Presented By : Ms. Dorjee Dolkar

Multiple Sclerosis

Multiple SclerosisChronic, progressive, degenerativedisorder of the CNS characterized bydisseminated demyelination of nerve

fibers of the brain and spinal cord

INCIDENCEUsually affects young to middle- aged adults, with onset between 15 and 50 years of age

Women affected more than men

EtiologyUnknown cause

Related to infectious, immunologic, and genetic factors

EtiologyPossible precipitating factors

include Infection Environmental factor-Vitamin D Immunologic reaction Sex hormone Genetic factorPoor state of health

PATHOPHYSIOLOGY

AN AUTOIMMUNE PROCESS TRIGGERED BY GENETIC AND ENVIRONMENTAL FACTORS.

INFLAMMATION OF VENULES IN THE CNS AND CAUSE DISRUPTION OF BLOOD-BRAIN BARRIER

ALLOWING LYMPHOCYTES TO ENTER CNS TISSUE.

THESE LYMPHOCYTES PROLIFERATE AND PRODUCE IgG WHICH RELEASE INFLAMMATORY CHEMICALS CAUSE EDEMA

ACUTE ATTACK

PATHOPHYSIOLOGY

REPEATED INFLAMMATORY ATTACK

MYELIN IS DEMAGED AND SEGMENT OF AXON BECOME TOTALLY DEMYELINATED AND

DEGENRATED

ASTROCYTE PROLIFERATES IN DEMAGE REGION OF CNS ( A PROCESS CALLED GLIOSIS).

PLAGUE ( GREY AND PINKISH LESION IN THE CNS).

CHRONIC LESION

WHEN NERVE IMPULSE TRAVEL DOWN AN AXON DEMAGED BY MS.

SLOW AND WEAK AS THEY PASS ACROSS THE DEMYLENATED AREAS.

IMPULSE BLOCKED ENTIRELY WHEN AXON DEGENRATED.

EXTREMITY WEAK, PARESTHESIA, VISUAL DISTURBANCES, ETC.

ABNORMAL NERVE IMPULSE

TRANSMISSION

Pathophysiology

Pathogenesis of MS

Fig. 57-1

Multiple SclerosisClinical ManifestationsVague symptoms occur

intermittently over months and years

MS may not be diagnosed until long after the onset of the first symptom

Multiple Sclerosis Clinical ManifestationsCommon signs and symptoms include

Visual, motor, sensory, cerebellar, and

emotional problems

Multiple Sclerosis Clinical ManifestationsMotor manifestations

◦Weakness or paralysis of limbs, trunk, and head.

◦Diplopia (double vision)◦Scanning speech◦Spasticity of muscles

Multiple Sclerosis Clinical Manifestations

Sensory manifestations◦Numbness and tingling◦Blurred vision◦Vertigo and tinnitus◦Decreased hearing◦Chronic neuropathic pain

Multiple SclerosisClinical Manifestations

Cerebellar manifestations◦Nystagmus Involuntary eye movements

◦Ataxia◦DysarthriaLack of coordination in articulating speech

◦DysphagiaDifficulty swallowing

Multiple SclerosisClinical Manifestations

Emotional manifestations

◦Anger◦Depression◦Euphoria

Multiple Sclerosis Other Clinical Manifestations

Bowel and bladder functions

◦Constipation◦Spastic bladder: small capacity for urine results in incontinenceFlaccid bladder: large capacity for urine and no sensation to urinate

Multiple Sclerosis Other Clinical ManifestationsSexual dysfunction Erectile dysfunction Decreased libidoDifficulty with orgasmic response

Painful intercourseDecreased lubrication

Clinical Courses Of MS Relapsing- Remitting MS

Primary Progressive MS

Secondary Progressive MS

Progressive Relapsing MS

Multiple Sclerosis Diagnostic StudiesBased primarily on history, clinical

manifestations, and physical examination.

Certain laboratory tests are used as adjuncts to clinical exam

Multiple SclerosisDiagnostic StudiesMRI – demonstrates presence of

plaques

Spinal Tap / Lumbar Puncture: tested for infection.

Evoked Potential Test: Monitor brain wave respond to what you see and hear.

Multiple Sclerosis Pharmacological Management

Drug Therapy◦CorticosteroidsTreat acute exacerbations by reducing edema and inflammation at the site of demyelination

Do not affect the ultimate outcome or degree of residual neurologic impairment from exacerbation

Cont….◦Immunosuppressive Therapy Azathioprine (Imuran) Cyclophosphamide ( cytoxan)Because MS is considered an autoimmune disease

Potential benefits counterbalanced against potentially serious side effects

Cont…..Antispasmotics (muscle relaxants)

Baclofen (Lioresal) Dantrolene ( Dantrium) Diazepam (Valium) To relieve muscle spasm.

Multiple Sclerosis Collaborative CarePhysical therapy helps

Relieve spasticity Increase coordination Train the patient to substitute

unaffected muscles for impaired ones

Multiple Sclerosis Collaborative CareNutritional therapy includes

megavitamins and diets consisting of low- fat, gluten-free food, and raw vegetables

High-protein diet with supplementary vitamins is often prescribed

PLASMAPHERESIS:

This therapy is to remove inflammatory agents such as T-lymphocytes through exchange plasma while suppressing immune response and inflammation.

Surgical Management:

ACHILLES TENOTOMY:

Indicated to severe spasticity and deformity.

Relieve foot drop from sever plantar flexion by transected the achilles tendon.

Multiple Sclerosis Nursing AssessmentHealth History

Risk factors

Precipitation factors

Clinical manifestations

Multiple Sclerosis Nursing DiagnosesIneffective airway clearance r/t

decreased cough mechanism. Risk for injury r/t blurred vision as

evidenced by unable to see clearily.

Altered nutrition less than body requirement r/t dysphagia as evidenced by inability to control spasticity.

Activity intolerence r/t fatigue as evidenced by unable to perform ADLs.

Myasthenia Gravis“Grave Muscle Weakness”

Myasthenia GravisAutoimmune disease affecting the

neuromuscular junction Not a brain disorder – brain

functions normally Characterized by fluctuating muscle

weakness and fatigability Disease may be generalized or

ocular specific

INCIDENCEOccurs in all races MG affects 14 per 100,000 people in the

United States Can affect any age groupWomen – peak incidence 20's to 30'sMen – peak incidence 50's to 60'sThree times more common in women

than men More common in asian race than other

CAUSESNo single cause has been identified Abnormal thymus tissue found in

most patients with MG Thymic tumors found in 15% of

patients Virus infections have been found in

some cases and are a suspected cause

Antibodies blocking Acetylcholine.

Genetic FactorsMyasthenia Gravis is not a

genetically inherited disease Some families appear to carry a

gene that increases the risk for developing the disease

No specific gene has been identified and there are no tests for genetic screening

Exacerbation Trigger Factors

InfectionStressFatigueCathartics (laxatives)Heat (sauna, hot tubs, sunbathing)

Pathophysiology

Signs and Symptoms Affects any of the muscles that you control

voluntarily, certain muscle groups are more commonly affected than others OCULAR AND FACIAL MUSCLE:

Difficulty speaking (dysarthria) Difficulty swallowing (dysphagia), Drooping eyelids (ptosis) Double vision (diplopia) Nasal-sounding speech and weak neck muscles that

give the head a tendency to fall forward or backward. 

Musculoskeletal System:

o Weakness and Fatigue

Immobility

Decreased function of limbs

Respiratory System

Weakening of intercostal muscle.

Decreased diaphragm movement

Breathlessness and dyspnea Poor gas exchange

Nutritional Dysphagia Decreased ability to move

tongue Inability to feed self Weight loss Dehydration Aspiration

Cont…..Symptoms tend to progress over

time, usually reaching their worst within a few years after the onset of the disease

Worsening muscle weakness with repeat activity

Diagnosis testEdrophonium test (Tensilon)

Antiacetylcholine receptor antibody serum level

Pulmonary Function Test

Single-fiber electromyography (EMG)

Imaging scans Eg: CT or MRI

Tensilon TestInjection may result in a sudden,

although temporary, improvement in muscle strength — an indication of myasthenia gravis. Acts to block an enzyme that breaks down acetylcholine, the chemical that transmits signals from nerve endings to muscle receptor sites.

Diet/NutritionEat small meals and snacks five to six

times a dayAvoid using low fat or diet products when

possibleAvoid eating lemons or tonic waterEat warm rather than hot food Runny or puree diet when swallowing is

difficultAlternate sips of liquid to avoid food from

stickingAVOID eating chewy or dry crumbly foods

Medications/TreatmentImmunosuppressive Therapy

PrednisoneAzathioprine

Acetylcholinesterase InhibitorsFirst line of therapy Neostigmine bromide

(Pyridostigmine)Edrophonium chloride (Tensilon)

Surgical ManagementThymectomy

Removal of thymus gland.• Recommended to those

who gets dysphagia due to thymus gland.

• Thymus tumor

Nursing Diagnosis: Risk for injury r/t ptosis as

evidenced by loss os motor control.

Ineffective airway clearance r/t nonproductive cough as manifested by decreased rib cage movement.

Impaired swallowing r/t fatigue and dysphagia as manifested by unable to swallow food.

Cont..

Impaired social interaction r/t change in body image as evidenced by decreased motor function.

Fatigue r/t increased energy need for muscle movement as evidenced by unable to perform ADL’s.

Ineffective therapeutic regimen r/t insufficient knowledge as evidenced by depression and potential for complication.

Myasthenic Crisis VS. Cholinergic CrisisMyasthenic Crisis

Under medication Increased HR/BP/RR Bowel and bladder

incontinence Decreased urine output Absent cough and

swallow reflex May need mechanical

ventilation Temporary improvement

of symptoms with administration of Tensilon

Cholinergic CrisisOvermedication

Decreased BP Abd cramps N/V, Diarrhea Blurred vision Pallor Facial muscle twitching Constriction of pupils Tensilon has no effect Symptoms improve with

administration of anticholinergics (Atropine)

Patient Teaching Teach patient/family disease process,

complications, and treatments Teach patient about their medications uses

dosage etc Teach medications to use with caution d/t

muscle exacerbationBeta blockers, calcium channel

blockers, quinine, quinidine, procainamide, some antibiotics, neuromuscular blocking agents

Avoid certain medications D-penicillinamine, A-interferon,

botulinum toxin

Cont……..Teach of both Myasthenic Crisis and

Cholinergic CrisisHelp patient plan daily activity to coincide

with energy peaksStress need for rest periods Explain that exacerbations, remissions,

and daily fluctuations are commonAvoid strenuous exercise, stress, infection,

exposure to hot or cold temperaturesTeach patient to wear medic-alert bracelet

PrognosisChronic disease with periods of

exacerbation and sometimes remissions

Disease course is highly variable Symptoms respond well to

treatment and in most cases the patient can live a normal or nearly normal life

Ocular Myasthenia has the best prognosis

SUMMARY

THANK YOU