Snake Venoms and the Neuromuscular Junction

Robert L. Lewis, M.D.; Ludwig Gutmann, M.D.

Disclosures

Semin Neurol. 2004;24(2) 

In This Article

Spontaneous Activity

A unique syndrome caused by a toxic snake venom is the generalized myokymia following envenomation by the timber rattlesnake (Crotalus horridus), a member of the family Crotalidae.[25,26] Clinically, myokymia manifests itself as spontaneous continuous undulating fine contractions of multiple individual motor units. The clinical appearance is similar to fasciculations but more rhythmic. Electromyographically, the myokymia results from spontaneous titanic bursts of motor unit potentials appearing as doublets and multiplets (Fig. 1).[26] These discharges originate at various sites along the axolemma including the terminal axon. Antibodies directed against voltage gated K channels (VGKCs) occur in association with other acquired myokymic and neuromyotonic (a more intense form of myokymia) syndromes. The anti-body alteration of the VGKCs causes axon membrane hyperexcitability by lowering the resting membrane potential. Although the precise mechanism of the myokymia associated with timber rattlesnake envenomation is not known, we postulate a transient toxic effect on axonal VGKCs.[4]

Recurrent multiplets recorded from the orbicularis oris muscle. The intraburst frequency of motor unit action potentials is 180 Hz.

The print version of this article was originally certified for CME credit. For accreditation details, contact the publisher. Indiana University School of Medicine, Division of Continuing Medical Education, 714 N. Senate Avenue, EF 200, Indianapolis, IN, 46202

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