摘要
Objective: To test the hypothesis that the N10 far field potential in median nerve somatosensory evoked potentials is generated by the motor axons by examini ng patients with amyotrophic lateral sclerosis (ALS). Methods: Subjects were 5 A LS patients showing pronounced or complete denervation of median inner vated s mall hand muscles. We evaluated N10 over scalp, and proximal plexus volleys (PPV s) at lateral or anterior cervical electrode. Results: N10 and PPVs were definit ely preserved for every ALS subject. N10 amplitudes of ALS subjects were even si gnificantly larger than control subjects. In one ALS patient completely lacking motor axons, N10 was larger than the largest one among control subjects. Conclus ions: Present results clearly indicate that N10 is not predominantly generated b y motor axons but by the whole median nerve dominated by sensory axons. We propo se a theory that N10 is a junctional potential generated by the entrance of the median nerve into bone at the intervertebral foramen, producing a positive pole at the non cephalic reference electrode. Significantly larger N10 in ALS subjec ts may be due to the lack of cancellation by slower motor axons. Significance: T he hypothesis that N10 is generated by motor axons is refuted, and a new theory of its generation is presented.
Objective: To test the hypothesis that the N10 far field potential in median nerve somatosensory evoked potentials is generated by the motor axons by examini ng patients with amyotrophic lateral sclerosis (ALS). Methods: Subjects were 5 A LS patients showing pronounced or complete denervation of median inner vated s mall hand muscles. We evaluated N10 over scalp, and proximal plexus volleys (PPV s) at lateral or anterior cervical electrode. Results: N10 and PPVs were definit ely preserved for every ALS subject. N10 amplitudes of ALS subjects were even si gnificantly larger than control subjects. In one ALS patient completely lacking motor axons, N10 was larger than the largest one among control subjects. Conclus ions: Present results clearly indicate that N10 is not predominantly generated b y motor axons but by the whole median nerve dominated by sensory axons. We propo se a theory that N10 is a junctional potential generated by the entrance of the median nerve into bone at the intervertebral foramen, producing a positive pole at the non cephalic reference electrode. Significantly larger N10 in ALS subjec ts may be due to the lack of cancellation by slower motor axons. Significance: T he hypothesis that N10 is generated by motor axons is refuted, and a new theory of its generation is presented.
出处
《世界核心医学期刊文摘（神经病学分册）》
2005年第2期23-23,共1页
Digest of the World Core Medical Journals:Clinical Neurology
