This document provides an overview of multiple sclerosis (MS). It describes MS as an autoimmune disease characterized by inflammation and damage to the protective myelin sheath surrounding nerves. The document discusses that MS most commonly affects people between the ages of 20-40, is more prevalent in women than men, and is more common in white populations. Genetic and environmental factors like viral infections are thought to contribute to MS risk. Magnetic resonance imaging, evoked potentials, and cerebrospinal fluid analysis are used to diagnose MS by detecting lesions in the brain and spinal cord. Available treatment options aim to reduce inflammation and prevent relapses.

1. MULTIPLE SCLEROSIS
SAYALI GUJJEWAR
MPT II

2. INTRODUCTION
• Multiple sclerosis (MS) is an autoimmune disease characterized by
inflammation, selective demyelination, and gliosis.
• MS affects approximately 2.1 million people worldwide.
• It was first defined by Dr. Jean Charcot in 1868 by its clinical and
pathological characteristics: paralysis and the cardinal symptoms of
intention tremor, scanning speech, and nystagmus, later termed
Charcot’s triad.

3. • The onset of MS typically occurs between ages 20 and 40 years.
• MS is rare in children, as is the onset of symptoms in adults
older than age 50 years.
• The disease is more common in woman than in men by a ratio
of 2:1 to 3:1.
• MS affects predominantly white populations; African
Americans demonstrate approximately half the risk of
acquiring the disease. Low rates are also reported in Asians
and Native Americans.

4. ETIOLOGY
Family
• The risk of MS is increased in persons with an affected family member.
• The risk is 3.0% for a sibling, 5.0% for a fraternal co-twin, and rises to 25.0% for an identical co-
twin.
Genetic
• Genetic studies have revealed many interacting alleles that may contribute to MS susceptibility
with mutations in the human leukocyte antigen major histocompatibility complex (MHC) gene
most strongly correlated.
Viral infection
Vitamin D deficiency
Smoking

5. PATHOPHYSIOLOGY

6. TYPES

8. SYMPTOMS

10. DIAGNOSIS
• The diagnosis of MS is made by the neurologist based on a careful
medical history, a complete neurological examination, and supportive
laboratory tests.
• Evidence of damage must be present in at least two separate areas of
the CNS (dissemination of lesions in space) and damage must have
occurred at two separate points in time at lease 1 month apart
(dissemination of lesions in time).

12. LABORATORY TESTS
• Magnetic Resonance Imaging (MRI)
• Evoked Potentials (EP)
• Lumbar Puncture (LP) With Cerebrospinal Fluid (CSF) Analysis

13. MAGNETIC RESONANCE IMAGING (MRI)
• MRI is highly sensitive for detecting MS plaques in the
white matter of the brain and spinal cord (Fig. 16.1).
• New lesions with active inflammation that occur during the
preceding 6 weeks or so are seen as areas of increased
signal intensity, “bright spots.”
• Contrast-enhanced T1- weighted images (gadolinium-
enhanced) are used todetect more long-term disease
activity (i.e., loss of myelin and axons, gliosis). These
lesions are seen as “black holes” on the MRI; the darker the
lesion, the more extensive the tissue damage.

14. EVOKED POTENTIALS (EP)
• Up to 90% of individuals with MS demonstrate abnormal EP.
• The presence of demyelinating lesions on visual, auditory, and
somatosensory pathways produces slowed conduction.
• Of the three, visual evoked potentials (VEPs) have been found to
be the most helpful in the diagnostic process.

15. LUMBAR PUNCTURE (LP) WITH
CEREBROSPINAL FLUID (CSF) ANALYSIS
• Patients with MS show elevated total immunoglobulin (IgG) in
CSF and the presence of oligoclonal IgG bands (seen in 90% to 95%
of patients) in response to inflammatory demyelinating lesions.
• Patients with PPMS have higher levels of immunoglobulins in
spinal fluid than patients with RRMS.

16. MEDICAL MANAGEMENT
• Immunosupression (ATCH)- initial phase
• Steroidal therapy- maintenance
• Beta-Interferon – treatment of relapses
• Immuno Globulin g - prevention of relapse