Yu, et al. (2001): Neurophysiological evidence of spared upper motor conduction fibers in clinically complete spinal cord injury

[Wise Young]

• Yu K, Rong W, Li J, Jia L, Yuan W, Yie X and Shi Z (2001). Neurophysiological evidence of spared upper motor conduction fibers in clinically complete spinal cord injury: discomplete SCI in rats. J Neurol Sci. 189 (1-2): 23-36. Summary: 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. <http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11535230> Deparment of Orthopaedic Surgery, Changzheng Hospital, Feng Yang Road 415#, 200003, Shanghai, People's Republic of China

[This message was edited by Wise Young on September 23, 2001 at 10:16 PM.]

[Wise Young]

Many clinicians assume that if there is no function, there must be no axons that cross the injury site. That is one of the reasons why many clinicians use the words "complete" spinal cord injury and "transections" of the spinal cord almost interchangeably. However, many of us who have looked at the spinal cords of humans and rats know that so-called "complete" spinal cord injury is not always associated with complete loss of all connections with the brain. Milan Dimitrijevic (a neurologist who use to work in Houston) called this condition "discomplete".

These authors report here that rats that appear to have complete loss of neurological function below the injury site may still have intact fibers crossing the injury site and that such fibers can be induced to conduct to some extent by 4-aminopyridine. These findings are important for several reasons. First and foremost, it suggests that complete spinal cord injury does not necessarily mean complete loss of connections. Second, it suggests that 4-AP may be useful for restoring function to some rats even though they may have so-called "complete" spinal cord injury.

Wise.