title: Neurophysiological evidence of spared upper motor conduction fibers in clinically complete spinal cord injury: discomplete SCI in rats.
abstract: Motor evoked potentials (MEP) were recorded and characterized by epidural electrodes (scMEP) and extracellular microelectrodes (exMEP) on T(13) level from 10 normal rats and 40 rats with chronic spinal cord injury (SCI). The spinal cord of 40 anesthetized rats were injured with various severity (sham, 35, 70, and 100 g/cm impact injury) at T(8)-T(9) cord using Allen's drop model. The incline plane and Tarlov techniques were investigated to assess clinical neurological function. MEPs in the normal rats elicited by applying transcortical suprathreshold stimulation consisted of 3-4 early negative peaks (N(1), N(2), N(3), N(4)) followed by several late waves. The N(1) and N(2) peaks had their maximal amplitudes in the anterior and ventrolateral funiculus, respectively, irrespective of the polarity of stimulation, which indicated that these impulses were conducted mostly through the extrapyramidal pathways. The 100 g/cm impact injury or transection of the cord caused abolishment of the MEP signals distal to the lesion, whereas the 35 g/cm injury resulted in a latency shift and amplitude decrement of the MEP peaks. Out of 20 rats with 70 g/cm injuries, 18 showed clinically paraplegia. Among them, seven had neurophysiological evidence of residual conduction pathways through the injured cord segment, such as the presence of N(1) and N(2) peaks in scMEP or exMEP. After 4-aminopyridine (4-AP) administration (1 mg/kg), the amplitude of spared exMEP increased significantly and spread more widely. These results suggest that MEPs evoked by transcortical stimulation travel mostly in the extrapyramid tract. The present study provides further direct and objective electrophysiological evidences of spared functional axons after discomplete SCI, since many other studies on this field have achieved similar results previously. Furthermore, pharmaceutical treatment with 4-AP or other K(+) channel blocking agents proved to be a potential therapeutic strategy for patient with chronic SCI.
authors.affiliation: Deparment of Orthopaedic Surgery, Changzheng Hospital, Feng Yang Road 415#, Shanghai 200003, People's Republic of China. kwyu@sh163b.sta.net.cn
authors.forename: K
authors.initials: K
authors.lastname: Yu
authors.forename: W
authors.initials: W
authors.lastname: Rong
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: L
authors.initials: L
authors.lastname: Jia
authors.forename: W
authors.initials: W
authors.lastname: Yuan
authors.forename: X
authors.initials: X
authors.lastname: Yie
authors.forename: Z
authors.initials: Z
authors.lastname: Shi
mesh_terms: D000818:Animals; D019054:Evoked Potentials, Motor; D006470:Hemorrhage / Q000473:pathology; D006801:Humans; D008297:Male; D009046:Motor Neurons / Q000502:physiology*; D009336:Necrosis; D009410:Nerve Degeneration; D009431:Neural Conduction; D010264:Paraplegia / Q000503:physiopathology; D011712:Pyramidal Tracts / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000473:pathology; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*