## Abstract Acquired neuromyotonia is characterized by hyperexcitability of motor nerves leading to muscle twitching, cramps, and weakness. The symptoms may improve following plasma exchange, and injection of immunoglobulin G (IgG) from 1 neuromyotonia patient into mice increased the resistance of
Strength-duration properties of peripheral nerve in acquired neuromyotonia
β Scribed by Paul Maddison; John Newsom-Davis; Kerry R. Mills
- Book ID
- 101253575
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 175 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0148-639X
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β¦ Synopsis
The strength-duration time constant (SDTC) of a myelinated axon is a property of the nodal membrane and is sensitive to changes in membrane potential. Strength-duration time constants for motor axons and cutaneous afferents of the median nerve were measured in 9 patients with acquired neuromyotonia (NMT), a condition of peripheral nerve hyperexcitability, and 15 control patients. Mean motor axon time constants were significantly prolonged (344 Β± 100 Β΅s) in patients compared to healthy controls (264 Β± 34 Β΅s; P = 0.038), but sensory axon time constants were not significantly different. Motor axon time constants were longer than sensory axon time constants in 4 of the patients with neuromyotonia, suggesting that the nodal membrane was depolarized by an ectopic focus at the site of nerve stimulation at the wrist, ionic conductances were altered at the node, or that the size of the node was increased, possibly as a result of immune-mediated damage. The anti-voltage-gated potassium channel antibodies thought to generate peripheral nerve hyperexcitability in acquired neuromyotonia may be indirectly responsible for changes in motor axon nodal membrane properties.
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In 2 patients with neuromyotonia, nerve blocks had no effect on the abnormal activity, while intramuscular injection of the botulinum toxin abolished the discharges in one and greatly diminished them in the other. Botulinum toxin thus helps to localize the origin of the neuromyotonic discharges to t