TY - JOUR
T1 - Cauda equina repair in the rat
T2 - Part 2. Time course of ventral root conduction failure
AU - Mackenzie, Samuel J.
AU - Smirnov, Igor
AU - Calancie, Blair
PY - 2012/5/20
Y1 - 2012/5/20
N2 - Treatment for cauda equina (CE) ventral root injury is currently limited. Furthermore, relatively little is known about the time course of nerve root functional degeneration after such injury has occurred. Using a previously developed method for identifying spinal nerve roots that innervate the rat tail, we transected S2, S3, and S4 ventral roots and measured their ability to activate tail muscles out to 72 h post-injury by way of stimulus-evoked electromyography (EMG) recording. Immediately following transection, all distal ventral root stumps successfully activated muscles in the tail upon stimulation with no change in stimulus threshold (0.07±0.04 to 0.07±0.06 V using 0.1-msec pulse duration; 0.04±0.02 to 0.04±0.02 V using 1.0-msec pulse duration). Thresholds increased incrementally at each later time point (24 h: 0.27±0.33 V using 0.1-msec pulse duration; 0.09±0.07 V using 1-msec pulse duration; 48 h: 0.57±1.00 V using 0.1-msec pulse duration; 0.56±1.09 V using 1-msec pulse duration), with the first complete absence of EMG noted at 48 h post-transection in a subset of nerve roots (4/12). We were not able to elicit EMG at 72 h post-transection without moving distally along the nerve root stump. Based on neurofilament staining, only 51% of axons were identifiably intact nearest the site of injury at 24 h post-injury. This percentage dropped to 39% at 48 h, and just 18% at 72 h. Moving 5 mm from the site of injury, we identified 83% intact axons at 24 h post-transection, 77% at 48 h, and 68% at 72 h. Regenerative implications aside, if electrophysiological mapping of injured nerve roots is to be carried out for repair purposes, the rapid nature of conduction failure needs to be considered.
AB - Treatment for cauda equina (CE) ventral root injury is currently limited. Furthermore, relatively little is known about the time course of nerve root functional degeneration after such injury has occurred. Using a previously developed method for identifying spinal nerve roots that innervate the rat tail, we transected S2, S3, and S4 ventral roots and measured their ability to activate tail muscles out to 72 h post-injury by way of stimulus-evoked electromyography (EMG) recording. Immediately following transection, all distal ventral root stumps successfully activated muscles in the tail upon stimulation with no change in stimulus threshold (0.07±0.04 to 0.07±0.06 V using 0.1-msec pulse duration; 0.04±0.02 to 0.04±0.02 V using 1.0-msec pulse duration). Thresholds increased incrementally at each later time point (24 h: 0.27±0.33 V using 0.1-msec pulse duration; 0.09±0.07 V using 1-msec pulse duration; 48 h: 0.57±1.00 V using 0.1-msec pulse duration; 0.56±1.09 V using 1-msec pulse duration), with the first complete absence of EMG noted at 48 h post-transection in a subset of nerve roots (4/12). We were not able to elicit EMG at 72 h post-transection without moving distally along the nerve root stump. Based on neurofilament staining, only 51% of axons were identifiably intact nearest the site of injury at 24 h post-injury. This percentage dropped to 39% at 48 h, and just 18% at 72 h. Moving 5 mm from the site of injury, we identified 83% intact axons at 24 h post-transection, 77% at 48 h, and 68% at 72 h. Regenerative implications aside, if electrophysiological mapping of injured nerve roots is to be carried out for repair purposes, the rapid nature of conduction failure needs to be considered.
KW - Wallerian degeneration
KW - electric stimulation
KW - electromyography
KW - neurofilament proteins
KW - rats
KW - spinal nerve roots
KW - tail
UR - http://www.scopus.com/inward/record.url?scp=84861970560&partnerID=8YFLogxK
U2 - 10.1089/neu.2010.1571
DO - 10.1089/neu.2010.1571
M3 - Article
C2 - 21361731
AN - SCOPUS:84861970560
SN - 0897-7151
VL - 29
SP - 1683
EP - 1690
JO - Journal of neurotrauma
JF - Journal of neurotrauma
IS - 8
ER -