Hyperbaric Oxygen Treatment Following Mid‐Cervical Spinal Contusion Injury

Mounting evidence suggests daily hyperbaric oxygen treatment (HBOT) can enhance functional motor recovery after thoracic spinal cord injury (SCI), possibly through alterations in inflammatory signaling and reduced apoptosis at or near the lesion epicenter. The purpose of this initial study was to explore using HBOT as a rehabilitative tool after cervical spinal contusion injury. Rats were randomly divided into the following groups: 1) naïve (no prior treatment), 2) sham operated (laminectomy only), 3) lateral contusion at C3/4 (cSCI) and, 4) cSCI + daily HBOT. The HBOT consisted of a 1 hr exposure to 2.0 atmospheres of 100% O2, beginning on the day of SCI and continued for 10 days. Forelimb function was analyzed on day 10 post‐surgery using open field forelimb locomotor scoring (FLS) and a “water grooming” test. Compared to naïve and sham rats, ipsilateral forelimb function was severely disrupted following cSCI in both the untreated and HBOT‐treated groups (p<0.05). However, HBOT‐treated rats showed a 17% increase in ipsilateral forelimb joint mobility (FLS score = 4.1 ± 1.6) when compared to the untreated cSCI group (FLS score = 1.25 ± 0.25; p = 0.074). In addition, a greater proportion of HBOT‐treated cSCI animals regained the ability to groom with the ipsilateral forelimb when compared to untreated cSCI animals (Chi‐Square Test, p = 0.016). After the 10th treatment day, cervical spinal tissues (C2–C5) were harvested for analyses of mRNA gene expression. Compared to non‐treated rats, the HBOT cohort showed increased mRNA expression (p<0.05) of genes involved in axon growth/guidance, including: SLIT2, CNTN1, ABLIM1, PLXNB1, and ARHGEF12. In addition HBOT treated rats showed decreased mRNA expression (p<0.05) of genes involved in the induction of apoptosis via DR3 and DR4/5 death receptors, such as: RELA, CASP9, NFKB1A, FADD, TNFSF12, and APAF1. Our data are consistent with prior reports of improved motor function following HBOT in SCI animal models, and the mRNA data raise the possibility that HBOT may be influencing axonal growth and regeneration, as well as attenuating cell death. Thus, HBOT following spinal cord injury may have exciting rehabilitative potential.Support or Funding InformationCTSA U54‐TR001012, Craig H. Neilsen Foundation 313369 (SMFT), 1 R01 NS080180‐01A1 (DDF), State of Florida Brain and Spinal Cord Injury Research Program (DDF and PJR)