
- Ax of the effects of fatigue in
physical, cognitive and psychosocial XIV. PT Goals
functioning during the past 4 weeks
- 21-item with scores ranging from 0 1. Increase/maintain ROM
(never) to 5 (always) 2. Improve sensory awareness
- Higher score = greater fatigue 3. Reduce pain
4. Decrease spasticity
 Minimal examination of Cognitive 5. Increase strength without overexertion
Function in MS (MACFIMS) 6. Improve motor control
- assessment of spatial processing 7. Increase static and dynamic bal/tol
and higher executive function 8. Improve coordination
abilities 9. Improve cognitive function
10. Reduce postural deviation
 McGill Questionnaire 11. Correct gait pattern
- Self-reporting measure of pain 12. Manage speech and swallowing
- scores range from 0 (no pain) to 13. Improve bowel and bladder control
78 (severe pain) 14. Enhance aerobic endurance
15. Improve functional status et ADL
 Patient History performance
 Cognitive status 16. Improve patient education on condition
 Sensation awareness
 ROM
 DTR
 MMT XV. Physical Agents and Modalities
 Muscle tone
 Appropriate Physical agents and
 Gait
modalities
 Coordination
a. TENS – to reduce pain
 Balance
b. Functional ES – to promote
 Fatigue motor control
 ADLs c. Cold packs – prevents heat-
 6MWT related flares
 Modified Ashworth Scale
 Berg Balance Scale
 d. Hydrotherapy – for
proprioceptive input, functional
mobility, balance and cardiac
conditioning

 Precautions and Contraindications

a. TENS

d. Hydrotherapy

b. Functional ES

c. Cold packs

XVI. Therapeutic Exercises

 Appropriate Manual therapy

POC Intervention
Increase - PROME ->
mobility AAROME -> exercises (with aid)
AROME
- PJM Speech and - correct posture to
swallowing improve feeding
Sensory - Sensory management process
awareness integration - stimulation of
- Eye patch (for muscles for speech
diplopia) and feeding
- Desensitization - resistive breathing
- Proper skin care training
on desensitized - good oral hygiene
areas Improve - Abdominal
- Frenkel’s exercise bowel and massage
Pain relief - Stretching bladder - Kegel exercises
- Postural retraining control (PFM contraction)
- Pressure stockings - Timed voiding
- Massage - Urge suppression
techniques
Reduce - Rhythmic rotation
spasticity w/ deep tendon Enhance - Regular
pressure aerobic walking/cycling
- PNF stretching endurance
- Proper positioning Improve - Functional mobility
- Orthotics/splints functional training
Increase - Free-weight status - Task-oriented
strength strengthening functional exercises
- Resistance training - Reaching activities
using elastic bands - Orthotics and
- Rest periods assistive devices
Improve - Hydrotherapy Patient - Energy
motor control - PNF techniques education conservation
- controlled mobility - Pacing
activities *Fatigue - Relaxation
Increase - Balance training *Positioning techniques
static and on wobble - Condition awareness
dynamic board/pool - Bed mobility
exercises
balance and
tolerance
Improve - Biofeedback
coordination - Coordination
 Precautions and Contraindications
exercises

Improve - Minimize 1. The therapist must be extra attentive to

cognitive distractions
patient’s fatigue and its triggering
function - Repetition of info
- Make list of tasks factors such as heat, stress and over
Reduce - Behavior exhaustion.
postural modification 2. Provide ample amount of rest period in
deviation - Correct faulty between exercises.
movement positions 3. Exercises for MS patients should be
- Pelvic mobilization
done in the morning when they are less
exercises
Correct gait - Pre-ambulation fatigued and the temperature is not as
pattern exercises warm.
- ambulation
4. Maintain cool body temperature when
participating in an exercise program by:
- staying hydrated with cool drinks
- wear proper lightweight clothes and
shoes
- use cooling garments or ice packs
- exercise in a cool environment
- avoid outdoor exercise during warm
parts of the day
5. Therapist must take into account the
medications taken by the patient before
exercising as some can cause side
effects such as dizziness, nausea and
shortness of breath.
 References

1. Human Anatomy, 7th Ed. By Frederic

Martini
2. Physical Rehabilitation, 5th Ed. by
Susan O’Sullivan
3. Physical Medicine and
Rehabilitation, 4th Ed. by Randall
Braddom
4. Pathology: Implications for the
Physical Therapist, 4th Ed. By
Catherine Goodman
5. Physical Agents in Rehabilitation, 4th
Ed. By Michelle Cameron
6. Physical, Medicine and
Rehabilitation Board Review, 2nd Ed.
By Sara Cuccurullo
7. Differential Diagnosis for Physical
Therapists, 5th Ed. By Catherine
Goodman