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
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