title: Why are sensory axons more vulnerable for ischemia than motor axons?
abstract: OBJECTIVE
  In common peripheral neuropathies, sensory symptoms usually prevail over motor symptoms. This predominance of sensory symptoms may result from higher sensitivity of sensory axons to ischemia.
  
  
  METHODS
  We measured median nerve compound sensory action potentials (CSAPs), compound muscle action potentials (CMAPs), and excitability indices in five healthy subjects during forearm ischemia lasting up to disappearance of both CSAPs and CMAPs.
  
  
  RESULTS
  ISCHEMIA INDUCED: (1) earlier disappearance of CSAPs than CMAPs (mean ± standard deviation 30±5 vs. 46±6 minutes), (2) initial changes compatible with axonal depolarization on excitability testing (decrease in threshold, increase in strength duration time constant (SDTC) and refractory period, and decrease in absolute superexcitability) which were all more prominent in sensory than in motor axons, and (3) a subsequent decrease of SDTC reflecting a decrease in persistent Na(+) conductance during continuing depolarisation.
  
  
  CONCLUSIONS
  Our study shows that peripheral sensory axons are more vulnerable for ischemia than motor axons, with faster inexcitability during ischemia. Excitability studies during ischemia showed that this was associated with faster depolarization and faster persistent Na(+) channel inactivation in sensory than in motor axons. These findings might be attributed to differences in ion channel composition between sensory and motor axons and may contribute to the predominance of sensory over motor symptoms in common peripheral neuropathies.
authors.affiliation: Clinical Neurophysiology, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands. jhofmeijer@rijnstate.nl
authors.forename: Jeannette
authors.initials: J
authors.lastname: Hofmeijer
authors.forename: Hessel
authors.initials: H
authors.lastname: Franssen
authors.forename: Leonard J
authors.initials: LJ
authors.lastname: van Schelven
authors.forename: Michel J A M
authors.initials: MJ
authors.lastname: van Putten
mesh_terms: D000200:Action Potentials; D000328:Adult; D001132:Arm / Q000098:blood supply* / Q000503:physiopathology; D001369:Axons / Q000502:physiology*; D015687:Cell Hypoxia; D005260:Female; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology*; D009431:Neural Conduction; D011434:Proprioception; D011984:Sensory Receptor Cells / Q000502:physiology*