MULTIPLE SCLEROSIS

MODERATOR : MRS Sibi RijuLecture CON

PRESENTER :Mr. Mahesh Kumar SharmaM.Sc. nursing 1st year

NEURON

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.

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.

INCIDENCEWomen 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.

DEFINITION • Multiple sclerosis is a chronic demyelinating disease

that affect the myelin sheath of neurons of central nervous system.

ETIOLOGY , RISK FACTORS

• ETIOLOGYExact etiology not knownEnvironmental agentGenetic susceptibility

• RISK FACTORSInfectionPhysical injuryEmotional stressPregnancyFatigue

CONT..

PATHOPHYSIOLOGY

T lymphocytes

Recognizes parts of CNS as foreign and attack

Trigger inflammatory process

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

Clinical manifestationCranial nerve dysfunction

Blurred visionDiplopiaDysphagiaFacial, weakness ,numbness , pain

CONTD..• Motor dysfunction

• Weakness• Paralysis• Spasticity• Abnormal gait

CONTD..• Sensory dysfunction

ParesthesiaLhermitte’s signDecreased proprioceptionDecreased temperature perception

CONTD..Cerebellar dysfunction

DysarthriaTremorIncoordinationAtaxiaVertigo

CONTD..

• Bowel and bladder dysfunction

• Fecal urgency ,constipation ,incontinence

• Urinary frequency ,urgency ,hesitancy ,nocturia, retention,incontinence

CONTD..Cognitive dysfunction

Decreased short term memoryDifficulty in learning Decreased concentrationMood alteration , short attention span

Sexual dysfunction

Fatigue

TYPES OF MSI. Relapsing –remitting MSII. Primary – progressive MSIII. Secondary – progressive MSIV. Progressive – relapsing MSV. Benign MSVI. Malignant or fulminant MS

TYPE OF MS..

PROGRESSIVE RELAPSING MS

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

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

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

CONTD..

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• reflexes

DIAGNOSISMRI brainMRI spineEvoked potentialsLumbar punctureEEGPET

CT- SCAN

CSF ANALYSIS• protein, IgG,oligoclonal

lgG bands ,Myelin basic protein

EVOKED POTENTIAL TEST

• To assess nerve conduction• Response measured using EEG readingsThree main types• visually evoked potential (VEP) • Brain stem auditory evoked response (BAER)• Somatosensory evoked potential {SSEP)

DIFFERENTIAL DIAGNOSIS

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

TREATMENT• Medical management

• Surgical management

• Nursing management

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

MEDICAL MANAGEMENT

• Treat acute relapse• IV or oral corticosteroids

(prednisolone ,ACTH )• Immunosuppressants (azathioprine ,

cyclophoshomide )

• Treat exacerbations• Interferon β1b• Interferon β1a• Glatiramir acetate

CONTD..• Symptomatic treatment

• Bladder dysfunction (oxybutin , propanthalene)

• Constipation ( psyllium hydrochloric mucilloid ,bisacosyl)

• Fatigue ( amantadine )• Tremor (propranalol ,clonazepam)

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.

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

CONTD..• Constipation R/T immobility and demyelination

high fiber diet ,bulk formers ,stool softnersFluid intake ,2L/dayLaxatives and enemas to be AVOIDED because it

cause dependenceA bowel program to be performedRectal evacuation by glcerin ,bisacodyl

suppositories ,digital stimulation

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 plannedCollaboration with physical and occupational

therapist helps a lot .Drug amantadine may help to reduce fatigue

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 contracturesUse of splints is helpfulAtaxia and tremor lessened by small weights applied to distal

extremities

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 aidsTable tops are adjusted at comfortable heightsWork in combination with physical therapist ,occupational

therapist and social worker

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

• thank all students for attention