Myasthenia gravis
Myasthenia gravis (MG) is a neuromuscular disease
that leads to uctuating muscle weakness and fatigue. In
the most common cases, muscle weakness is caused by
circulating antibodies that block nicotinic acetylcholine
receptors at the postsynaptic neuromuscular junction. By
blocking the ability of the neurotransmitter acetylcholine
to bind to these receptors in the muscle, these antibod-
ies keep motor neurons from signaling the muscle to con-
tract. Alternatively, in a much rarer form, muscle weak-
ness is caused by a genetic defect in some portion of the
neuromuscular junction that is inherited at birth as op-
posed to developing through passive transmission from
the mothers immune system at birth or through autoim-
munity later in life.[1]
Myasthenia is treated with medications such as
acetylcholinesterase inhibitors or immunosuppressants,
and, in selected cases, thymectomy (surgical removal of
the thymus gland).
The disease is diagnosed in 3 to 30 people per million
per year.[2] Diagnosis is becoming more common due to
increased awareness.[2] The condition occurs more fre-
quently in women than in men and begins most com-
monly between ages 20 and 40 years of age.[3] The word
is from Greek muscle, Greek asthenia weakness,
and Latin: gravis serious. 1.3
1 Signs and symptoms
The initial, main symptom in MG is painless weakness of
specic muscles, not fatigue.[4] The muscle weakness be-
comes progressively worse during periods of physical ac-
tivity, and improves after periods of rest. Typically, the
weakness and fatigue are worse towards the end of the
day.[5] MG generally starts with ocular (eye) weakness;
it might then progress to a more severe generalized form,
characterized by weakness in the extremities or while per-
forming basic life functions.[6]
1.1 Eyes
In about two-thirds of individuals, the initial symptom
of MG is related to the muscles around the eye.[4] There
may be eyelid drooping (ptosis due to weakness of levator
palpebrae superioris)[7] and double vision (diplopia,[4]
due to weakness of the extraocular muscles).[5] Eye
symptoms tend to get worse when watching television,
reading or driving, particularly in bright conditions.[4]
1
Consequently, some aected individuals choose to wear
sunglasses.[4] The term ocular myasthenia gravis de-
scribes a subtype of MG where muscle weakness is con-
ned to the eyes, i.e. extraocular muscles, levator palpe-
brae superioris and orbicularis oculi.[7] Typically, this
subtype evolves into generalized MG, usually after a few
years.[7]
1.2 Eating
Weakness of the muscles involved in swallowing may
lead to swallowing diculty (dysphagia). Typically, this
means that some food may be left in the mouth after
an attempt to swallow,[8] or food and liquids may re-
gurgitate into the nose rather than go down the throat
(velopharyngeal insuciency).[5] Weakness of the mus-
cles that move the jaw (muscles of mastication) may
cause diculty chewing. In individuals with MG, chew-
ing tends to become more tiring when chewing tough,
brous foods.[4] Diculty in swallowing, chewing and
speaking is the rst symptom in about one-sixth of
individuals.[4]
Voice
Weakness of the muscles involved in speaking may lead
to dysarthria and hypophonia.[4] Speech may be slow
and slurred,[9] or have a nasal quality.[5] In some cases
a singing hobby or profession must be abandoned.[8]
1.4 Head and neck
Due to weakness of the muscles of facial expression and
muscles of mastication, there may be facial weakness,
manifesting as inability to hold the mouth closed[4] (the
hanging jaw sign), and a snarling appearance when at-
tempting to smile.[5] Together with drooping eyelids, fa-
cial weakness may make the individual appear sleepy
or sad.[4] There may be diculty in holding the head
upright.[9]
1.5 Other
The muscles that control breathing (dyspnea) and limb
movements can also be aected, but rarely do these
present as the rst symptoms of MG, and they develop
over months to years.[10] In a myasthenic crisis, a paralysis
2 3 PATHOPHYSIOLOGY

of the respiratory muscles occurs, necessitating assisted

ventilation to sustain life.[11] Crises may be triggered by
various biological stressors such as infection, fever, an ad-
verse reaction to medication, or emotional stress.[11]

2 Cause
This neuromuscular disease is caused by transmission de-
fects in nerve impulses to muscles. The neuromuscu-
lar junction is apparently aected: acetylcholine, which
produces muscle contraction under normal conditions no
longer produces the contractions necessary to muscle
movement.[12]
The nicotinic acetylcholine receptor

3 Pathophysiology system malfunctions and attacks the bodys tissues. The

antibody in myasthenia gravis attacks normal human pro-
tein, targeting a protein called an acetylcholine receptor,
or a related protein called a muscle-specic kinase.[13]
Human leukocyte antigens have been associated with MG
susceptibility. Many of these genes are present among
other autoimmune diseases. Relatives of MG patients
have a higher percentage of other immune disorders.[14]
The thymus gland cells form part of the bodys immune
system. In those with myasthenia gravis, the thymus
gland is large and abnormal. It sometimes contains clus-
ters of immune cells which indicate lymphoid hyperpla-
sia, and it is believed the thymus gland may give wrong
instructions to immune cells.[15]

3.1 Associated conditions

Myasthenia gravis is associated with various autoimmune
Neuromuscular junction: 1. Axon 2. Muscle cell membrane
diseases, including:
3. Synaptic vesicle 4. Nicotinic acetylcholine receptor 5.
Mitochondrion Thyroid diseases,[16]
CNS disease[17]
Lupus[18]

3.2 In pregnancy
For women who are pregnant and already have MG, in a
third of cases they have been known to experience an ex-
acerbation of their symptoms, and in those cases it usu-
ally occurs in the rst trimester of pregnancy.[19] Signs
and symptoms in pregnant mothers tend to improve dur-
ing the second and third trimesters. Complete remission
can occur in some mothers.[20] Immunosuppressive ther-
apy should be maintained throughout pregnancy, as this
reduces the chance of neonatal muscle weakness, as well
A juvenile thymus shrinks with age.
as controls the mothers myasthenia.[21]
Myasthenia gravis is believed to be caused by variations 10-20% of infants with mothers aected by the con-
in certain genes. The disorder occurs when the immune dition are born with Transient Neonatal Myasthenia,
4.3 Blood tests 3

which generally produces feeding and respiratory di- 4.3 Blood tests
culties that develop within 12 hours to several days af-
ter birth.[19][21] A child with TNM typically responds If the diagnosis is suspected, serology can be performed:
very well to acetylcholinesterase inhibitors, and the con-
dition generally resolves over a period of three weeks as One test is for antibodies against the acetylcholine
the antibodies degregate and generally does not result in receptor,[22] the test has a reasonable sensitivity of
any complications.[19] Very rarely, an infant can be born 8096%, but in ocular myasthenia, the sensitivity
with arthrogryposis multiplex congenita, secondary to falls to 50%.
profound intrauterine weakness. This is due to maternal
antibodies that target an infants acetylcholine receptors. A proportion of the patients without antibodies
In some cases, the mother remains asymptomatic.[21] against the acetylcholine receptor have antibodies
against the MuSK protein.[26]

In specic situations, testing is performed for

4 Diagnosis Lambert-Eaton syndrome.[27]

MG can be dicult to diagnose, as the symptoms can be

subtle and hard to distinguish from both normal variants 4.4 Electrodiagnostics
and other neurological disorders.[22]
Three types of myasthenic symptoms in children can be
distinguished:[23]

1. Transient Neonatal: occurs in 10 to 15% of babies

born to mothers aicted with the disorder, and dis-
appears after a few weeks.
2. Congenital: the rarest form; genes are present in
both parents.
3. Juvenile myasthenia gravis: most common in fe-
males

Congenital myasthenias cause muscle weakness and fati-

A chest CT-scan showing a thymoma (red circle)
gability similar to those of MG. The signs of congen-
ital myasthenia usually are present in the rst years of
childhood although they may not be recognized until
adulthood.[24]

4.1 Classication
When diagnosed with MG, a person is assessed for his
or her neurological status and the level of illness is estab-
lished. This is usually done using the accepted Myasthe-
nia Gravis Foundation of America Clinical Classication
scale, which is as follows:
4.2 Physical examination
During a physical examination to check for MG, a doc-
tor might ask the potentially aected person to look at
a xed point for 30 seconds and to relax the muscles of
their forehead. This is done because a person with MG
and ptosis of their eyes might be involuntarily using their
forehead muscles to compensate for the weakness in their
eyelids.[22] The clinical examiner might also try to elicit
the curtain sign in a patient by holding one of the per-
sons eyes open, which in the case of MG will lead the
other eye to close.[22]
Photograph of a patient showing right partial ptosis (left picture),
the left lid shows compensatory pseudo lid retraction because of
equal innervation of the levator palpabrae superioris (Herings
law of equal innervation): Right picture: after an edrophonium
test, note the improvement in ptosis.
Muscle bers of patients with MG are easily fatigued,
and a test called the repetitive nerve stimulation test can
be performed. In single-ber electromyography, which is
considered to be the most sensitive (although not the most
specic) test for MG,[22] a thin needle electrode is in-
serted into dierent areas of a particular muscle to record
the action potentials from several samplings of dierent
individual muscle bers. Two muscle bers belonging
to the same motor unit are identied, and the temporal
variability in their ring patterns is measured. Frequency
and proportion of particular abnormal action potential
patterns, called jitter and blocking, are diagnostic.
Jitter refers to the abnormal variation in the time inter-
val between action potentials of adjacent muscle bers
4 5 MANAGEMENT

in the same motor unit. Blocking refers to the failure of 5.1 Medication
nerve impulses to elicit action potentials in adjacent mus-
cle bers of the same motor unit.[28]

4.5 Ice test N O

Applying ice for two to ve minutes to the muscles re- N
portedly has a sensitivity and specicity of 76.9% and
98.3%, respectively, for the identication of MG. Acetyl-
cholinesterase is thought to be inhibited at the lower tem-
O
perature, and this is the basis for this diagnostic test. This
generally is performed on the eyelids when a ptosis is
present and is deemed positive if there is a 2mm raise
Neostigmine, chemical structure
in the eyelid after the ice is removed.[29]

4.6 Edrophonium test

This test requires the intravenous administration of

edrophonium chloride or neostigmine, drugs that block
the breakdown of acetylcholine by cholinesterase
(acetylcholinesterase inhibitors).[30] This test is no longer
typically performed as its use can lead to life-threatening
bradycardia (slow heart rate) which requires immediate
emergency attention.[31] Production of edrophonium was
discontinued in 2008.[11]

4.7 Imaging

A chest X-ray may identify widening of the mediastinum

suggestive of thymoma, but computed tomography or
magnetic resonance imaging (MRI) are more sensitive
ways to identify thymomas and are generally done for this
reason.[32] MRI of the cranium and orbits may also be
performed to exclude compressive and inammatory le-
sions of the cranial nerves and ocular muscles.[33]

4.8 Pulmonary function test

The forced vital capacity may be monitored at intervals to
detect increasing muscular weakness. Acutely, negative
inspiratory force may be used to determine adequacy
of ventilation; it is performed on those individuals with
MG.[34][35]
5 Management
Treatment is by medication and/or surgery. Med-
ication consists mainly of acetylcholinesterase in-
hibitors to directly improve muscle function and
immunosuppressant drugs to reduce the autoimmune
process.[36] Thymectomy is a surgical method to treat
MG.[37]
Azathioprine, chemical structure
Acetylcholinesterase inhibitors can provide symptomatic
benet and may not fully remove a persons weakness
from MG.[38] While they might not fully remove all symp-
toms of MG, they still may allow a person the ability
to perform normal daily activities.[38] Usually, acetyl-
cholinesterase inhibitors are started at a low dose and
increased until the desired result is achieved. If taken
30 minutes before a meal, symptoms will be mild dur-
ing eating, which is helpful for those who have di-
culty swallowing due to their illness. Another medica-
tion used for MG is atropine, which can reduce the mus-
carinic side eects of acetylcholinesterase inhibitors.[39]
Pyridostigmine is a short-lived drug, with a half-life of
about four hours with relatively few side eects.[40] Gen-
erally, it is discontinued in those who are being mechan-

ically ventilated as it is known to increase the amount of
salivary secretions.[40] There have been few high-quality
studies directly comparing cholinesterase inhibitors with
other treatments (or placebo); it has been suggested that
their practical benet is such that it would be dicult to
conduct studies in which they would be withheld from
some people.[41] The steroid prednisone might also be
utilized to achieve a better result, but it can lead to the
worsening of symptoms for 14 days and take 68 weeks
for it to achieve its maximal eectiveness.[40] Due to the
myriad symptoms that steroid treatments can cause, it is
not the preferred method of treatment.[40]
5.2 Plasmapheresis and IVIG
If the myasthenia is serious (myasthenic crisis),
plasmapheresis can be used to remove the putative
antibodies from the circulation. Also, intravenous
immunoglobulins (IVIGs) can be used to bind the
circulating antibodies. Both of these treatments have
relatively short-lived benets, typically measured in
weeks, and often are associated with high costs which
make them prohibitive; they are generally reserved for
when MG requires hospitalization.[40][42]
5.3 Surgery
Main article: Thymectomy
As thymomas are seen in 10% of all people with the MG,
patients are often given a chest X-ray and CT scan to eval-
uate their need for surgical removal of their thymus and
any cancerous tissue that may be present.[11][31] Even if
surgery is performed to remove a thymoma, it generally
does not lead to the remission of MG.[40] Surgery in the
case of MG involves the removal of the thymus although
there is no clear consensus that it would be benecial ex-
cept in the presence of a thymoma. However, thymec-
tomy should not be done in ocular myasthenia.[43] Cur-
rently, there is no literature that gives meaningful con-
clusions in regard to the benet of thymectomy in af-
fected individuals. Some observational studies indicate
that thymectomy could be prudent in MG.[43]
5.4 Physical measures
Patients with MG should be educated regarding the uc-
tuating nature of their symptoms, including weakness and
exercise-induced fatigue. Exercise participation should
be encouraged with frequent rest.[44] In people with gen-
eralized MG, some evidence indicates a partial home
program including training in diaphragmatic breathing,
pursed lip breathing, and interval-based muscle therapy
may improve respiratory muscle strength, chest wall mo-
bility, respiratory pattern, and respiratory endurance.[45]
5
6 Prognosis
The prognosis of MG patients is generally good, as is
quality of life, given very good treatment.[46] In the
early 1900s the mortality associated with MG was 70%;
now that number is estimated to be around 35% which
is attributed to increased awareness and medications
to manage symptoms.[40] Monitoring of a person with
MG is very important as at least 20% of people diag-
nosed with it will experience a myasthenic crisis within
two years of their diagnosis requiring emergent medical
intervention.[40] Generally, the most disabling period of
MG might be years after the initial diagnosis.[38]
7 Epidemiology
Myasthenia gravis occurs in all ethnic groups and both
sexes. It most commonly aects women under 40 and
people from 50 to 70 years old of either sex, but it has
been known to occur at any age. Younger patients rarely
have thymoma. The prevalence in the United States is
estimated between 0.520.4 cases per 100,000, with an
estimated 60,000 Americans aected.[11][47] Within the
United Kingdom, it is estimated that there are 15 cases
of MG per 100,000 people.[31]
8 History
The rst to write about MG were Thomas Willis,
Samuel Wilks, Erb, and Goldam.[7] The term myas-
thenia gravis pseudo-paralytica was proposed in 1895
by Jolly, a German physician.[7] Mary Walker treated a
person with MG with physostigmine in 1934.[7] Simp-
son and Nastuck detailed the autoimmune nature of the
condition.[7] In 1973, Patrick and Lindstrom used rab-
bits to show that immunization with puried muscle-like
acetylcholine receptors caused the development of MG-
like symptoms.[7]
9 Research
Immunomodulating substances, such as drugs that pre-
vent acetylcholine receptor modulation by the immune
system, are currently being researched.[48] Some research
recently has been on anti-c5 inhibitors for treatment re-
search as they are safe and used in the treatment of
other diseases.[49] Ephedrine seems to benet some peo-
ple more than other medications, but it has not been prop-
erly studied as of 2014.[50][51] In the laboratory myas-
thenia gravis is mostly studied in model organisms, such
as rodents. In addition, in 2015 scientists developed an
in vitro functional all-human neuromuscular junction as-
say from human embryonic stem cells and somatic mus-
6 11
cle stem cells. After addition of pathogenic antibodies
against the acetylcholine receptor and activation of the
complement system the neuromuscular co-culture shows
signs of disease such as weaker muscle contractions.[52]
10 Notable cases
Indian actor Amitabh Bachchan was diagnosed with
it in 1983.
Brandon Cox, starting Auburn quarterback from
2005-2007, nished with a record of 29-9.[53]
Weeb Ewbank, New York Jets coach
Henrique Mecking, Brazilian chess grandmaster
Christopher Robin Milne, the son of A. A. Milne,
author of the Winnie-the-Pooh books and the person
on whom Christopher Robin was based, lived with
myasthenia gravis for several years before his death
in 1996.[54]
Aristotle Onassis (1906-1975), Greek shipping
magnate and businessman, suered from the disease
[12] Information, National Center for Biotechnology; Pike, U.
during the last years of his life. S. National Library of Medicine 8600 Rockville; MD,
Actor Roger Smith, husband of Ann-Margret, was
diagnosed in 1980.[55]
Days Of Our Lives actress Suzanne Rogers has
the condition and so does the character she plays,
Maggie Horton.
Powhatan chief Opchanacanough (Uncle of
Pocahontas ) was thought to have the condition.
Stephen Garrett, also known as Static Major. He
made up half of the R&B group Playa.
Anselmo Ralph, Angolan singer.
11 References
[1] Kandel E, Schwartz J, Jessel T, Siegelbaum S, Hudspeth A
(2012). Principles of Neural Science (5 ed.). pp. 31819.
[2] McGrogan A, Sneddon S, de Vries CS (2010). The
incidence of myasthenia gravis: a systematic litera-
ture review. Neuroepidemiology 34 (3): 171183.
doi:10.1159/000279334. PMID 20130418.
[3] Tamparo, Carol (2011). Fifth Edition: Diseases of the Hu-
man Body. Philadelphia, PA: F.A. Davis Company. p.
233. ISBN 978-0-8036-2505-1.
[4] Engel AG (3 April 2012). Myasthenia Gravis and Myas-
thenic Disorders (2nd ed.). Oxford University Press, USA.
pp. 109110. ISBN 978-0-19-973867-0.
REFERENCES
[5] Scully C (21 July 2014). Scullys Medical Problems in Den-
tistry. Elsevier Health Sciences UK. ISBN 978-0-7020-
5963-6.
[6] Myasthenia Gravis: Practice Essentials, Background,
Anatomy. 2015-06-06.
[7] Nair, AG; Patil-Chhablani, P; Venkatramani, DV;
Gandhi, RA (October 2014). Ocular myasthenia
gravis: a review.. Indian journal of ophthalmology 62
(10): 98591. doi:10.4103/0301-4738.145987. PMC
4278125. PMID 25449931.
[8] Scherer K, Bedlack RS, Simel DL (2005). Does this pa-
tient have myasthenia gravis?". JAMA 293 (15): 1906
14. doi:10.1001/jama.293.15.1906. PMID 15840866.
[9] Rajendran A; Sundaram S (10 February 2014). Shafers
Textbook of Oral Pathology (7th ed.). Elsevier Health Sci-
ences APAC. p. 867. ISBN 978-81-312-3800-4.
[10] Myasthenia gravis: MedlinePlus Medical Encyclopedia.
www.nlm.nih.gov. Retrieved 2015-07-09.
[11] Marx, John A. Marx (2014). Rosens emergency medicine :
concepts and clinical practice (8th ed.). Philadelphia, PA:
Elsevier/Saunders. pp. 14411444. ISBN 1455706051.
Bethesda; Usa, 20894. Myasthenia Gravis - National Li-
brary of Medicine. PubMed Health. Retrieved 2015-07-
09.
[13] Myasthenia gravis. Genetics Home Reference. Retrieved
2015-07-10.
[14] Sathasivam, Sivakumar (January 1, 2014). Diagnosis
and management of myasthenia gravis. Progress
in Neurology and Psychiatry 18 (1): 614.
doi:10.1002/pnp.315. ISSN 1931-227X.
[15] Myasthenia Gravis Fact Sheet: National Institute of Neu-
rological Disorders and Stroke (NINDS)". www.ninds.
nih.gov. Retrieved 2015-07-10.
[16] Autoimmune Myasthenia Gravis and Thyroid Disease in
Argentina (P02.200) -- Bettini et al. 80 (1001): P02.200
-- Neurology. www.neurology.org. Retrieved 2015-07-
10.
[17] Kaminski, Henry J. (2009-03-02). Myasthenia Gravis
and Related Disorders. Springer Science & Business Me-
dia. ISBN 9781597451567.
[18] Jallouli, M.; Saadoun, D.; Eymard, B.; Leroux, G.;
Haroche, J.; Le Thi Huong, D.; De Gennes, C.; Chapelon,
C.; Benveniste, O. (Jul 2012). The association of sys-
temic lupus erythematosus and myasthenia gravis: a series
of 17 cases, with a special focus on hydroxychloroquine
use and a review of the literature. Journal of Neurology
259 (7): 12901297. doi:10.1007/s00415-011-6335-z.
ISSN 1432-1459. PMID 22160434. via ScienceDirect
(Subscription may be required or content may be available
in libraries.)

[19] Varner, Michael (June 2013). Myasthenia Gravis
and Pregnancy. Clinical Obstetrics and Gynecology
(Lippincott Williams & Wilkins) 56 (2): 37281.
doi:10.1097/GRF.0b013e31828e92c0.
[20] Tllez-Zenteno JF, Hernndez-Ronquillo L, Salinas V,
Estanol B, da Silva O (2004). Myasthenia gravis and
pregnancy: clinical implications and neonatal outcome.
BMC Musculoskeletal Disorders 5: 42. doi:10.1186/1471-
2474-5-42. PMC 534111. PMID 15546494. Retrieved
10 July 2008.
[21] Warrell, David A; Timothy M Cox; et al. (2003). Ox-
ford Textbook of Medicine Fourth Edition Volume
3. Oxford. p. 1170. ISBN 0-19-852787-X.
[22] Scherer K, Bedlack RS, Simel DL (2005). Does this pa-
tient have myasthenia gravis?". JAMA 293 (15): 1906
14. doi:10.1001/jama.293.15.1906. PMID 15840866.
[23] Rudd, Kathryn; Kocisko, Diane (2013-10-10). Pediatric
Nursing: The Critical Components of Nursing Care. F.A.
Davis. ISBN 9780803640535.
[24] Congenital Myasthenia Information Page: National In-
stitute of Neurological Disorders and Stroke (NINDS)".
www.ninds.nih.gov. Retrieved 2015-07-11.
[25] Wolfe, Gil I.; Barohn, Richard J. (2009). Myasthenia
Gravis: Classication and Outcome Measurements.
Myasthenia Gravis and Related Disorders. Cur-
rent Clinical Neurology (Humana Press): 293302.
doi:10.1007/978-1-59745-156-7_18. ISBN 978-1-
58829-852-2.
[26] Leite MI, Jacob S, Viegas S, et al. (July 2008).
IgG1 antibodies to acetylcholine receptors in 'seroneg-
ative' myasthenia gravis. Brain 131 (Pt 7): 1940
52. doi:10.1093/brain/awn092. PMC 2442426. PMID
18515870.
[27] Lambert-Eaton syndrome: MedlinePlus Medical Ency-
clopedia. www.nlm.nih.gov. Retrieved 2015-07-11.
[28] Selvan VA. (2011). Single-ber EMG: A review. Ann
Indian Acad Neurol 14 (1): 6467. doi:10.4103/0972-
2327.78058. PMC 3108086. PMID 21654930.
[29] Kearsey, Christopher; Fernando, Prabhath; D'Costa,
Domnick; Ferdinand, Phillip (June 1, 2010). The use
of the ice pack test in myasthenia gravis. JRSM Short Re-
ports 1 (1): 14. doi:10.1258/shorts.2009.090037. ISSN
2054-2704. PMID 21103106.
[30] Tensilon test: MedlinePlus Medical Encyclopedia.
www.nlm.nih.gov. Retrieved 2015-07-11.
[31] Spillane, J.; Higham, E.; Kullmann, D. M. (21 De-
cember 2012). Myasthenia gravis. The BMJ 345:
e8497. doi:10.1136/bmj.e8497. ISSN 1756-1833.
PMID 23261848.
[32] de Kraker M, Kluin J, Renken N, Maat AP, Bogers AJ
(2005). CT and myasthenia gravis: correlation be-
tween mediastinal imaging and histopathological nd-
ings. Interact Cardiovasc Thorac Surg 4 (3): 26771.
doi:10.1510/icvts.2004.097246. PMID 17670406.
7
[33] Allan H. Ropper, Robert H. Brown Adams and Victors
Principles of Neurology McGraw-Hill Professional; 8 edi-
tion (29 March 2005)
[34] Pulmonary function tests: MedlinePlus Medical Ency-
clopedia. www.nlm.nih.gov. Retrieved 2015-07-11.
[35] Emergent Management of Myasthenia Gravis:
Overview, Patient History, Physical Examination.
2015-06-06.
[36] Mehndiratta, Man Mohan; Pandey, Sanjay; Kuntzer,
Thierry (2014). Acetylcholinesterase inhibitor
treatment for myasthenia gravis. The Cochrane
Database of Systematic Reviews 10: CD006986.
doi:10.1002/14651858.CD006986.pub3. ISSN 1469-
493X. PMID 25310725.
[37] National Guideline Clearinghouse | Practice parame-
ter: thymectomy for autoimmune myasthenia gravis (an
evidence-based review). Report of the Quality Standards
Subcommittee of the American Academy of Neurology..
www.guideline.gov. Retrieved 2015-07-11.
[38] Mehndiratta, Man Mohan; Pandey, Sanjay; Kuntzer,
Thierry (2014-10-13). Acetylcholinesterase inhibitor
treatment for myasthenia gravis. John Wiley & Sons, Ltd.
doi:10.1002/14651858.CD006986.pub3.
[39] Choices, N. H. S. (2014). Atropine - Myasthenia-gravis
medicines and drugs - NHS Choices. Retrieved 2015-
07-11.
[40] Kumar, Vikas; Kaminski, Henry J. (7 October 2010).
Treatment of Myasthenia Gravis. Current Neu-
rology and Neuroscience Reports 11 (1): 8996.
doi:10.1007/s11910-010-0151-1. ISSN 1528-4042.
[41] Mehndiratta, MM; Pandey, S; Kuntzer, T (Oct 13, 2014).
Acetylcholinesterase inhibitor treatment for myasthenia
gravis.. The Cochrane database of systematic reviews 10:
CD006986. doi:10.1002/14651858.CD006986.pub3.
PMID 25310725.
[42] Juel VC (2004). Myasthenia gravis: management of
myasthenic crisis and perioperative care. Semin Neu-
rol 24 (1): 7581. doi:10.1055/s-2004-829595. PMID
15229794.
[43] Surgical removal of the thymus for myasthenia gravis
that is not caused by a tumour of the thymus | Cochrane.
www.cochrane.org. Retrieved 2015-07-11.
[44] Goldenberg, W.D.; Shah, A.K. Myasthenia Gravis.
eMedicine. Retrieved 5 May 2012.
[45] Cup E.H., Pieterse A.J., ten Broek-Pastoor J.M.,
Munneke M., van Engelen B.G., Hendricks H.T., van
der Wilt G.J., Oostendorp R.A., EH; Pieterse, AJ; Ten
Broek-Pastoor, JM; Munneke, M; Van Engelen, BG; Hen-
dricks, HT; Van Der Wilt, GJ; Oostendorp, RA (2007).
Exercise therapy and other types of physical therapy
for patients with neuromuscular diseases: a systematic
review. Archives of Physical Medicine and Rehabilita-
tion 88 (11): 145264. doi:10.1016/j.apmr.2007.07.024.
PMID 17964887.
8 13 FURTHER READING

[46] Sieb, J P (2014). Myasthenia gravis: an update for the The Myasthenia Gravis Association (MGA) for the
clinician. Clinical and Experimental Immunology 175 Republic of Ireland
(3): 408418. doi:10.1111/cei.12217. ISSN 0009-9104.
PMC 3927901. PMID 24117026. The Myasthenia Gravis Coalition of Canada

[47] Cea, Gabriel; Benatar, Michael; Verdugo, Renato J; Sali-

nas, Rodrigo A (November 14, 2013). Thymectomy
for non-thymomatous myasthenia gravis. Cochrane 13 Further reading
Database of Systematic Reviews (John Wiley & Sons, Ltd).
doi:10.1002/14651858.CD008111.pub2. Zhang, Zhenchang; Guo, Jia; Su, Gang; Li,
Jiong; Wu, Hua; Xie, Xiaodong (Novem-
[48] Losen M, Martnez-Martnez P, Phernambucq M, Schu-
ber 17, 2014). Evaluation of the Quality
urman J, Parren PW, DE Baets MH (2008). Treatment
of myasthenia gravis by preventing acetylcholine receptor
of Guidelines for Myasthenia Gravis with the
modulation. Annals of the New York Academy of Sci- AGREE II Instrument. PLoS ONE 9 (11):
ences 1132: 1749. doi:10.1196/annals.1405.034. PMID e111796. doi:10.1371/journal.pone.0111796.
18567867. PMC 4234220. PMID 25402504.

[49] Conti-Fine, Bianca; Milani, Monica (December 1, NCBI - Diagnostic. www.ncbi.nlm.nih.gov. Re-
2006). Myasthenia gravis: past, present, and fu- trieved 2015-07-11.
ture. The Journal of Clinical Investigation 116: 2843
2854. doi:10.1172/JCI29894. PMC 1626141. PMID
17080188.

[50] Vrinten, C; van der Zwaag, AM; Weinreich, SS;

Scholten, RJ; Verschuuren, JJ (17 December 2014).
Ephedrine for myasthenia gravis, neonatal myas-
thenia and the congenital myasthenic syndromes..
The Cochrane database of systematic reviews 12:
CD010028. doi:10.1002/14651858.CD010028.pub2.
PMID 25515947.

[51] Vrinten, Charlotte; van der Zwaag, Angeli M; Wein-

reich, Stephanie S; Scholten, Rob JPM; Verschuuren,
Jan JGM (December 17, 2014). Ephedrine for
myasthenia gravis, neonatal myasthenia and the con-
genital myasthenic syndromes. Cochrane Database
of Systematic Reviews (John Wiley & Sons, Ltd) 12:
CD010028. doi:10.1002/14651858.CD010028.pub2.
PMID 25515947.

[52] Steinbeck, JA; Jaiswal, MK; Calder, EL; Kishinevsky,

S; Weishaupt, A; Toyka, KV; Goldstein, PA; Studer,
L (7 January 2016). Functional Connectivity under
Optogenetic Control Allows Modeling of Human Neu-
romuscular Disease.. Cell stem cell 18 (1): 13443.
doi:10.1016/j.stem.2015.10.002. PMID 26549107.

[53] Nielsen, Chad. Toughness is a Choice. ESPN Magazine.

Retrieved 11 November 2010.

[54] Who Was Christopher Robin Milne?". 2007-06-18.

Archived from the original on 18 June 2007. Retrieved
2015-07-12.

[55] Hollywood Legend Ann-Margret on Faith, Love and Re-

covery. Retrieved 2015-07-12.

12 External links
The Myasthenia Gravis Foundation of America

The Myasthenia Gravis Association (MGA) for the

United Kingdom
 9

14 Text and image sources, contributors, and licenses

14.1 Text
Myasthenia gravis Source: https://en.wikipedia.org/wiki/Myasthenia_gravis?oldid=728309349 Contributors: General Wesc, Vicki
Rosenzweig, Mav, The Anome, RoseParks, ErdemTuzun, Alex.tan, Gabbe, Jiang, Lancevortex, Tpbradbury, Dcsohl, Romanm, Diberri,
Cutler, DocWatson42, Lproven, Piquan, Michael Devore, Jfdwol, Eequor, Decoy, Chowbok, Zeimusu, Kiteinthewind, Maikel, Rich Farm-
brough, Guanabot, Nina Gerlach, Bender235, Balok, Jpgordon, Stesmo, Davidruben, Arcadian, Pacula, Terrypearson, Arthena, Wouter-
stomp, Sleigh, Throbblefoot, Japanese Searobin, Woohookitty, Lkjhgfdsa, Prashanthns, Palica, RichardWeiss, Graham87, Rjwilmsi, Ge-
oO, Brighterorange, FlaBot, Nihiltres, Brimcmike, Stevenfruitsmaak, Celebere, Bgwhite, YurikBot, Mikalra, RussBot, Pigman, Gaius
Cornelius, Mccready, Nephron, Osnimf, Killdevil, Igin, Drdr1989, David Biddulph, Zvika, SmackBot, Delldot, Eskimbot, Yam-
aguchi , RDBrown, Moshe Constantine Hassan Al-Silverburg, Lesnail, Rcktmanil, Cybercobra, DMacks, Kukini, Khazar, Howardj,
Optakeover, Novangelis, MrDolomite, Jetman, StephenBuxton, Theyer, ChrisCork, JForget, BrettMontgomery, CmdrObot, Philbradley,
Martiniminister, Salicyna, Mig11, TheTito, Kupirijo, Cunningpal, Clarifythis, ST47, LMAnthony, Alaibot, DavidSteinle, PizzaMan,
Thijs!bot, Gacggt, Omicron619, Ninad 1999, Headbomb, Marek69, Copperman, Marlberg, Cyclonenim, QuiteUnusual, DR, NSH001,
Freazer, Patxi lurra, Ph.eyes, TAnthony, Hb2019, RHSydnor, Ojh2, Think outside the box, Philgress, Scottalter, Mmoneypenny, Anax-
ial, Nono64, Lilac Soul, Xargque, J.delanoy, MITBeaverRocks, Spidrak, Nbauman, Xris0, Rod57, Joe Back, Jeepday, Mikael Hg-
gstrm, Betswiki, Tbone762, RJASE1, Wikieditor06, Magaera, AndyLeja~enwiki, TXiKiBoT, Dj stone, Rei-bot, Melsaran, LeaveSleaves,
Bengisuk, Shanata, Sevela.p, Doc James, AlleborgoBot, Daveh4h, SieBot, Mikemoral, WereSpielChequers, Rhcastilhos, Moletrouser, Nip-
sonanomhmata, Efe, D cavel-greant, Elbonia, ClueBot, The Thing That Should Not Be, Abe (or Abraham), FritzLaurel, GoDawgs1, Shin-
pah1, Boing! said Zebedee, Mallapurbharat, Ecuadmd, Sanjpatel1, Estirabot, Peter.C, Dekisugi, Delldot on a public computer, Matt362,
Dthomsen8, Triptropic, JzoJames, Alexius08, Addbot, Giftiger wunsch, DOI bot, Kongr43gpen, Cadence13, Diptanshu.D, Looie496,
Eivindbot, Diculttoguess, Orlandoturner, SpBot, SamatBot, JGKlein, Dayewalker, Verazzano, Jarble, TundraGreen, Luckas-bot, Delux-
Nate, QueenCake, AnomieBOT, 1exec1, Choij, StormBlade, BASWIM, Ulric1313, Materialscientist, Citation bot, DirlBot, Xqbot,
LA1213, Gigemag76, Gilo1969, XZeroBot, Tjonez, Levesque2177, Swua, Jestorg, SD5, Theletterone, Jzivku, FrescoBot, Xadrezista,
TimonyCrickets, Citation bot 1, Scootercatter, Rokaszil, TobeBot, Wlduggan, Minimac, Ajmelville1, Stephane.rainville, Ripchip Bot,
Whywhenwhohow, EmausBot, Milkunderwood, SingleIntegral, Kittainter, Dcirovic, Ocaasi, Cforrester101, Orange Suede Sofa, Toralinda,
Jehovahrapha, Gwen-chan, ClueBot NG, This lousy T-shirt, Shka, Pepetiktak, DAAllegretto, Helpful Pixie Bot, Maxsherman, BG19bot,
Everybodyjones, Davidiad, Watermelon mang, Vartan Balian, BattyBot, Valleyforge2012, Cyberbot II, TheGnerd, Biolprof, YFdyh-bot,
TylerDurden8823, Allenor Tan, Crepuscular ray, Mdscottis, Vetteranger, Lugia2453, SynapticSage, Corinne, Me, Myself, and I are Here,
Sadkins1953, Ozzie10aaaa, Christensenka, Pratibha1, Anrnusna, Glee gg, Butcan, Koteswara rao manne, Monkbot, Myasthenia Gravis,
Cbb002, Stacie Croquet, Matthew Ferguson 57, Niscarpi, Mastermindful, Waldo is Somewhere, Hulkstrong, Stewader91, Monicatulia,
7phillip7, TaylerH20, Mariapilavakis and Anonymous: 287

14.2 Images
File:Azathioprine.svg Source: https://upload.wikimedia.org/wikipedia/commons/2/2a/Azathioprine.svg License: Public domain Contrib-
utors: PubChem Original artist: Ayacop
File:Gray1178.png Source: https://upload.wikimedia.org/wikipedia/commons/8/80/Gray1178.png License: Public domain Contributors:
Henry Gray (1918) Anatomy of the Human Body (See Book section below)
Original artist: Henry Vandyke Carter
File:Myasthenia_gravis_ptosis_reversal.jpg Source: https://upload.wikimedia.org/wikipedia/commons/5/57/Myasthenia_gravis_
ptosis_reversal.jpg License: CC BY 2.0 Contributors: Rare association of thymoma, myasthenia gravis and sarcoidosis : a case report.
Journal of Medical Case Reports. 2008;2:245. doi:10.1186/1752-1947-2-245 Original artist: Mohankumar Kurukumbi, Roger L Weir,
Janaki Kalyanam, Mansoor Nasim, Annapurni Jayam-Trouth.
File:Neostigmine.svg Source: https://upload.wikimedia.org/wikipedia/commons/c/ca/Neostigmine.svg License: Public domain Contrib-
utors: ? Original artist: ?
File:Nicotinic_Acetylcholine_receptor.png Source: https://upload.wikimedia.org/wikipedia/commons/6/6e/Nicotinic_Acetylcholine_
receptor.png License: Public domain Contributors: No machine-readable source provided. Own work assumed (based on copyright claims).
Original artist: No machine-readable author provided. S. Jhnichen assumed (based on copyright claims).
File:Synapse_diag4.png Source: https://upload.wikimedia.org/wikipedia/commons/2/2b/Synapse_diag4.png License: CC-BY-SA-3.0
Contributors: ? Original artist: ?
File:Tumor_Thymoma1.JPG Source: https://upload.wikimedia.org/wikipedia/commons/3/3f/Tumor_Thymoma1.JPG License: GFDL
Contributors: Own work Original artist: Tdvorak

14.3 Content license

Creative Commons Attribution-Share Alike 3.0