Multiple sclerosis is a chronic autoimmune disease that affects the central nervous system by destroying myelin sheaths surrounding neurons. It is the most common disabling neurological disease in young adults. The exact cause is unknown but is thought to involve genetic and environmental factors. There are several types but most common is relapsing-remitting MS where periods of relapse with new or worsening symptoms are followed by periods of remission. Diagnosis involves MRI, lumbar puncture, and evoked potential tests. While there is no cure, treatments aim to reduce frequency and severity of relapses and manage symptoms. Nursing care focuses on managing symptoms like bladder dysfunction, fatigue, mobility issues, and providing emotional support.

1. MULTIPLE SCLEROSIS
MODERATOR : MRS Sibi Riju
Lecture CON
PRESENTER :Mr. Mahesh Kumar Sharma
M.Sc. nursing 1st year

2. NEURON

3. INTRODUCTION
It is an Auto Immune Disease which is when the body
starts to destroy itself.
 It is a life-long disease with no cure.
 In MS, the body attacks and destroys the fatty tissue
called myelin that insulates an axon/nerve, and is called
demyelination.
 If damage is severe it can also destroy the nerve/axon
itself.

4. CONT ..
 MS affects the central nervous system and inflames
the white matter in the brain which creates plaques.
White matter is below the top layer of our brain and
spinal cord. Plaques block a signal from being passed
from the body to the spinal cord and brain.
 Currently in the US, 250,000-300,000 people have
been diagnosed with MS and there are 200 new cases
diagnosed every week.

5. INCIDENCE
Women makes up 70-75 % cases of MS
Whites are commonly affected
Age of onset ranges from 10 to 50 yrs .the distribution
is bimodal ,with one peak at in mid 20s and other at mid
40s.

6. DEFINITION
• Multiple sclerosis is a chronic demyelinating disease
that affect the myelin sheath of neurons of central
nervous system.

7. ETIOLOGY , RISK FACTORS
• ETIOLOGY
Exact etiology not known
Environmental agent
Genetic susceptibility
• RISK FACTORS
Infection
Physical injury
Emotional stress
Pregnancy
Fatigue

11. CONT..

12. PATHOPHYSIOLOGY
T lymphocytes
Recognizes parts of CNS as foreign and
attack
Trigger inflammatory process

13. Damaging effects
Demyelination
Demyelination also plays an
important role with repeated attack
less affective demyelination
Multiple lesions are produced in the
CNS
Multiple lesions are produced in
the CNS

14. Clinical manifestation
Cranial nerve dysfunction
Blurred vision
Diplopia
Dysphagia
Facial, weakness ,numbness , pain

15. CONTD..
• Motor dysfunction
• Weakness
• Paralysis
• Spasticity
• Abnormal gait

16. CONTD..
• Sensory dysfunction
Paresthesia
Lhermitte’s sign
Decreased proprioception
Decreased temperature perception

17. CONTD..
Cerebellar dysfunction
Dysarthria
Tremor
Incoordination
Ataxia
Vertigo

18. CONTD..
• Bowel and bladder
dysfunction
• Fecal urgency
,constipation
,incontinence
• Urinary frequency
,urgency ,hesitancy
,nocturia,
retention,incontinence

19. CONTD..
Cognitive dysfunction
Decreased short term memory
Difficulty in learning
Decreased concentration
Mood alteration , short attention span
Sexual dysfunction
Fatigue

20. TYPES OF MS
I. Relapsing –remitting MS
II. Primary – progressive MS
III. Secondary – progressive MS
IV. Progressive – relapsing MS
V. Benign MS
VI. Malignant or fulminant MS

21. TYPE OF MS..

22. PROGRESSIVE RELAPSING
MS

23. RELAPSING-REMITTING
• Describes the initial course of 85 % to 90% of
individual with MS
• Characterized by unpredictable relapses followed by
periods of months to years of recovery
• Deficit suffered during the attacks may either
resolve or may be permanent
• When deficits always resolve between attacks this is
referred to as benign MS

24. CONT.
2 Primary progressive MS
• Gradual progression
• Superimposed relapse
• No remission
3 Secondary progressive MS
• It is characterized by gradual deterioration with or with out
acute relapse
• Initially remission and then gradually progress
• Neurological symptoms
• Cognitive functions worsens

25. CONT..
4 Progressive relapsing
• From the onset, gradual progression of disability
• Continuous disease progression
• Significant recovery immediately following a relapse
• Between relapses there is a gradual worsening of
symptoms

26. CONTD..

27. DIAGNOSTIC EVALUATION
• HISTORY
• viral infection
• precipitating factors
• family history
• signs and symptoms
• Sexual history
• mental status examination
• cranial nerve examination
• motor deficit
• sensory examination
• Cerebellar functions

28. DIAGNOSIS
MRI brain
MRI spine
Evoked potentials
Lumbar puncture
EEG
PET

29. CT- SCAN

30. CSF ANALYSIS
• protein, IgG,oligoclonal
lgG bands ,Myelin
basic protein

31. EVOKED POTENTIAL TEST
• To assess nerve conduction
• Response measured using EEG readings
Three main types
• visually evoked potential (VEP)
• Brain stem auditory evoked response (BAER)
• Somatosensory evoked potential {SSEP)

32. DIFFERENTIAL DIAGNOSIS
• Lyme disease
• Neurosyphilis
• Sarcoidosis
• SLE
• HIV associated myelopathy
• Polyarteritis nodosa
• tumors, cervical spondolysis
• Vitamin B12 deficiency

33. TREATMENT
• Medical management
• Surgical management
• Nursing management

34. CONT..
Aim
• Delay the progression of disease
• Manage chronic symptoms
• Treat acute exacerbations
• Generally palliative
• Immunotherapeutic drugs
• Methyl prednisolone
• ACTH
• Nonsteroidal immunosuppressive agents
• Azathioprine
• Cyclophosphamide
• Cyclosporine
• interferon's

35. MEDICAL MANAGEMENT
• Treat acute relapse
• IV or oral corticosteroids (prednisolone
,ACTH )
• Immunosuppressants (azathioprine ,
cyclophoshomide )
• Treat exacerbations
• Interferon β1b
• Interferon β1a
• Glatiramir acetate

36. CONTD..
• Symptomatic treatment
• Bladder dysfunction (oxybutin ,
propanthalene)
• Constipation ( psyllium hydrochloric
mucilloid ,bisacosyl)
• Fatigue ( amantadine )
• Tremor (propranalol ,clonazepam)

37. SURGICAL MANAGEMENT
• Intrathecal baclofen via surgically implantable pump
• Adductor tenotomy
• Dorsal rhizotomy
• Surgical diversion for urinary incontinence , retention
etc.
• Plastic surgery to cure decubitus ulcer
• No surgical intervention to alter the disease course of
MS.

38. NURSING MANAGEMENT
• Impaired urinary elimination R/T bladder dysfunction
• Fluid intake should be maintained at 2L/day
• Avoid fluid intake after evening meals
• Voiding to be attempted at every 3 hrs when
awake
• If voiding not successful-intermittent
catheterization
• Teach self catheterization

39. CONTD..
• Constipation R/T immobility and demyelination
high fiber diet ,bulk formers ,stool softners
Fluid intake ,2L/day
Laxatives and enemas to be AVOIDED because it
cause dependence
A bowel program to be performed
Rectal evacuation by glcerin ,bisacodyl
suppositories ,digital stimulation

40. CONTD..
• Activity intolerance R/T fatigue and muscle weakness
Assist client in planning his activities at his peak
energy level ,which is usually the morning
Periods of rest through out he day to be planned
Collaboration with physical and occupational
therapist helps a lot .Drug amantadine may help to
reduce fatigue

41. CONTD..
• Impaired physical mobility R/T weakness, contractures ,spasticity ,
ataxia
Spastic muscles can be stretched at least twice a day through
their full range of motion
Correct body alignment to prevent contractures
Use of splints is helpful
Ataxia and tremor lessened by small weights applied to distal
extremities

42. CONTD..
• Risk for self care deficit R/T muscle weakness
Client may require aids like wheel chairs ,or canes to perform
ADL and to ambulate
Teach client to use ADL aids
Table tops are adjusted at comfortable heights
Work in combination with physical therapist ,occupational
therapist and social worker

43. REFERENCES
• Ellen barker ; neurosciences nursing ; 2nd edition ; pg 685 –
718
• Joyce M Black ; medical surgical nursing ; 7th edition ; pg
2177-2189
• burner medical surgical nursing ;5th edition p.g. 1765- 17
• www . wikipedia .com

44. • thank all students for
attention