Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system that typically affects young adults between the ages of 20-40. It is characterized by immune-mediated damage to the myelin sheath and axons in the brain and spinal cord, leading to demyelination and potentially axonal loss. Symptoms vary depending on the location of lesions in the CNS but may include sensory and visual disturbances, motor impairments, cognitive issues, and others. The disease course is unpredictable and can be relapsing-remitting, primary progressive, secondary progressive, or progressive relapsing. There is no known cure for MS and treatment aims to manage symptoms and reduce disease progression.

1. Multiple Sclerosis

2. • Introduction
• Epidemiology
• Etiology
• Pathophysiology
• Types of M.S.
• Clinical features

3. • Its chronic inflammatory demylinating disease of CNS.
• Affects largely young adults between ages of 20-40
• Also described as ‘great crippler of young adults’.
• Dr. Jean Charcoat first described- ‘Charcoat triad’
• Intentional tremors.
• Scanning speech.
• Nystagmus

4. Epidemiology
• Onset of M.S. typically occurs between 15-50.
• Peak age- 30 years
• Rare in children.
• Females are more prone for M.S. than male- 2:1

5. Etiology
• Precise etiology is unknown
• Most widely accepted theory is that- an auto immune disease
induced by viral infectious agent.
• Herpes-I,II.VI along with chlamydial pneumonia are general agents
of great interest in this infectious hypothesis.
• Increased IgG & oligoclonal bands in C.S.F.- 65-95%; M.S. patients
provides convincing evidence of precipating infections an auto
immune response.

6. • About 33% patients found with positive history viral infections
• 15% patients found with positive genetic history.

7. Pathophysiology
• Immune response triggers the antibody production of T- Lymhocytes
& macrophages.
• Antigen is triggered in response to command
• Produces cytotoxic effects within CNS- ( friendly Fire)
• BBB fails to & T- Lymphocytes enter the CNS & attack mylin
sheath, surrounds the nerve.
• It serves as insulator & conserves energy for nerve

8. • Demylination- slowing of neural transmission, nerves fatigue early.
• Severe disruption- conduction block- disruptions of functions
• Local inflammation & edema, infiltrates surround the acute lesion
and can cause a ‘mass effect’ ,further interferes with the
conductivity of the nerve fiber.
• During the early stages of M.S. Oligodendrocytes (myelin -
producing cells) survive the initial insult and can produce
remyelination.
• This process is often incomplete and as the disease becomes more
chronic.

9. • Demyelinated areas eventually become filled with fibrous
astrocytcs and undergo a process called ‘Gliosis’.
• Gliosis refers to the proliferation of neurological tissue within
the CNS and results ‘Glial scars (plaques}’
• At this stage, the axon itself becomes interrupted and
undergoes retrograde degeneration (dying axonopathy).
• Axonal loss varies from 10 to 20 % shows, milder form of the
disease where as 80 % shows severe MS

10. Clinical course & Types
• M.S. is highly variable & unpredictable in person to person.
• RRMS- relapse with either fully recovery of some remaining
neurological signs and symptoms & residual deficit, the period
between relapse are characterized by lack of disease progression.
• PPMS- characterized by disease progression from onset, without
pleatues or remission or temporary minor improvements.
• SPMS- characterized by relapsing- remitting course, followed by
progression at variable rate including minor relapsing and remitting

11. • PRMS- characterized by progressive disease from onset but without
clear acute relapse that may or may not have recovery or remission
commonly seen patients above 40 year.
• Benign MS- characterized by mild disease in which patient remain
fully functional in all neurological systems after 15 years of onset .
• Malignant/ Marburg MS- characterized by rapid progression
leading to significant disability or death within relatively short time
period after onset.

12. Sensory Impairement
• Sensory Symptoms
• Hypothesia or numbness
• Paresthesias
• Pain
• Dysesthesias .
• Optic or trigeminal neuralgia
• Lhermitte's sign
• Chronic pain

13. Motor Impairement
• Weakness or paralysis
• fatigue
• Spasticity
• in-coordination
• Intentional tremor
• Impaired balance
• Gait disturbances

14. Visual impairement
• Blurred or diminished vision
• Diminished acuity of vision
• Scotoma
• Nystagmus

15. Bladder impairment
• Urinary urgency, frequency
• Nocturia
• incontinence
• Urinary hesitancy, dribbling

16. Cognitive impairment
• Memory or recall problems
• Decreased attention, concentration
• Diminished abstract reasoning
• Dimmished problem solving, judgment
• Diminished speed of information processing
• Diminished visual-spatial abilities

17. Sexual impairments
• Impotence
• Decreased libido
• Decreased vaginal lubrication
• Impaired ability to achieve orgasm

18. bowl impairment
• Constipation
• Diarrhea
• Incontinence.

19. Speech and swolling imapirment
• Dysarthia.
• Diminished verbal fluency
• Dysphonia
• Dysphagia

20. Emotional &other impairments
• Depression
• Pseudo bulbar affect
• Anxiety
• Cardiovascular Dysautonomia

21. Pattern of symptoms
• Varies from person-to-person
• Varies Over time in each individual affected
• First symptoms usually transient
• Early symptoms are typically sensory & visual
• Involves more than one functional component of the CNS