Myasthenia Gravis Differential Diagnoses

  • Author: William D Goldenberg, MD; Chief Editor: Nicholas Lorenzo, MD   more...
 
Updated: Jan 20, 2012
 
 

Diagnostic Considerations

Myasthenia gravis (MG) can mimic other diagnoses in elderly persons and vice versa. Examples of such pathology include diagnoses such as congestive heart failure, pulmonary embolism, and acute myocardial infarction.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Botulism
  • Compressive lesions of cranial nerves
  • Congenital myasthenic syndromes
  • Depression
  • Drug-induced myasthenialike syndrome - This may be related to D-penicillamine, antibiotics (ciprofloxacin, erythromycin, ampicillin, polymyxins, or aminoglycosides), antispasmodic drugs (trihexyphenidyl), beta-adrenergic receptor blocking agents (propranolol, timolol), or cardiac drugs (procainamide, verapamil, quinidine)
  • Kearns-Sayre syndrome
  • Mitochondrial cytopathies
  • Mitochondrial myopathies, with or without external ophthalmoplegia
  • Neurasthenia
  • Oculopharyngeal muscular dystrophy

Differential Diagnoses

Proceed to Workup
 
 
Contributor Information and Disclosures
Author

William D Goldenberg, MD  Assistant Professor, Department of Emergency Medicine, Uniformed Services University of Health Sciences; Staff Emergency Physician, Naval Hospital San Diego

William D Goldenberg, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Aashit K Shah, MD  Professor of Neurology, Director, Comprehensive Epilepsy Program, Program Director, Clinical Neurophysiology Fellowship, Detroit Medical Center, Wayne State University School of Medicine

Aashit K Shah, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Neurological Association

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD  Consulting Staff, Neurology Specialists and Consultants

Nicholas Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives

Disclosure: Nothing to disclose.

Additional Contributors

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University School of Medicine; Director of Neurology Clinic, St Louis ConnectCare; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and Phi Beta Kappa

Disclosure: Baxter Grant/research funds Other; Amgen Grant/research funds None

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
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Normal neuromuscular junction showing a presynaptic terminal with a motor nerve ending in an enlargement (bouton terminale): Synaptic cleft and postsynaptic membrane with multiple folds and embedded with several acetylcholine receptors.
Acetylcholine receptor. Note 5 subunits, each with 4 membrane-spanning domains forming a rosette with a central opening. The central opening acts as an ion channel.
A typical recording of compound muscle action potentials with repetitive nerve stimulation at low frequency in a patient with myasthenia gravis. Note the gradual decline in the amplitude of the compound muscle action potential with slight improvement after the fifth or sixth potential.
CT scan of chest showing an anterior mediastinal mass (thymoma) in a patient with myasthenia gravis.
Increasing left ptosis developing upon sustained upward gaze in patient with myasthenia gravis (A through F). Note limited elevation of left eye, denoting superior rectus palsy (A). A initially, C after around 20 seconds, F after 1 minute.
Cogan sign. Patient changes gaze from downward position (A) to primary position (B). Both lids are seen to overshoot in twitch (B) before gaining their initial ptotic position (D). In this case, Cogan sign is seen more obviously on right, whereas left lid is more ptotic.
CT scan of chest and mediastinum showing thymoma in patient with myasthenia gravis.
Repetitive nerve stimulation at frequency of 2 Hz showing increasing decrement in amplitude of compound muscle action potential up to fourth response (42% amplitude loss), after which it stabilizes.
Single-fiber electromyography showing so-called jitter phenomenon (second action potential wave group).
Table. Prevalence and Titers of Antibody to Acetylcholine Receptor in Patients with Myasthenia Gravis
Osserman MG Class*Mean Anti-AChR Titer (× 10–9 M)Positive Results, %
R0.7924
I2.1755
IIA49.880
IIB57.9100
III78.5100
IV205.389
AChR = acetylcholine receptor; MG = myasthenia gravis.



*Osserman classification: R = remission, I = ocular only, IIA = mild generalized, IIB = moderate generalized, III = acute severe, IV = chronic severe.



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