Spinal Cord Injuries

An estimated 291,000 persons live with a spinal cord injury (SCI), with roughly 17,730 new cases occurring each year(1). Current research and treatments focus on reducing the “secondary injury cascade” that begins immediately after the initial spinal cord trauma(2). This cascade occurs during either the sub-acute (weeks to months after initial injury) or chronic phase (months to years after initial injury), or during both (3). The severity of this secondary damage directly impacts further bodily damage and the restorative process.

Fortunately, research has shown a correlation between reduced secondary damage and improved neurological outcomes(4, 5). Therapies that can reduce the severity of the secondary injury cascade, such as hyperbaric oxygen therapy, have the potential to reduce the cellular damage that occurs post-injury, and therefore improve neurological outcomes.

 

Extivita Therapies for Spinal Cord Injuries:

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Extivita Therapies Spinal Cord Injury Recovery:

Hyperbaric Oxygen Therapy for Spinal Cord Injury (SCI)

Hyperbaric Oxygen Therapy

Neurofeedback for Spinal Cord Injury (SCI)

Neurofeedback

Supplements for Spinal Cord Injury (SCI)

Supplements

Nutritional IV Therapy for Spinal Cord Injury (SCI)

Nutritional IV Therapy

Pulsed Electromagnetic Field Therapy (PEMF) for Spinal Cord Injury (SCI)

Pulsed Electromagnetic Field Therapy

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Hyperbaric Oxygen Therapy
to treat his
Spinal Cord Injury

Hyperbaric Oxygen Therapy for Spinal Cord Injury:

Hyperbaric Oxygen Therapy - Chapel Hill

Hyperbaric Oxygen Therapy (HBOT) increases oxygen to the damaged spinal cord tissue, thereby decreasing the cell death and damage that can occur for weeks to months after initial injury (6, 7). Additionally, HBOT decreases spinal cord edema (swelling) and inflammation(3) and has been shown to reduce synaptic and dendritic degeneration in animal models(8).

 

Synaptic and dendritic degeneration refers to the degradation of connections between nerve cells, which are essential for healthy neurological function. Reducing such degeneration via HBOT may preserve connections in the spinal cord and brain and thus decrease the severity of neurological impairment. 

 

HBOT Research Shows Improvement To:

  • Reduces cell death
  • Reduces inflammation and swelling
  • Reduces oxidative stress
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Effects of HBOT on Spinal Cord Injury:

Decreases Inflammation

Decreased Inflammation

Hyperbaric oxygen therapy reduces systemic inflammation by increasing anti-inflammatory gene expression and decreasing proinflammatory genes.
Grows New Blood Vessels

New Blood Vessel Formation

Hyperbaric oxygen therapy stimulates the formation of new blood vessels, healing injured tissues that were unable to get nutrients and oxygen.
Increases Stem Cell Production

Increased Stem Cell Activity

Hyperbaric oxygen therapy mobilizes stem progenitor cells (SPCs) from the bone marrow, creating the opportunity for tissue regeneration.
Neurofeedback Therapy in Durham, NC

Neurofeedback for Spinal Cord Injury:

Neurofeedback may help relieve the central neuropathic pain (CNP) that 50% of SCI patients experience(9-10). CNP is characterized by burning, aching, and prickling sensations that often lead to anxiety and sleep issues, as well as a lower quality of life(9, 11-12). There is some evidence that neurofeedback therapy can reduce ratings of pain in SCI patients with CNP. One study found that 80% of study participants experienced statistically significant pain reduction following sessions of alpha reward training(10). Given this, we recommend neurofeedback therapy for people with SCI who may not be responding to traditional CNP treatment, and for those looking for an alternative method of pain relief.

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IV Therapy for Spinal Cord Injury:

Nutritional IV therapy has strong potential to limit that damage of the secondary injury cascade that occurs post-SCI. A hallmark of the secondary phase of SCI is oxidative stress, which occurs when levels of reactive oxygen and/or nitrogen species are elevated(13-14). Brain cells are particularly susceptible to damage from oxidative stress, but such damage can be reduced by improving antioxidant defenses(15).

We recommend our NAD+ IV trio for people with SCI. This trio includes NAD+, a Myer’s Cocktail IV, and a glutathione IV. Both the Myer’s Cocktail IV and glutathione IV have powerful antioxidant effects that may reduce the secondary injury cascade by combating oxidative stress(16-17). The NAD+ can also provide benefits for SCI by improving mitochondrial function, which is impaired in those with SCI(13, 18).

Learn More About Nutritional IV Therapy
Nutritional IV Therapy in Durham, NC
Pulsed Electromagnetic Field Therapy (PEMF) in Durham, NC

Pulsed Electromagnetic Field Therapy for Spinal Cord Injury:

There is some evidence to suggest that pulsed electromagnetic field (PEMF) therapy may promote functional recovery and reduce the secondary injury cascade in those with SCI. These benefits are likely due to PEMF’s ability to reduce inflammation and oxidative stress, both of which are involved in the secondary injury phase of SCI(19).​

Learn More About PEMF

News & Research for Spinal Cord Injury:

Perfluorocarbon in Delayed Recompression with a Mixed Gender Swine Model of Decompression Sickness.

Dec 14, 2017 |

Perfluorocarbons (PFC) are fluorinated hydrocarbons that dissolve gases to a much greater degree than plasma and hold promise in treating decompression sickness (DCS). The efficacy of PFC in a mixed gender model of DCS and safety in recompression therapy has not been previously explored. Swine (25 kg; N = 104; 51 male and 53 female) were randomized into normal saline solution (NSS) or PFC emulsion treatment groups and subjected to compression on air in a hyperbaric chamber at 200 fsw for 31 min. Then the animals were decompressed and observed for signs of DCS. Afterwards, they were treated with oxygen and either PFC (4 cc · kg-1) or NSS (4 cc · kg-1). Surviving animals were observed for 4 h, at which time they underwent recompression therapy using a standard Navy Treatment Table 6. After 24 h the animals were assessed and then euthanized. Survival rates were not significantly different between NSS (74.04%) and PFC (66.67%) treatment groups.

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Neuroprotective effects of hyperbaric oxygen (HBO) therapy on neuronal death induced by sciatic nerve transection in rat.

Oct 30, 2017 |

Recent studies shows that hyperbaric oxygen (HBO) therapy exerts some protective effects against neural injuries. The purpose of this study was to determine the neuroprotective effects of HBO following sciatic nerve transection (SNT). Rats were randomly divided into five groups (n = 14 per group): Sham-operated (SH) group, SH + HBO group, SNT group, and SNT + pre- and SNT + post-HBO groups (100% oxygen at 2.0 atm absolute, 60 min/day for five consecutive days beginning on 1 day before and immediately after nerve transaction, respectively). Spinal cord segments of the sciatic nerve and related dorsal root ganglions (DRGs) were removed 4 weeks after nerve transection for biochemical assessment of malodialdehyde (MDA) levels in spinal cord, biochemical assessment of superoxide dismutase (SOD) and catalse (CAT) activities in spinal cord, immunohistochemistry of caspase-3, cyclooxigenase-2 (COX-2), S100beta (S100ß), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in spinal cord and DRG. The results revealed that MDA levels were significantly decreased in the SNT + pre-HBO group, while SOD and CAT activities were significantly increased in SNT + pre- and SNT + post-HBO treated rats. Attenuated caspase-3 and COX-2 expression, and TUNEL reaction could be significantly detected in the HBO-treated rats after nerve transection. Also, HBO significantly increased S100ß expression. Based on these results, we can conclude that pre- and post-HBO therapy had neuroprotective effects against sciatic nerve transection-induced degeneration.

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Hyperbaric oxygen ameliorated the lesion scope and nerve function in acute spinal cord injury patients: A retrospective study.

Oct 20, 2017 | ,

This is a retrospective study to assess the therapeutic effect of hyperbaric oxygen (HBO) in early treatment of acute spinal cord injury (SCI) using magnetic resonance imaging (MRI) and electrophysiology in diagnosing. Forty acute SCI patients from Sun Yat-Sen Memorial Hospital who were assigned into HBO treatment were included during August 2013 to October 2014.The patients with adverse reactions or contraindications for HBO were assigned as controls. Both of two groups (HBO and Control) received medicine treatment with Urbason, GM-1 and mecobalamine after surgery. ASIA and the Frankel scores were used to evaluate the therapeutic effect of HBO at the 15th and 30th day after HBO treatment by using MRI and electrophysiology features. Significant therapeutic effect of HBO treatment on acute SCI patients was observed compared with the control group (P<0.05). Comparison for ASIA and Frankel scores showed that motor and neurological functions were significantly improved in HBO group at day 15 and day 30 post treatment. MRI images showed that the grade III injury in HBO group was significant lower than the control group. In comparison with the control, the peak of somatosensory evoked potential (SEP) and motor evoked potential (MEP) amplitude increased, the latency was shortened, and the conduction velocity of sensory nerve (SCV) and motor nerve (MCV) was significantly increased in the HBO group (P<0.05). HBO treatment has a great efficacy in acute SCI patients. HBO therapy at early stage of acute SCI is beneficiary to the recovery.

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References
  1. “Home Page – NSCISC Application.” Accessed June 19, 2019. https://www.nscisc.uab.edu/.
  2. “Spinal Cord Injury Information: Levels, Causes, Recovery.” Accessed June 19, 2019. https://www.shepherd.org/patient-programs/spinal-cord-injury/about#FAQ3.
  3. Oyinbo, Charles Aidemise. “Secondary Injury Mechanisms in Traumatic Spinal Cord Injury: A Nugget of This Multiply Cascade.” Acta Neurobiologiae Experimentalis 71, no. 2 (2011): 281–99. https://pdfs.semanticscholar.org/8131/2216495186e1d35f6958c59587714efca557.pdf
  4. Dumont, R. J., D. O. Okonkwo, S. Verma, R. J. Hurlbert, P. T. Boulos, D. B. Ellegala, and A. S. Dumont. “Acute Spinal Cord Injury, Part I: Pathophysiologic Mechanisms.” Clinical Neuropharmacology 24, no. 5 (October 2001): 254–64. https://www.ncbi.nlm.nih.gov/pubmed/11586110
  5. Kwon, Brian K., Wolfram Tetzlaff, Jonathan N. Grauer, John Beiner, and Alexander R. Vaccaro. “Pathophysiology and Pharmacologic Treatment of Acute Spinal Cord Injury.” The Spine Journal 4, no. 4 (July 1, 2004): 451–64. https://doi.org/10.1016/j.spinee.2003.07.007
  6. Kelly, D. L., K. R. Lassiter, A. Vongsvivut, and J. M. Smith. “Effects of Hyperbaric Oxygenation and Tissue Oxygen Studies in Experimental Paraplegia.” Journal of Neurosurgery 36, no. 4 (April 1972): 425–29. https://doi.org/10.3171/jns.1972.36.4.0425.
  7. Emery, E., P. Aldana, M. B. Bunge, W. Puckett, A. Srinivasan, R. W. Keane, J. Bethea, and A. D. Levi. “Apoptosis after Traumatic Human Spinal Cord Injury.” Journal of Neurosurgery 89, no. 6 (December 1998): 911–20. https://doi.org/10.3171/jns.1998.89.6.0911.
  8. Ying, Xinwang, Wenzhan Tu, Sisi Li, Qiaoyun Wu, Xiaolong Chen, Ye Zhou, Jie Hu, Guanhu Yang, and Songhe Jiang. “Hyperbaric Oxygen Therapy Reduces Apoptosis and Dendritic/Synaptic Degeneration via the BDNF/TrkB Signaling Pathways in SCI Rats.” Life Sciences 229 (July 15, 2019): 187–99. https://doi.org/10.1016/j.lfs.2019.05.029.
  9. Siddall, Philip J., et al. “A Longitudinal Study of the Prevalence and Characteristics of Pain in the First 5 Years Following Spinal Cord Injury.” Pain, vol. 103, no. 3, June 2003, pp. 249–57. ScienceDirect, doi:10.1016/S0304-3959(02)00452-9.
  10. Vučković, Aleksandra, et al. “EEG Correlates of Self-Managed Neurofeedback Treatment of Central Neuropathic Pain in Chronic Spinal Cord Injury.” Frontiers in Neuroscience, vol. 13, Frontiers, 2019. Frontiers, doi:10.3389/fnins.2019.00762.
  11. Finnerup, Nanna B., et al. “Neuropathic Pain Clinical Trials: Factors Associated with Decreases in Estimated Drug Efficacy.” Pain, vol. 159, no. 11, Nov. 2018, pp. 2339–46. PubMed Central, doi:10.1097/j.pain.0000000000001340.
  12. Middleton, James, et al. “Relationship Between Quality of Life and Self-Efficacy in Persons With Spinal Cord Injuries.” Archives of Physical Medicine and Rehabilitation, vol. 88, no. 12, Dec. 2007, pp. 1643–48. ScienceDirect, doi:10.1016/j.apmr.2007.09.001.
  13. Azbill, Robert D., et al. “Impaired Mitochondrial Function, Oxidative Stress and Altered Antioxidant Enzyme Activities Following Traumatic Spinal Cord Injury.” Brain Research, vol. 765, no. 2, Aug. 1997, pp. 283–90. ScienceDirect, doi:10.1016/S0006-8993(97)00573-8.
  14. Pizzino, Gabriele, et al. “Oxidative Stress: Harms and Benefits for Human Health.” Oxidative Medicine and Cellular Longevity, vol. 2017, 2017. PubMed Central, doi:10.1155/2017/8416763.
  15. Jia, Z., et al. “Oxidative Stress in Spinal Cord Injury and Antioxidant-Based Intervention.” Spinal Cord, vol. 50, no. 4, 4, Nature Publishing Group, Apr. 2012, pp. 264–74. www.nature.com, doi:10.1038/sc.2011.111.
  16. Carr, Anitra C., and Silvia Maggini. “Vitamin C and Immune Function.” Nutrients, vol. 9, no. 11, Nov. 2017. PubMed Central, doi:10.3390/nu9111211.
  17. Forman, Henry Jay, et al. “Glutathione: Overview of Its Protective Roles, Measurement, and Biosynthesis.” Molecular Aspects of Medicine, vol. 30, no. 1–2, Apr. 2009, pp. 1–12. PubMed, doi:10.1016/j.mam.2008.08.006.
  18. Johnson, Sean, and Shin-ichiro Imai. “NAD + Biosynthesis, Aging, and Disease.” F1000Research, vol. 7, Feb. 2018. PubMed Central, doi:10.12688/f1000research.12120.1.
  19. Wang, Chunyan, et al. “Lowfrequency Pulsed Electromagnetic Field Promotes Functional Recovery, Reduces Inflammation and Oxidative Stress, and Enhances HSP70 Expression Following Spinal Cord Injury.” Molecular Medicine Reports, vol. 19, no. 3, Spandidos Publications, Mar. 2019, pp. 1687–93. www.spandidos-publications.com, doi:10.3892/mmr.2019.9820.