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Basic image of the spinal cord vertebrae and where the nerves are located transcending the length.

Acute Spinal Cord Injury (ASCI)[edit]

Acute spinal cord injury (ASCI) involves severe damage to or even complete severance of the spinal cord, this can change the overall function of the spinal cord[1]. ASCI injuries are typically irreversible and impair one's sensory and motor function. Although most ASCI cases do not result in casualty, quality of life is decreased substantially because of the loss of sensation, muscle function, and some autonomic function. ASCI is mostly induced through various means of physical trauma like automobile accidents or sports related injuries. Although most ASCI cases are due to physical trauma, there are also cases where physical trauma does not cause ASCI[2]. Sometimes cancerous tumors that develop internally can press on the spinal cord and mimic damage caused by physical traumas. The spinal cord connects the peripheral nervous system (PNS) and central nervous system (CNS) through a complex integration of neurons and interneurons. The location and size of the injury determines how severe the consequences could be. In less severe cases, patients can experience numbness or pain. In more severe cases, a patient could experience total paralysis and complete loss of sensory and muscular function[3].

Specific nerves, like sensory neurons, have projections in both central and peripheral neurological domains. Most ASCI injuries impact the sensory nerves because they traverse the length of the entire spinal cord. Sensory nerves bridge PNS and CNS communication because the cell body has a peripheral projection extending from the cell body to the skin and a central (afferent) projection that extends from the cell body into the spinal cord via the dorsal root entry zone (DREZ). Severance or severe injury to nerves that directly bridge the PNS/CNS gap breaks the connection between the CNS and PNS and the two domains are no longer able to communicate. Sensory nerves serve as one example of a CNS/PNS break occurring during ASCI but, motor neurons, interneurons, and several other types of neurons responsible for specific tasks can be influenced and break neural circuitry as well. Disruption of neural circuitry can have serious implications on regeneration and wound healing[4].

Snapshot of peripheral nerve regeneration in zebrafish, specifically an axon interacting with Schwann cells.

Regeneration[edit]

Many cells in the body have the capacity to fully or at least partially regenerate. The regenerative capacity of nerves is extremely limited, especially inside the spinal cord. The ability to regenerate post-injury is dependent upon the location, size, and severity of the injury. Most ASCI cases involve injury to sensory nerves, in these cases, only the peripheral projection of the nerve has the capacity to regenerate fully. The central (afferent) projection into the spinal cord does not exhibit the same regenerative capacity and typically fails to regenerate. This is one specific example, but displays how injury and improper regeneration can have detrimental impacts on PNS/CNS communication. Unfortunately, there is no direct treatment for ASCI patients, especially in more severe cases[5]. But, there are ways to combat pain, improve neurological function in injured areas, and make the patient more comfortable. Early ASCI treatment involves the overall comfort of the patient and light physical therapy[6]. This involves re-aligning the spine, simple surgeries to decompress the spinal cord, drain fluid, and relieve pressure to provide immediate relief[7]. Later treatment involves more aggressive rounds of physical therapy and the possibility of more invasive and exploratory surgical procedures. More recent approaches to healing involves rounds of hormonal steroid treatment and stem cell implantation[8].

Treatments[edit]

ASCI injuries can start less severe and become more detrimental the longer they go untreated. If ASCI injuries are not treated almost immediately, or within a few hours post-injury, the regenerative, sensory, and motor consequences become more severe and are more likely to fail. Recent steroid hormone studies have shown how impactful immediate ASCI treatment can be. Methylprednisolone and naloxone are two steroid hormones that are potential therapeutics for ASCI. Methylprednisolone was tested in the early 90's over a 10 day period, but induced infection and complications within ASCI patient[9][10]. Since then, more efficient antibiotics and regimens to treat infection have been developed to combat these consequences. Recently, methylprednisolone and naloxone have been used in several trials involving ASCI, general spinal cord injury (SCI), and traumatic spinal cord injury (TSCI)[11]. Both therapeutics improve sensory and motor function, but the drugs must be administered within a short window post-initial injury to achieve maximum efficiency. These two therapeutics provide a means to improve neurological function in severe injury cases, but a disadvantage is they must be administered almost immediately following injury. For patients involved in a car accident, immediate treatment may not be an option.

More research efforts are being made to find more long term treatments for ASCI patients because not much can be done for patients unable to be treated immediately following injury. The current tools do allow for the patient to be more comfortable, participate in physical therapy, and have access pain medications. But, this is a current gap in the medical field and demands a greater need for research in therapeutics and further development of ASCI injury models[4].

  1. ^ Cortez, Ricardo; Levi, Allan D. (2007-03-01). "Acute spinal cord injury". Current Treatment Options in Neurology. 9 (2): 115–125. doi:10.1007/s11940-007-0037-y. ISSN 1092-8480.
  2. ^ "What you should know about spinal cord injuries". International Journal of Trauma Nursing. 7 (2): 74–75. 2001-04-01. doi:10.1067/mtn.2001.115395.
  3. ^ Morganti-Kossmann, Cristina; Raghupathi, Ramesh; Maas, Andrew (2012-07-19). Traumatic Brain and Spinal Cord Injury: Challenges and Developments. Cambridge University Press. ISBN 9781107007437.
  4. ^ a b Masri(y), Wagih Shafik El; Kumar, Naveen (2011-03-19). "Traumatic spinal cord injuries". The Lancet. 377 (9770): 972–974. doi:10.1016/S0140-6736(11)60248-1. ISSN 0140-6736. PMID 21377200 21377200, 21377200. {{cite journal}}: Check |pmid= value (help)
  5. ^ Bracken, Michael B.; Shepard, Mary Jo; Collins, William F.; Holford, Theodore R.; Young, Wise; Baskin, David S.; Eisenberg, Howard M.; Flamm, Eugene; Leo-Summers, Linda (1990-05-17). "A Randomized, Controlled Trial of Methylprednisolone or Naloxone in the Treatment of Acute Spinal-Cord Injury". New England Journal of Medicine. 322 (20): 1405–1411. doi:10.1056/NEJM199005173222001. ISSN 0028-4793. PMID 2278545.
  6. ^ Adams, James G. (2012-09-05). Emergency Medicine E-Book: Clinical Essentials (Expert Consult -- Online). Elsevier Health Sciences. ISBN 1455733946.
  7. ^ Shah, Kaushal H.; Egan, Daniel; Quaas, Joshua (2012-02-17). Essential Emergency Trauma. Lippincott Williams & Wilkins. ISBN 9781451153187.
  8. ^ Newman, Mark F.; Fleisher, Lee A.; Fink, Mitchell P. (2008). Perioperative Medicine: Managing for Outcome. Elsevier Health Sciences. ISBN 1416024565.
  9. ^ Walker, Michael D. (2010-01-14). "Acute Spinal-Cord Injury". http://dx.doi.org/10.1056/NEJM199106273242608. doi:10.1056/nejm199106273242608. Retrieved 2017-09-26. {{cite web}}: External link in |website= (help)
  10. ^ Bracken, Michael B.; Shepard, Mary Jo; Collins, William F.; Holford, Theodore R.; Baskin, David S.; Eisenberg, Howard M.; Flamm, Eugene; Leo-Summers, Linda; Maroon, Joseph C. (2009-05-27). "Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data". Collections. 112 (2): 23–31. doi:10.3171/jns.1992.76.1.0023@col.2.
  11. ^ Nesathurai, Shanker (December 1998). "Steroids and Spinal Cord Injury: Revisiting the NASCIS 2 and NASCIS 3 Trials". Journal of Trauma and Acute Care Surgery. 45 (6): 1088–1093. ISSN 2163-0755.