Lambert-Eaton vs. Myasthenia Gravis

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Discussion Overview

The discussion focuses on the differences in clinical presentation between Lambert-Eaton Myasthenic Syndrome (LEMS) and Myasthenia Gravis (MG), both of which involve autoimmune attacks at the neuromuscular junction. Participants explore the underlying mechanisms, symptoms, and diagnostic features of each condition.

Discussion Character

  • Technical explanation
  • Conceptual clarification
  • Debate/contested

Main Points Raised

  • Some participants note that LEMS and MG both involve antibody attacks at the neuromuscular junction but target different components, with LEMS affecting calcium channels and MG affecting receptor muscles.
  • One participant suggests that the differences in symptoms may arise from the specific muscle groups affected by each disorder, mentioning that LEMS often affects limbs first while MG typically affects bulbar muscles.
  • A participant references that LEMS is often associated with small-cell carcinoma and that its symptoms improve with exertion, contrasting with MG where weakness does not improve in the same way.
  • Another participant discusses the diagnostic features of LEMS, highlighting a specific electromyogram (EMG) pattern that distinguishes it from MG, where end plate potential inhibition occurs.
  • There is mention of the variability in neuromuscular transmission abnormalities being more pronounced in MG patients compared to those with LEMS.

Areas of Agreement / Disagreement

Participants express differing views on the reasons behind the clinical differences between LEMS and MG, with no consensus reached on the underlying mechanisms or the significance of the symptoms presented.

Contextual Notes

Some limitations include the lack of detailed explanations for why specific muscle groups are targeted by the autoimmune responses in each condition, as well as unresolved aspects of the electrodiagnostic testing guidelines for MG.

greghouse
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How comes the clinical presentation differs between LE and MG? In both cases anti-bodys attack the neuromuscular junction, LE attacks the calcium channels on the pre-synaptic axon terminal, and MG the receptor muscles Na/K-channels... Why is there difference in symptoms?
 
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Here are two links explaining the diseases and symptoms with general descriptions of the causes (you may have seen these already, but for the sake of ensuring everyone else knows what is being talked about, this should help).
http://www.emedicine.com/emerg/TOPIC325.HTM
http://www.emedicine.com/NEURO/topic181.htm

The simplest answer (and only one) I can offer on this is that they affect different muscle groups. Autoimmune disorders can be tissue specific, or more general, and I don't have any explanation for you of why they target the muscle groups they do. Otherwise, the symptoms are similar in terms of inducing muscle weakness or loss of function, it's just that one affects the limbs first while the other is more likely to affect the bulbar muscles first (the ones used for swallowing, speaking, chewing).
 
"LEMS is most often a paraneoplastic syndrome associated with small-cell carcinoma, which it may precede. Like myasthenia gravis, it is an autoimmune disorder. Unlike myasthenia gravis, the weakness improves with exertion, and oculobulbar involvement is rare except for ptosis."

"Repetitive electric stimulation at 50-Hz applied to the ulnar nerve at the wrist normally elicits from the abductor of the fifth finger an evoked response of ≥ 5 mV, which may increase no more than 50%. In the case we describe, the electromyogram (EMG) showed that the initial lowamplitude potential was at 0.54 mV and increased progressively to 1.82 mV, a change of 237%. This EMG pattern is a diagnostic feature of Lambert-Eaton myasthenic syndrome (LEMS)."
(Lambert-Eaton myasthenic syndrome: Monique D'Amour, Gilles Gariepy, Joseph Braidy. Canadian Medical Association. Journal. Ottawa: Jan 2, 2007. Vol. 176, Iss. 1; pg. 38, 1 pgs)


"This variability is highly sensitive to neuromuscular transmission abnormalities and is increased in MG patients. Neuromuscular blocking is the failure of transmission of one of the potentials, when one of the muscle fibers fails to transmit an action potential because the EPP does not reach the necessary threshold. The American Association of Neuromuscular & Electrodiagnostic Medicine has developed guidelines for electrodiagnostic testing for evaluation of MG (88)."
(Myasthenia gravis: past, present, and future: Bianca M Conti-Fine, Monica Milani, Henry J Kaminski. Journal of Clinical Investigation. Ann Arbor: Nov 2006. Vol. 116, Iss. 11; pg. 2843, 12 pgs)

It looks like End Plate Potential is inhibited in MG and increased in LEMS and fast twitch or slow twitch muscles are more or less susceptible.
 
Care to link that?