Article
Nerve conduction abnormalities and neuromyotonia in genetically engineered mouse models of human hereditary neuropathies.
Annals of the New York Academy of Sciences - 14 Sept 1999
Zielasek J, Toyka K V
Abstract excerpt
We performed electrophysiological studies in myelin protein mutant mice in order to characterize nerve conduction changes. We performed neurographic studies on the facial and sciatic nerves and needle electromyography (EMG). Mice homozygously deficient for the peripheral myelin protein 22 gene (Pmp22-/-) exhibited increased motor latencies, reduced nerve conduction velocities, and polyphasia of the M-response,...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
