2. Multiple Sclerosis
Chronic, progressive, degenerative
disorder of the CNS characterized
by
disseminated demyelination of
nerve
fibers of the brain and spinal cord
5. Etiology
Possible precipitating factors include
Infection
Environmental factor-Vitamin D
Immunologic reaction
Sex hormone
Genetic factor
Poor state of health
7. 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
8. 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
9. 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
12. Multiple Sclerosis
Clinical Manifestations
Vague symptoms occur intermittently
over months and years
MS may not be diagnosed until long
after the onset of the first symptom
18. 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
19. Multiple Sclerosis
Other Clinical Manifestations
Sexual dysfunction
Erectile dysfunction
Decreased libido
Difficulty with orgasmic
response
Painful intercourse
Decreased lubrication
20. Clinical Courses Of MS
Relapsing- Remitting MS
Primary Progressive MS
Secondary Progressive MS
Progressive Relapsing MS
21. Multiple Sclerosis
Diagnostic Studies
Based primarily on history, clinical
manifestations, and physical
examination.
Certain laboratory tests are used as
adjuncts to clinical exam
22. Multiple Sclerosis
Diagnostic Studies
MRI – demonstrates presence of
plaques
Spinal Tap / Lumbar Puncture: tested
for infection.
Evoked Potential Test: Monitor brain
wave respond to what you see and
hear.
23. Multiple Sclerosis
Pharmacological Management
Drug Therapy
◦ Corticosteroids
Treat 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
24. Cont….
◦ Immunosuppressive Therapy
Azathioprine (Imuran)
Cyclophosphamide ( cytoxan)
Because MS is considered an
autoimmune disease
Potential benefits
counterbalanced against
potentially serious side effects
26. Multiple Sclerosis
Collaborative Care
Physical therapy helps
Relieve spasticity
Increase coordination
Train the patient to substitute unaffected
muscles for impaired ones
27. Multiple Sclerosis
Collaborative Care
Nutritional therapy includes
megavitamins and diets consisting of
low- fat, gluten-free food, and raw
vegetables
High-protein diet with supplementary
vitamins is often prescribed
28. PLASMAPHERESIS:
This therapy is to remove
inflammatory agents such as T-
lymphocytes through exchange
plasma while suppressing immune
response and inflammation.
29. Surgical Management:
ACHILLES TENOTOMY:
Indicated to severe spasticity and
deformity.
Relieve foot drop from sever plantar
flexion by transected the achilles
tendon.
31. Multiple Sclerosis
Nursing Diagnoses
Ineffective 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.
35. Myasthenia Gravis
Autoimmune 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
36. INCIDENCE
Occurs in all races
MG affects 14 per 100,000 people in
the United States
Can affect any age group
Women – peak incidence 20's to 30's
Men – peak incidence 50's to 60's
Three times more common in women
than men
More common in asian race than other
37. CAUSES
No 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.
38. Genetic Factors
Myasthenia 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
43. 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.
47. 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
48. Diagnosis test
Edrophonium test (Tensilon)
Antiacetylcholine receptor antibody serum
level
Pulmonary Function Test
Single-fiber electromyography (EMG)
Imaging scans Eg: CT or MRI
49. Tensilon Test
Injection 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.
50. Diet/Nutrition
Eat small meals and snacks five to six
times a day
Avoid using low fat or diet products
when possible
Avoid eating lemons or tonic water
Eat warm rather than hot food
Runny or puree diet when swallowing
is difficult
Alternate sips of liquid to avoid food
from sticking
AVOID eating chewy or dry crumbly
foods
53. 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.
54. 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.
55. Myasthenic Crisis VS. Cholinergic Crisis
Myasthenic 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 Crisis
Overmedication
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)
56. 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 exacerbation
Beta blockers, calcium channel
blockers, quinine, quinidine,
procainamide, some antibiotics,
neuromuscular blocking agents
Avoid certain medications
D-penicillinamine, A-interferon,
botulinum toxin
57. Cont……..
Teach of both Myasthenic Crisis and
Cholinergic Crisis
Help patient plan daily activity to coincide
with energy peaks
Stress need for rest periods
Explain that exacerbations, remissions,
and daily fluctuations are common
Avoid strenuous exercise, stress, infection,
exposure to hot or cold temperatures
Teach patient to wear medic-alert bracelet
58. Prognosis
Chronic 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