• Samuel J Mackenzie, Igor Smirnov, and Blair Calancie.
• Department of Neuroscience, Upstate Medical University, Syracuse, NY, USA.
• J. Neurotrauma. 2012 May 20;29(8):1683-90.

AbstractTreatment 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.

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