2. DEFINITION:
Myasthenia
gravis (abbreviated
as MG) is an
autoimmune neuro
muscular
disease leading to
fluctuating muscle
weakness and fatigibility.
It is a type
of autoimmune
disorders.

3. CLASSIFICATION:
•Class I: Any eye muscle weakness, possible ptosis, no other evidence of
muscle weakness elsewhere
•Class II: Eye muscle weakness of any severity, mild weakness of other
muscles
1)Class II a: Predominantly limb or axial muscles
2)Class II b: Predominantly bulbar and/or respiratory muscles
•Class III: Eye muscle weakness of any severity, moderate weakness of
other muscles
1)Class III a: Predominantly limb or axial muscles
2)Class III b: Predominantly bulbar and/or respiratory muscles
•Class IV: Eye muscle weakness of any severity, severe weakness of other
muscles
1)Class IV a: Predominantly limb or axial muscles
2)Class IV b: Predominantly bulbar and/or respiratory muscles (Can
also include feeding tube without intubation)
•Class V: Intubation needed to maintain airway.

5. SYMPTOMS:
The first noticeable symptom is
weakness of the eye
muscles, difficulty in swallowing
and slurred speech may also be the
first signs.
Muscles that control eye and
eyelid movement, facial
expressions, chewing, talking
and swallowing becomes
weaker.
The muscles that
control breathing and neck and
limb movements can also be
affected.

6. Symptoms: Ptosis(dropping of eye lid)
(1) (2)

7. CAUSES OF
MYASTHENIA GRAVIS:
It occurs when normal
communication between the
nerve and muscle is
interrupted at the
neuromuscular junction
.Normally when impulses
travel down the nerve, the
nerve endings release a
neurotransmitter substance
called acetylcholine which
travels from the
neuromuscular junction and
binds to acetylcholine
receptors which are activated
and generate a muscle
contraction.

8. Causes:
In MG, the auto antibodies
most commonly act
against the nicotinic
acetylcholine
receptor (nAChR),the r
eceptor in the motor
end plate for the
neurotransmitter acet
ylcholine that stimulates
muscular contractions.
Some forms of the
antibody impair the ability
of acetylcholine to bind to
receptors thus preventing
muscle contraction.

9. ROLE OF THYMUS:
The antibodies are produced
by plasma cells, derived from
B-cells. B-cells convert into
plasma cells by T-helper cell
stimulation. To carry out this
activation, T-helpers must
first be activated
themselves, which is done by
binding of the T-cell
receptor (TCR) to the
acetylcholine receptor
antigenic peptide fragment
(epitope). Since the thymus
plays an important role in the
development of T-cells, so it
is closely related with
myasthenia gravis.

10. DURING PREGNANCY:
Up to 10% of infants with parents affected by the condition
are born with transient (periodic) neonatal myasthenia
(TNM), which generally produces feeding
and respiratory difficulties. TNM usually presents as
poor suckling and generalized hypotonia (low muscle
tone). Immuno suppressive therapy should be
maintained throughout pregnancy, as this reduces the
chance of neonatal muscle weakness, as well as controls
the mother's myasthenia.

11. DIAGNOSIS:
• Physical examination(eyes, feet, arms)
• Blood tests(for antibodies against acetylcholine
receptors)
• Electrodignostics(measure fatiguability of the
muscle)
• Ice test
• Edrophonium test(intravenous administration
of edrophonium chloride to increase acetylcholine)
• Imaging(x-ray of thymus)
• Pulmonary function test(lung function testing)
• Pathological findings(Muscle biopsy)

12. MEDICATION:
Acetylcholinesterase
inhibotors:
Neostigmine
Immunosuppressive
drugs:
prednisone

13. MANAGEMENT:
• Plasmapheresis can be used to remove the
putative antibodies from the circulation.
Plasmapheresis is a blood purification procedure
used to treat several autoimmune diseases.
• Surgery:Thymectomy, the surgical removal
of the thymus, is essential in cases
of thymoma.
• Physical activity:Exercise participation