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               Central Nervous System Trauma

               Simon R. Platt, BVM&S, FRCVS, DACVIM (Neurology), DECVN

               Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA, USA


                 Spinal Trauma                                      vides a window for therapeutic intervention, we are cur-
                                                                    rently less capable of halting these processes,  which
               Traumatic spinal cord injury (SCI) is a devastating disease   include vasospasm and localized ischemia, delayed cell
               in human and veterinary medicine. The majority of SCIs   damage and apoptosis, ion‐mediated cell damage and
               result from vehicle‐related accidents but other impor-  excitotoxicity, and neuroinflammation, as well as mito-
               tant causes include gunshots, dog fights, falls, accidental   chondrial dysfunction and oxidative cell damage.
               owner‐induced injuries, and falling objects.       Clinical signs associated with spinal trauma are caused
                                                                  by injury to the spinal cord, the spinal nerves as they exit
               Pathophysiology of Spinal Cord Injury              the vertebral canal, and the vertebral column itself. The
                                                                  different injuries resulting from trauma include vertebral
               The normal spinal cord is a stable structure throughout   fractures, subluxations and luxations, flexion/extension
               life, but it exhibits modest decrements in myelinated   injuries, and traumatic disk herniations. Subluxation
               axon  and  neuron  numbers  with  advancing  age.  Its   and luxation can occur in combination with a vertebral
               complexity greatly exceeds that of other tissues, and its   fracture or due to soft tissue disruption only, without
               thin cellular processes can extend long distances, thereby   evidence of vertebral injury. These injuries occur most
               increasing their vulnerability. It has unique vascular   frequently  at  the  lumbosacral,  thoracolumbar,  and
               barriers and fluid compartments. Its cellular compo-  atlantoaxial junctions. Cats are more likely to suffer sac-
               nents and the tissues that they form are highly suscepti-  rocaudal fractures than dogs, and typically have a com-
               ble to injury. Together with the brain, this organ has the   bination of fracture and luxation, whereas approximately
               least ability to undergo self‐repair. Increasing evidence   20% of dogs suffer a luxation only.
               indicates  that  the  spinal  cord  also  has  distinct  differ-  These events can cause spinal cord contusion and
               ences from the brain in its injury responses.        laceration, and can result in compression by bone, soft
                 The pathophysiology of SCI can be divided into two
               phases: the initial primary injury and subsequent second-  tissue or blood (hematomas). Ongoing instability can
                                                                  result in repeated contusive injuries, additional laceration
               ary injury.
                                                                  of the cord, and increasing severity of compression.
                  Primary injury refers to the initial traumatic insult to   Compression of the spinal cord reduces perfusion, poten-
               ●
                 the spinal cord, which results in immediate severing of   tially causing neuronal and glial cell death by the second-
                 axons and death of spinal cord cells.            ary injury mechanisms described above. Demyelination
                  Secondary injury invariably follows and leads to pro-  is a common finding histopathologically, as a result of
               ●
                 gressive tissue damage for weeks after the initial insult.   both direct damage to myelin and death of oligodendro-
                 It results from a complex series of related events on a   cytes. Physical deformation of axons can cause failure of
                 number of physiologic levels. Hypotension and hypoxia   ion channels, changing membrane permeability and pro-
                 are important preventable causes of secondary injury at   ducing conduction block that rapidly reverses when
                 a clinical level and must be recognized and either pre-  decompressed. Ongoing spinal cord compression can
                 vented or treated proactively.  Numerous  secondary   also cause development of syringohydromyelia cranial to
                 injury mechanisms also occur on the   cellular level, and   the compression site, potentially causing neuropathic
                 although their delayed time course theoretically pro-  pain in addition to further neurologic deterioration.

               Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
               © 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
               Companion website: www.wiley.com/go/bruyette/clinical
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