Multiple sclerosis
Introduction
# Definition
# History of MS
# Epidemiology
# Pathophysiology
# Clinical
Presentation #
Classification of MS
# Diagnosis
# PT
Assessment #
PT Management
DEFINITION
• Multiple sclerosis is a Chronic
inflammatory, demyelinating disease of
the central nervous system (CNS).
• Also known as disseminated sclerosis or
disseminated encephalomyelitis.
Brief Overview of disease condition
• It is an inflammatory
and demyelinating
disease.
• Inflammation: body’s
own immune cells
attack the nervous
system.
• Demyelination: myelin
(protective covering of
the nerves) is destroyed
leaving multiple areas of
History
• Dr.Jean-Martin Charcot had first described
Multiple Sclerosis as a clinical pathology in
1868.
• He found hardened, patchy areas disseminated
in the CNS during autopsy and first used the
term “islands of sclerosis” to describe areas
of hardened tissue discovered on autopsy.
• However, it was characterized by its clinical
pathological characteristics : paralysis and
cardinal symptoms of ‘ intention tremor,
scanning speech, and nystagmus’ later
Epidemiology
• Prevalence: 7to10/100,000
• Age onset: MS affects people between
the ages of 20 and 50 years.
• Referred to as “great crippler of
young adults”
• The disease is more common in women
than in men by a ratio of 2:1
Etiology
• There is no defined etiology of MS
• Still, some of the etiological/risk factors are:
Epstein Barr Virus
Human Herpes Virus 6
Low level of Vit D
Mutation in DNA – HLA –DR-2 (dendritic cells)
Phagocytosis
Pathophysiology
• In patients with MS, the immune response
triggers activation of immune cells (e.g. T
cells, CD4+ helper T cells and B cells).
• These immune cells cross the BBB, enter into
the CNS, these cells activate autoantigens,
producing autoimmune cytotoxic effects
within CNS which cause demyelination of the
axonal tissue.
• Disruption of myelin sheath leads to
slowing of neural transmission
•
• This local pathology causes an acute
inflammatory reaction which heightens up to
a mass effect.
• Thus, conduction reduce even further.
• During early stages of MS, remaining
oligodendrocytes may survive initial insult &
produce remyelination
• As disease becomes chronic no
oligodendrocytes are preserved & hence
remyelination do not occur
• These demyelinated areas are filled with
• Gliosis consequently forms the plaques.
• After gliosis, the axon undergoes
degeneration and cause permanent
neurological deficit.
Classification of MS
• According to progression of disease
• Benign MS 0r Inactive MS
• Malignant MS or Fulminant MS or Marburg
MS.
• According to clinical manifestation
• Relapsing remitting MS
• Secondary progressive MS
• Primary progressive MS
• Progressive relapsing MS
Benig
•
n
Characterized by mild relapse of symptoms
followed by remission with no or minimal
deficit
• Patient remains fully functional in all
systems
Maligna
•
nt
Rare occurrence and highly aggressive in
nature.
• There is rapid symptom onset and progression.
• The patient may become so disabled that they
require assistance for locomotion within 5
years of onset.
Relapsing
•
remitting
Time on x – axis, where time refers to the
lifespan of the individual, and disability on y –
axis.
• Bouts (short period of intense activity) of
autoimmune attacks happening in months or
even years and causing increasing the level
of disability
Relapsing
•
remitting
For example, during a bout a person may lose
some vision, but then it may be followed by
improvements, if there is remyelination.
• Unfortunately, remyelination process is not
completed, so there is often some residual
disability that remains & that which attacks more
& more CNS get irreversibly damaged.
• In the RRMS there is typically no increase in
disability b/w bouts, so line stays flat.
• About 85% of people have such type of MS.
Secondary
• progressive
Pretty similar to the
RRMS type, but over
time the immune
attack, becomes
constant which
causes steady
progression of
disability.
• There is progressive
axonal loss which
shows an increase in
Primary
•
progressive
Constant attack on myelin which cause a
steady progression of disability over a
person’s lifetime.
• Characterized by disease progression from
onset without platues or remission
• Or sometimes with occasional platues &
temporary minor improvement.
Progressive
•
relapsing
Continuous deterioration in disease
from onset with occasional relapse.
• Intervals between relapse are
characterized by continuous
disease progression
• Least common of all subtypes
CLINICAL PRESENTATION
• Onset:
• It can be sudden or insidious.
• Initially it starts with a single lesion in the white
matter giving symptoms of disability of one or
more limbs.
• This can be accompanied by visual symptoms,
such as impaired vision in one eye or double
vision (diplopia).
• Paresthesia may or may not accompany.
• The common symptoms and signs of MS can
be as follows:
CLINICAL PRESENTATION
• Spasticity:
• It indicates sign of UMN involvement.
• It can be present in the upper limb and lower
limb.
• Spasticity can result in impaired voluntary
control and thus can affect muscle work.
• Blurred vision:
• Involvement of optic nerve results into
impaired visual acuity.
• Blindness can be seen in rare cases.
CLINICAL PRESENTATION
• Blurred vision:
• The light reflex can also be affected on
examination.
• The pupil reflex is an involuntary response
originating at the brainstem and under the
control of the autonomic nervous system.
CLINICAL PRESENTATION
• Blurred vision:
• Pupils constrict in bright light (to prevent
overstimulation of photoreceptors) and dilate in
dim light (to maximise light exposure)
• In bright light, parasympathetic nerves trigger
circular muscles to contract and cause the
pupils to constrict
• In dim light, sympathetic nerves trigger radial
muscles to contract and cause the pupils to
dilate
CLINICAL PRESENTATION
• Diplopia:
• This can be due to impaired gaze.
• 3rd, 4th and 6th cranial nerve palsy can give
rise to double vision known as diplopia.
• The main reason behind this is affected
motor coordination of muscles of both
eyes.
CLINICAL PRESENTATION
• Weakness:
• Due to multiple factors:
• Decreased motor control from CNS: Patient with
UMN syndrome will show altered muscle
performance which can lead to secondary
muscle weakness.
• Immobility and deconditioning
• Spasticity: in this muscle consume more
energy to perform any action.
CLINICAL PRESENTATION
• Weakness:
• Heat and fatigue: Lack of energy will make the
patient feel weak which ultimately leads to
loss of muscle performance and weakness.
• Pain:
• Patients can present with acute or chronic
pain.
• Head ache and limb pains are some of the
common pains.
CLINICAL PRESENTATION
• Sensory impairments:
• Complete loss of any sensation anaesthesia is
very rare, whereas patients with MS generally
show paraesthesia (burning or tingling
numbness).
• Incoordination:
• Intentional tremors:
• While attempting to reach a particular
object, the patient shows tremors of
the hand known as intentional
CLINICAL PRESENTATION
• Dysarthria and dysphagia:
• Incontinence:
• Urinary bladder and bowel dysfunction
occurs due to demyelinating lesions
affecting lateral and posterior spinal
tracts.
• Spastic bladder is very commonly seen.
CLINICAL PRESENTATION
• Fatigue:
• It is a lack of mental or physical energy
which affects patient’s day to day
performance.
• Altered muscle tone, weakness and
incoordination can all result in
unnecessary energy consumption
leading to decrease to decrease in the
overall capacity to work.
Clinical presentation
• Cognitive deficit
• Visual impairment
• Sensory impairment
• Motor impairment
• Bowel & bladder
involvement
Exacerbating factors
• Viral or bacterial infection
• Disease of major organ
• Stress (physical & mental)
• Heat (Uthoff’s symptom)
• Hyperventillation
• Exhaustion, dehydration,
malnutrition
❑ Uthoff’s Phenomenon:
❑ An adverse reaction to heat seen in
patients with MS or body gets
overheated from hot weather; the
effect is usually immediate and
dramatic in terms of reduced function
and increased fatigue.
❑ Lhermitte’s sign:
# A sign of posterior column
damage in the spinal cord; a
flexion of the neck produces an
electric shock – like sensation
running down the spine and into
the lower extremities.
Cognitive & behavioral dysfunction
• Depression, anxiety, anger
• Emotional dysregulation
syndrome
• Suicidal tendencies
CSF
• Increased immunoglobulin concentration in
>90% of patients
• IgG index (CSF/serum) elevated
• Oligoclonal bands—85%
• Elevated protein—50%
MRI
• Demyelinating plaques in areas of increased
signal intensity
• Scattered throughout the brain & spinal cord
• Gadolinium enhancement identifies active
lesions
PT Assessment
• Higher functions
✔ examination:
Cognition
✔
✔ Perceptio
✔ n Speech
✔ Memory
✔ Behavior
Pain assessment
• Type and site
• Aggravating and relieving factors
✔ Cranial nerve integrity: (All cranial nerves should be
examine in detail)
• Optic, oculomotor, trigeminal nerve
PT Assessment
• Musculoskeletal
examination
• Joint ranges: Active &
passive
• Contracture, deformity.
• Sensory examination:
• Check for paresthesia
PT Assessment
• Tone examination
✔ Hypertonia
✔ Balance examination
• Static and dynamic balance
✔ Coordination examination
✔ Gait examination: Spastic, ataxic or mixed
gait
• Cardiovascular and pulmonary
examination:
• Endurance evaluation
• Fatigue assessment
• Frequency, duration, severity of fatigue, precipitating
factors
• Assessment of temperature sensitivity
• Tympanic thermometer during & after moderate exercise
• Determine co relation between temp & worsening of
symptoms
• Functional assessment
• BADL, IADL, social functioning (FIM)
• Environmental assessment
• Barriers, access, safety, specific task analysis in
relevant environment
• General health & disease specific measure
• SF 36, Expanded dysability status scale (EDSS)
Interventions
• Fatigue • Ambulation &
management mobility
• Strength training • Reduce ataxia
• Normalise tone • Cognitive training
• Improve balance • General
& coordination conditioning &
• Sensory fitness
reeducation • Functional training
• Reduce pain • Psychological
• Improve swallowing counseling
Fatigue management
• Energy conservation techniques:
• Use of Adaptive equipments & assistive
technology & planned exercise & rest
• Modifying task & environment e.g. scooter
for mobility
• Complex task are broken into component
parts
• Sub maximal aerobic training & cooling
reduces fatigue
Strength training
• Active assisted, active exercise & resistive
exercise
• Compensatory strengthening of unaffected
muscle groups & prevent weakness from
disuse.
• Stretching exercise should be given
before strengthening
• Combining strength training with aerobic,
balance & spasticity reducing exercise
Normalize tone
• Stretching routine & relaxation exercise
• Prolonged icing
• Slow rocking, stroking, joint approximation,
weight bearing exercise
• positioning
• Pneumatic pressure splints
Improve balance & coordination
• Dynamic balance exercises on physio
ball or balance board.
• Frenkel's exercise
• Sit to stand from vestibular ball.
• Progression from wide BOS to narrow BOS,
static to dynamic, from low to high COG
• Strengthening of postural muscles, visual
cues & biofeedback
• Include dual task activities s/a speaking
while walking, carrying an object during
Sensory reeducation & skin care
• Unpleasant dysesthesia is treated by cold application
• Minimizing safety & increase awareness of
impairment
• Routine skin inspection & pressure relieving
techniques
• dragging, bumping or scraping body parts during
transfer should be avoided
• Maintaining good nutrition & drinking plenty of fluids
Reduce pain
• Regular stretching, massage & US
• Hydrotherapy
• Soft collar for neck to reduce Lhermitt’s
sign
• Pressure stockings & gloves
• Stress management
• Cognitive & behavioral training for pain
control
Improve swallowing & speech
• Speech therapy aims in compensating dysfunction
• Reducing phrase length & Increasing voice volume
• Using augmented devices s/a writing, computers &
pointers
• Oral exercise
• Treatment for dysphagia focuses on body
positioning to prevent aspiration
• Selection of soft, semi solid food
• Resistive sucking through straw
• Iceing of tongue, back of mouth, laryngeal area of
neck stimulates swallowing
Improve ambulation & mobility
• Maintenance & improvement of trunk control &
balance following normalization of tone &
maximizing ROM
• Pool walking will reduce fatigue & improve balance
• Specific ambulation aid to improve safety,
decrease energy expenditure & improve
function
• E.g. AFO with rocker shoes, canes, walker
• Wheelchair transfer as disease progress
• Motorizes scooter in severe conditions
Cognitive training
• Compensatory techniques are more
effective in improving daily functioning
• Compensatory strategies for memory deficits,
such as keeping a diary and noting down
important things to remember
• Personal digital assistant device to improve
functional task
• Pill dispenser to help patient take medicine at a
scheduled time
• Clear written sequence steps of exercise or clear
direction for functional task in environment.
General conditioning & fitness
• Prescription is based on freq., intensity,
mode & time
• Daily exercise at sub maximal level are safe
in MS
• Aerobic training s/a running, walking,
cycle ergometer are suitable
• Adequate rest periods should be provided to
avoid fatigue
Functional training
• Focuses on development of problem solving
skills & appropriate compensatory strategies
• Specific training in technique of dressing,
bathing, toileting, personal hygeine, feeding &
bed mobility to improve ADL
• Long handle reachers, button hooks sock aids or
velcro closures can assist in dressing
Bladder management
• Flaccid bladder: crede’s maneuver of emptying
(application of downward manual pressure over
lower abdomen)
• Intermittent self catheterization
• Dysynergic bladder
• Intermittent or continuous catheterization
• Dietory modifications : reducing fluids
Bowel management
• Dietary: increase fluid intake, high fiber food
& processed food
• Maintain hygiene & prevent infection
Psychological counseling
• Personal & family councelling
• Promotion of self management skills
• Referral to support group
• Positive attitude & honest open
approach
Thank
you
