Introduction: Neonatal brachial plexus palsy (NBPP) results from over-stretching of the brachial plexus (BP) during complicated delivery1 with reported incidence of 0.9-2.6 per 1000 live births2-6. Permanent disability is reported in 30-45% of clinical cases, with concomitant spinal cord injury (CSci) in over 80% of these cases 7-11. Although CSci prevention seems critical to limiting the incidence of permanent disability occurring during NBPP, no data exists on the BP strains and forces that are transmitted to the spinal cord (SC) leading to CSci. The aim of this study is to determine the histological changes in the spinal cord post BP avulsion injuries.
Materials and
Methods: Four newborn piglets (3-4 days old) were anesthetized and intubated according to the approved IACUC protocol, Drexel University. The exposed brachial plexus (Musculocutaneous nerves were subjected to failure tensile testing using a custom-built biomechanical testing set-up) was put through mechanical stretching until failure to induce avulsion injuries by clamping the nerve (Figs.1 and 2). Samples of injured nerve and spinal cord were harvested and prepared using H&E staining methods. These samples were then imaged using a stitch microscope at 10X magnification. The spinal cord samples were then analyzed, determining the amount of damage for each section of the spinal cord in the dorsal and ventral horns, bilaterally. These are the areas where the rootlets attach to the spinal cord (Fig. 3). A scale of 0-2 was used to rate the injury (0 being no injury, 1 being some injury, and 2 being severe injury) for each region of the C5 spinal cord (Left and Right Ventral and Dorsal horns (Fig. 2)). Two C5 level spinal cord regions (innervating MSC (Med School Competitiveness) nerve) with three sections each were scored.
Results, Conclusions, and Discussions: Using the modified scoring system, we report an increase in the extent of SC damage with increasing failure load (Table 1). Only one rupture was reported during mechanical testing and all other samples were avulsed at the MSC BP level. The current study contributes to understanding the avulsion injury mechanisms in neonatal brachial plexus using a large animal piglet model. Future studies can further characterize structural changes such as the extent of neuronal damage and vascular disruption in avulsed BP thereby increasing our understanding of NBPI (Neonatal Brachial Plexus Injury) and concomitant SCI (Spinal Cord Injury). Such knowledge is critical to guiding the care of neonates.
Acknowledgements (Optional): This research was supported by funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health under Award Number R15HD093024 and R01HD104910A and NSF (National Science Foundation) CAREER Award Number 1752513.
