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Myasthenia Gravis

This is a mind map of myasthenia gravis. You can make and share your own mind maps easily. Just try EdrawMind mind mapping software for free! Myasthenia gravis (MG) is a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles. Myasthenia gravis affects the voluntary muscles of the body, especially those that control the eyes, mouth, throat, and limbs.

Edited at 2023-02-16 01:35:02

Ibrahim Saad ALSAFYAH AL-qahtani

Recent works View more works>>

Myasthenia Gravis

Ibrahim Saad ALSAFYAH AL-qahtani

Recent works View more works>>

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Myasthenia Gravis

Over view

a chronic, fluctuating, antibody-mediated autoimmune disorder

directed against the post-synaptic neuromuscular junctions of skeletal muscles

resulting in a wide spectrum of manifestations ranging from mild to potentially fatal

characterized by weakness and rapid fatigability of skeletal muscle

the patient is unable to maintain voluntary muscular contraction for more than brief periods

Pathophysiology of MG

In this disease, antibodies are produced against the main immunogenic region found on α1 subunits of the nicotinic receptor-channel complex.

Antibodies are detected in 85% of myasthenic patients

The antibodies reduce nicotinic receptor function in many ways

Cross-linking receptors, a process that stimulates their internalization and degradation

Causing lysis of the postsynaptic membrane; and Binding to the nicotinic receptor and inhibiting function

Reduced postsynaptic nicotinic (Nm)Rs normal muscles receptor density

Results in end-plate potentials of diminished amplitude which fail to

trigger action potentials in some fibres causing a failure in initiation of muscle fibre contraction – power of the whole muscle is reduced

The amount of ACh released per impulse normally declines on repeated activity (termed presynaptic rundown)

Etiology and Epidemiology of MG

IgG antibodies attack Ach nicotinic NmRs on SK. muscles.

Antibody-antigen complex and inflammation inhibit neuromuscular transmission.

Breakdown of immune tolerance involves thymus.

Afffects Women > men before age 50.

Peak onset 20-40 years

Men more commonly diagnosed ages 60-80.

It also occurs in children and adolescents.

MG is a hereditary disease transmitted genetically from parents.

Clinical Features of MG

Painless, Fluctuating weakness of voluntary muscles (fatigability)

Worsen after exertion and improve with rest.

Exacerbating factors include

emotional stress

rapid changes in body temperature

infection

trauma

multiple medications

Ocular manifestations is common

diplopia

ptosis

Ocular MG 10-40% of all cases

Generalized MG symptoms vary based on muscle groups

oropharyngeal

skeletal

respiratory

Ocular symptoms

Initial symptoms involve the ocular muscles in 60% of cases

All patients will have ocular involvement within 2 years of disease onset

Ocular manifestations

Ptosis

uni- or bilateral is very common and may occur while patients reading, or during long period of driving

Diplopia

Extraocular muscle weakness may also present asymmetrically

Limb muscles weakness

Initial symptoms in fewer than 10%

Upper extremities weakness is more common than lower extremities, asymmetrical.

Involve proximal muscles than distal

Involve neck muscles: neck flexion weaker than neck extension

Respiratory insufficiency

The initial presentation is rare

Occurring precipitously in a patient with recent worsening of symptoms

MG: Classification

MG Foundation of America Clinical Classification

Grade I: Any ocular muscle weakness

Grade II: Mild weakness affecting other than ocular muscles

IIa: limb and/or axial weakness; less oropharyngeal involvement

IIb: oropharyngeal and/or respiratory weakness

Grade III: Moderate weakness affecting other than ocular muscles (a,b)

Grade IV: Severe weakness affecting other than ocular muscles (a,b)

Grade V: Defined by tracheal intubation.

Myasthenia Gravis: Diagnosis

Clinical manifestations

chronic intermittent muscle weakness;

Fatigability.

Provocative test

Physiologic tests

Look up for several minutes; counting aloud to100; repetitively testing the proximal muscles

Pharmacological tests

Pharmacological test

Curare test

to demonstrate generalized MG

Edrophonium test

Using edrophonium chloride: short acting acetylcholinesterase inhibitor

10 mg of edrophonium (0.15-0.2 mg/kg, iv) used

It causes rapid dramatic improvement of MG symptoms

A small test dose (2 mg) iv; If after 1 min. no improvement and side effect appeared, the remainder given slowly.

The effect of edrophonium: appears in 30 sec. and last fewer than 10 min.

Treatment

The goal is to achieve remission

Goal

Symptoms free and taking no medication

By increased neuromuscular transmission

Reduce autoimmunity

Others: having a normal quality of life even if some signs

remaining and cholinesterase inhibitors taking

No single treatment is ideal for all patients

Each patient needs an individual plan

Treatment may have to be changed time to time

Types of Mg therapy

Symptomatic therapy

Acetylcholinesterase (AChE) inhibitors

Immune-directed therapy

Corticosteroids (high dose Prednisolone 100 mg/day)

Non-steroid immunomodulators

Azathioprine

Mycophenolate mofetil

Cyclosporine

Cyclophosphamide

Tacrolimus

Rituximab

Acetylcholinesterase inhibitors (AChEIs)

Ex Neostigmine, Pyridostigmine

Benefit most patients but incomplete after weeks or months treatment; require further therapeutic measures

Ex Neostigmine, Pyridostigmine

Mechanism

Synthetic acetylcholinesterase inhibitors, inhibit the hydrolysis of the acetylcholine neurotransmitter in the synaptic cleft

These agents increase the number of interactions between the acetylcholine and the acetylcholine Nm receptors in the neuromuscular junction.

AChEIs do not cross the blood–brain barrier, thereby limiting central nervous system toxicity, and may be mildly effective in ocular and generalized MG.

Pyridostigmine (Mestinon)

This compound, which structurally resembles neostigmine, share its pharmacological actions

It has, longer duration of action and lower incidence of side effects

It is used in the treatment of myasthenia gravis

Ambenonium (Mytelase)

This is a synthetic quaternary ammonium compound

has longer duration of action and lower incidence of side effects than neostigmine

It is available for oral use in the treatment of myasthenia gravis in a dose of 10-30 mg every 4 hours

Edrophonium (Tensilon)

Edrophonium, structurally related to neostigmine

has a rapid onset and a brief duration of action

It is used in the diagnosis of suspected cases of myasthenia gravis.

and in the treatment of curare poisoning (10 mg I.V. repeated as required)

It can also be used to terminate attacks of paroxysmal supraventricular tachycardia.

Other uses of AChEIs

Antidote to competitive neuromuscular blockers

To hasten recovery from respiratory paralysis produced by overdose from competitive neuromuscular blocking agents (e.g. d-tubocurarine) , neostigmine 1-3 mg I.V. combined with 0.6-1.2 mg atropine may be used

Side effects

The reversible anti-ChE produce side effects attributable mainly to their muscarinic actions

salivation

sweating

lacrimation

diarrhea

sense of constriction in the chest

abdominal cramps

bradycardia and hypotension

Contraindications

Bronchial asthma.

Peptic ulcer.

Coronary insufficiency.

Hyperthyroidism.

Other Treatment of MG

Acute management therapies

Plasmapheresis (plasma transfusion)

IV IG Infusion

Surgical intervention (Thyroidectomy) .

Cholinergic crisis (Ch-Cr)

It is a condition results from toxicity by anticholinesterases agents either the reversible or the irreversible (organophosphate-OPC) groups.

Its Symptoms similar to that of MG including; fatigue, muscle weakness, and even paralysis.

Differential diagnosis of (Ch-Cr from MG)

Clinical investigation

Ch-Cr is accompanied with progressive muscarinic symptoms (salivation, lacrimation, colic, bradycardia,…etc)

Edrophonium (eserine) test

(5 mg/kg I.V.)

If the case is MG

Improvement of symptoms

If the case is Ch-Cr

Worsening the symptoms