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Multiple sclerosis

Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system, characterized by immune-mediated damage to myelin. The disease presents with a variety of symptoms including weakness, sensory impairments, and cognitive deficits, and can be classified into different types based on progression and clinical manifestation. Management involves physical therapy, cognitive training, and addressing psychological aspects to improve quality of life for affected individuals.

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0% found this document useful (0 votes)
42 views65 pages

Multiple sclerosis

Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system, characterized by immune-mediated damage to myelin. The disease presents with a variety of symptoms including weakness, sensory impairments, and cognitive deficits, and can be classified into different types based on progression and clinical manifestation. Management involves physical therapy, cognitive training, and addressing psychological aspects to improve quality of life for affected individuals.

Uploaded by

Heer Thakkar
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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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

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