Multiple sclerosis is an autoimmune demyelinating disease of the central nervous system characterized by inflammation, demyelination and scarring of nerve tissue. It typically affects people in their 20s-40s and is more common in women. Symptoms vary depending on the location of lesions but may include visual problems, numbness, weakness, fatigue and cognitive issues. Diagnosis involves MRI of the brain and spine, lumbar puncture and evoked potential tests. Treatment focuses on reducing relapses and managing symptoms, and may include medications like beta interferons, steroids, and disease-modifying drugs.

1. MULTIPLE SCLEROSIS
KEERTHI PRIYA MPT NEURO,
ASSISTANT PROFESSOR

2. CONTENTS
INTRODUCTION
ETIOLOGY
PATHOPHYSIOLOGY
TYPES
CLINCAL FEATURES
INVESTIGATIONS & DD
MEDICAL
MANAGEMENT
COMPLICATIONS

3. Autoimmune demyelinating disease of nervous system.
Characterized by chronic inflammation, demyelination and
gliosis of nervous tissue.
Clinically it is characterized by Charcot's triad.
Charcot's triad :
Intention tremor
Scanning speech
Nystagmus
INTRODUCTION
sclerosis
Stiffening of a
tissue

4. Age of onset: 20 - 40 years
Females > Males =3:1
Incidence=3.50.000/year
Prevalence
<1 in equatorial region
6-14 in southern U.S & Europe
30-80 in Canada, North Europe & North U.S
INTRODUCTION
EPIDEMIOLOGY

5. ETIOLOGY
 Exposure to Virus during early
childhood
 Environmental changes
 Mutation in HLA, IL2RA, IL7RA
 Molecular Mimicry
RISK FACTORS
 Vitamin D Deficiency
 Smoking
 Heredity

6. Immune response
Tlymphocytes,
macrophages & anti bodies
Crosses blood brain barrier
Myelin sheath
Demyelination
Depletion of
oligodendrocytes
Astrocytes deposition
Gliosis
PATHOPHYSIOLOGY

7. TYPES1. Relapsing & Remitting Multiple
Sclerosis
2. Secondary Progressive
Multiple Sclerosis
3. Primary Progressive Multiple
Sclerosis
4. Progressive Relapsing Multiple
Sclerosis

8. TYPES
RRMS
Most common.
Seen in 85%
Relapse followed by remission
Symptoms may become Permanent if
seen during remission

9. TYPES
SPMS
Transition of RRMS
Progressive worsening of
neurological symptoms

10. TYPES
PPMS
15%
Progression of symptoms without
relapse & remission

11. TYPES
PRMS
5%
Worsening of disease from
beginning with relapse alone

12. CLINICAL FEATURES
Early symptoms
Visual disturbance
Paraesthesia
Weakness
Fatigability
Sensory
Paraesthesia's
Numbness
Loss of position &
vibration sense
Pain
80% of patient
Electric shock followed
by burning sensation
Paroxysmal limb pain
Trigeminal neuralgia
Headache
Hyperpathia

13. CLINICAL FEATURES
Visual
80%
Optic neuritis
Blurred vision
Double vision
Lateral gaze palsy
Nystagmus
Consensual light reflex
Motor
Weakness
Spasticity
Babinski +ve
Flexor & extensor
spasm
clonus
Fatigue
Tiredness
Exhaustion
Lack of concentration
Mental dullness

14. CLINICAL FEATURES
Coordination &
balance
Ataxia
Tremors
Truncal weakness
Dizziness
Vertigo
Drunken gait
Speech & swallowing
Dysarthria
Dysphonia
Dysphagia
cognitive
10%
Short term memory
Loss of attention &
concentration
Problem solving
Emotional incontinence
in 10%, euphoria
Depression 50%

15. CLINICAL FEATURES
Bladder
Spastic
Flaccid
Dysynergic
Speech & swallowing
Constipation
Diarrhoea
Sexual
Impotent
Infertility
Libido

16. INVESTIGATIONS
1. MRI
2. VEP
3. SSEP
4. BEP
5. CSF
6. SEROLOGICAL INVESTIGATIONS

18. DIFFERENTAIAL DIAGNOSIS
1. Lymes disease
2. Ankylosing spondylitis
3. Neuromyelitis optica spectrum disorder
4. Sjogrens syndrome
5. Myasthenia gravis
6. Acute disseminated encephalopathy

19. TRAETMENT
 Beta Interferon
 Teriflunomide
 dimethyl fumarate
 Prednisone
 Methyl prednisone
 Dexamethasone
 Natalizumab
 Dimethyl furamate
RRMS
ACUTE
PREVENT
RELAPSE

20. TRAETMENT
 Baclofen
 Tizanidine
 Anticholinergics
 Deitary
 Laxatives
 Amantidine
 Beta blockers
 Analgesics
 Anti depressants
SPASTICITY
BOWEL
FATIGUE
BLADDER

21. REFERENCES
 PHYSICAL REHABILITATION BY SUSAN O SULLIVAN
 CLINICAL NEUROLOGY BY AMINOFF
 ADAMS & VICTOR PRINCIPLE OF NEUROLOGY BY ALLAN
HOOPER
 NEUROLOGY & NEUROSURGERY ILLUSTRATED BY
LINDSAY