[Nerve excitability studies in the assessment of dysimmune neuropathies].
BACKGROUND
Various changes in axonal membrane excitability might explain negative symptoms in dysimmune neuropathies, e.g., acute or chronic inflammatory demyelinating neuropathies or multifocal neuropathies with persistent conduction blocks. Several electrophysiological methods have recently been designed to specifically assess such axonal membrane excitability changes.


BACKGROUND
Resting and action potentials are related to ionic movements through the axonal membrane, mainly involving various types of sodium and potassium channels, as well as the ATP-dependent Na+/K+ pump. The functional status of these channels and pumps can be assessed in man, by studying the excitability recovery cycle after a single impulse, the strength-duration and stimulus-response curves, and the effects of hyperpolarization and depolarization depending on activity (voluntary contraction), ischemia or application of prolonged subthreshold currents. Various features of altered axonal membrane excitability might characterize dysimmune neuropathies, according to the course of the disease and its treatment.


CONCLUSIONS
This electrophysiological approach allowed changes in axonal membrane properties to be objectively determined. In particular, some results obtained with these methods could explain the rapid action of intravenous immunoglobulins, and various pathophysiological mechanisms of conduction block or axonal degeneration.


CONCLUSIONS
Nerve excitability studies appeared to be useful for the diagnosis and the follow-up of dysimmune neuropathies. New therapeutical strategies for such neuropathies will be probably developed in the future intending to improve nerve function by acting on axonal membrane excitability.
Lefaucheur
J-P
JP
Service de Physiologie-Explorations Fonctionnelles, Hôpital Henri-Mondor, AP-HP, Créteil. jean-pascal.lefaucheur@hmn.ap-hop-paris.fr
Boërio
D
D
Hogrel
J-Y
JY
Créange
A
A
D000818:Animals; D020274:Autoimmune Diseases of the Nervous System / Q000175:diagnosis* / Q000503:physiopathology; D004594:Electrophysiology; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D009474:Neurons / Q000502:physiology
D007473:Ion Channels