Key result
Sodium channel modifiers effectively control myotonia symptoms by targeting repetitive electrical activity.
Drugs modifying sodium channel activation kinetics can effectively control myotonia symptoms by targeting the final common pathway of repetitive electrical activity.
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May support sodium channel modulators for myotonia symptom control; leaves open need for randomized trials before practice change.
The clinical and electrophysiologic features of myotonia can be seen in a number of human diseases as well as in several well-studied animal models. In some cases, the underlying pathophysiologic mechanism has been defined, but different and as yet undetermined membrane abnormalities are present in others. In spite of the differing mechanisms that can produce the repetitive electrical activity characteristic of myotonia, the involvement of the voltage-dependent sodium channel as the final common pathway in the expression of this activity provides a target for therapeutic intervention. A number of drugs that modify sodium channel activation kinetics can be used to effectively control the symptoms of myotonia.
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Robert L. Barchi (1988) conducted a review in Myotonia. Drugs that modify sodium channel activation kinetics was evaluated. Drugs that modify sodium channel activation kinetics can effectively control the symptoms of myotonia by targeting the final common pathway of repetitive electrical activity.
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