Critical roles of decompression in functional recovery of ex vivo spinal cord white matter

Abstract

Object The correlations between functional deficits, the magnitude of compression, and the role of sustained compression during traumatic spinal cord injury remain largely unknown. Thus, the functional outcome of this type of injury with or without surgical intervention is rather unpredictable. To elucidate how severity and duration of compression affect cord function, the authors have developed a method to study electrophysiological characteristics and axonal membrane damage in white matter from guinea pig spinal cord. Methods Ventral white matter strips isolated from adult guinea pigs were compressed by a compression rod at a level of either 60 or 80% and held briefly, for 30 minutes, or for 60 minutes. In half the experimental groups, a decompression phase consisting of probe withdrawal and 30 minutes of recovery was also applied. For all cord samples, functional response was continuously monitored through compound action potential (CAP) recording. In addition, axonal membrane damage was assessed by a horseradish peroxidase (HRP) exclusion assay. Results After 30 minutes of sustained compression at levels of 60 or 80%, a spinal cord decompression procedure caused a significant CAP recovery, with specimens reaching 97.5 ± 6.84% (p < 0.05) and 56.2 ± 6.14% (p < 0.05) of preinjury amplitude, respectively. After 60 minutes of compression, the amount of CAP recovery following the decompression stage was only 65.5 ± 9.33% for 60% compression (p < 0.05) and 29.8 ± 6.31% for 80% compression (p < 0.05). Unlike the CAP response, HRP uptake did not increase during sustained compression, and the data showed that HRP staining was primarily time dependent. Conclusions The degree of axonal membrane damage is not exacerbated during sustained compression. However, the electrical conductivity of the cord white matter weakens throughout the duration of compression. Therefore, decompression is a viable procedure for preservation of neurological function following compressive injury.