Overview of spinal cord injuries

Original Editor - Kudzanayi Ronald Muzenda

Top Contributors - Naomi O'Reilly and Kudzanayi Ronald Muzenda  

What is a Spinal Cord Injury

Spinal Cord Injury (SCI) is a sudden onset disruption to the neuronal tissue within the spinal canal resulting in spinal cord damage, which occurs as a result of trauma, disease or degeneration.[1][2] Any damage to the spinal cord is a very complex injury. Each injury is different and can affect the body in many different ways. It can present as either an upper motor neuron lesion or lower motor neuron lesion with varying loss of motor, sensory and autonomic function, either temporary or permanent depending on the level and type of injury to the Spinal Cord or Cauda Equina. [2][3] Effective management of spinal cord injury is reliant upon accurate clinical examination and classification of the neurological injury combined with detailed radiological assessment of the vertebral column injury. [4]

Clinically Relevant Anatomy

The spinal column is comprised of 33 Vertebra; 7 Cervical Vertebrae, 12 Thoracic Vertebrae, 5 Lumbar Vertebrae, 5 Fused Sacral Vertebrae and 4 Fused Coccygeal Vertebrae, which provide support and protection for the spinal cord. The spinal cord is the major conduit between the peripheral nerves and the brain, and transmits motor information from the brain to the muscles, tissues and organs, and sensory information from these areas back to the brain. [5][6]

The nervous system is divided into the central nervous system (brain and spinal cord) and the peripheral nervous system (nerves that enter and exit the spinal cord). Information to and from the muscles, glands, organs and sensory receptors are carried through the peripheral nervous system, which is divided into the autonomic nervous system carrying information to and from the organs, and the somatic nervous system carrying information to and from the muscles and the external environment. [5]

The autonomic nervous system consists of the parasympathetic nervous system that governs resting function and the sympathetic nervous system that governs excitatory functions. The spinal cord and peripheral nerves provide all impulses to control muscle contraction, cardiac rhythm, pain and other bodily functions so therefore any lesion to the spinal cord prevents or reduces transmission of this information to and from the brain to the peripheries, affecting movement, sensation and visceral function. [6]

Read more about Spinal Cord Anatomy

Spinal Column [7]
Spinal Cord Sectional Anatomy [8]

Etiology and Epidemiology

Spinal Cord injury can occur as a result of non-traumatic causes (16%) secondary to disease, infection and congenital defect. and trauma (84%), with themost common occurring as a result of motor vehicle and motor-bike accidents, followed by falls. Sport, in particular water based activities and work-related injuries are also common, while violence related injuries from gun, stab or war-related injuries are high in some countries. 

Global Prevalence of spinal cord injury varies from 236 to 1298 per million of population with a recent trend in increasing prevalence over the last decade. A recent systematic review found the prevalence of spinal cord injury to be dependent on the region the studies were conducted in, ranging from the highest prevalence of 906 per million in the USA and the lowest prevalence of 250 per million in Rhone-Alpes, France.[9] While further studies found similar results with prevalence ranging from 1298 per million to 50 per million. [10]

Global incidence also shows huge variance from 8 to 246 cases per million of population in one study while further research found similar results with 246 per million to 3.3 per million. [9][10] Annual incidence rates also varied significantly between region, ranging from 246 per million in Taiwan, 49.1 per million in New Zealand to just 10.0 per million in Fiji. [9] Similarly studies available also show a high male-to-female ratio of 5:1 with peak incidence of spinal cord injury occurring at 42 years old, increased from 29 years old in 1970.

These results indicate that the incidence, and prevalence of Spinal Cord Injury can differ significantly between countries and regions, and identifies the need for development of preventative and management strategies that are tailored towards regional trends.There is limited available research that examines the reasons for this variation suggesting the need for further comparative studies, and for international standards and guidelines for reporting on spinal cord injury. [9]

Read more about Epidemiology of Spinal Cord Injury

Clinical Presentation

Injuries to the spinal cord are complex, and each individuals injury is unique in terms of the functions affected and therefore the clinical presentation. Most spinal cord injuries do not involve full transection or severing of the spinal cord. Rather, the spinal cord remains intact and the neurological damage is due to secondary vascular and pathogenic events, including oedema, inflammation and changes to the blood-spinal cord barrier. [11] Signs and symptoms vary depending on where the spine is injured and the extent of the injury but can include loss of power, sensation, respiration, temperature regulation, bladder, bowel and sexual function.

Paraplegia refers to impairment or loss of motor, sensory or autonomic function in areas of the body served by the thoracic, lumbar or sacral segments of the spinal cord. Depending on the level of the injury trunk, pelvic organs and lower limbs may be involved with upper limb function preserved.[1]

Tetraplegia, sometimes referred to as quadriplegia in some countries, refers to impairment or loss of motor, sensory or autonomic function in areas of the body served by the cervical segments of the spinal cord. This results in impairment in upper and lower limbs, trunk and pelvic organs with respiratory function impaired in those with high cervical injuries.[1]

Classification of the spinal cord injury is conducted by means of a neurologic assessment including motor, sensory and autonomic evaluation to determine the degree of sparing of motor, sensory and autonomic function below the level of the Injury using the American Spinal Injury Association (ASIA) Impairment Scale. [4][11]

Types

Spinal cord injury can result in complete or incomplete injury to the spinal cord, which can prevent the transmission of all or just some neural messages across the site of the lesion, resulting in highly varied presentations of injury. Some individuals will have extensive preservation of motor and sensory pathways with a more favourable outcome, while in others there is limited preservation. Partial preservation of the spinal cord tends to be more common in cervical, lumbar and sacral level injuries.

The American Spinal Injury Association (ASIA) classification system, based on a standardized motor and sensory assessment, is used to classify spinal cord injuries.It is used to define two motor, two sensory and one neurological level. It is also used to classify injuries as either complete (ASIA A) or incomplete (ASIA B, C, D or E), with distinction between different ASIA impairments made on the basis of: 

  • Motor function in S4 - S5, reflected by the ability to voluntarily contract the anal sphincter. 

  • Sensory function in S4 - S5, reflected by appreciation of deep anal pressure or preservation of either light touch or pinprick sensation in the perianal area.
  • Strength in muscles below the motor and neurological level. 


  The S4 - S5 segments is linked to prognosis, with preservation a strong predictor of neurological recovery. Similarly preservation of pinprick sensation anywhere on the body helps predict motor recovery. 

Complete (ASIA A)

A complete spinal cord injury has no motor or sensory function in S4 - S5 area of the spinal cord. Complete ASIA A lesions can also have zones of partial preservation reflecting some preservation of motor or sensory function below the neurological level, however, if there is motor or sensory function in S4 - S5 the lesion is no longer complete but rather incomplete. 

Incomplete (ASIA B, C, D and E)

An incomplete spinal cord injury has some preservation of sensory and/or motor function in the S4 - S5 area of the spinal cord. There are a number of recognised patterns of incomplete cord injury. More commonly these tend to present clinically as combinations of syndromes rather than in isolation with signs and symptoms related to the anatomical areas of the spinal cord affected. Central Cord Lesion: The most common of the incomplete spinal cord injury syndromes, central cord syndrome is ypically seen in older patients with cervical spondylosis secondary to degenerative changes in the spinal column, with osteophytes and possible disc bulges, combined with spondylitic joint changes in the anterior part of the vertebral column with thickening of the ligamentum flavum posteriorly. Predominantly occurs as a result of a hyperextension injury, which compresses the central cord in the narrowed canal and leads to interference of the blood supply causing hypoxia and haemorrhage of the central cord grey matter, which is often already compromised in an older person and so has less potential for recovery. This presents with upper limbs more profoundly affected than lower limbs, often flaccid weakness of the arms, due to lower motor neuron lesions, and spastic patterning in the arms and legs due to upper motor neuron lesions as the central cervical tracts are predominantly affected with some partial dysfunction of bowel and bladder common. Prognosis varies and is often age dependent with ambulation seen in 97% of younger patients under 50 years compared with only 41% in those over 50 years. [12]

Brown Sequard Syndrome: Occurs when just one side of the spinal cord in damaged. Presents as sagittal hemicord damage with dorsal column interruption resulting in ipsilateral paralysis and loss of proprioception with contralateral loss of temperature and pain sensation. As a result of the spinothalamic tract crossing over to the opposite side of the cord, relatively normal pain and temperature sensation remain on the ipsilateral side. While it is rare for the spinal cord to be truly hemisected, this syndrome was originally described by Galen and most commonly occurs as a result of a penetrating injury to the spinal column eg. gunshot or knife, accounting for between 2 - 4% of all spinal cord injuries. It is thought that axons in the contralateral cord may facilitate recovery leading to a good prognosis, with almost all patients ambulating successfully.[13][14]

Anterior Cord Syndrome: Presents as complete motor loss caudal to the lesion secondary to anterior cord damage affecting the spinothalamic and corticospinal tracts, with and loss of pain and temperature sensation as these sensory tracts are located anterolaterally in the spinal cord. Vibration and proprioception remain intact on the ipsilateral side due to preservation of the posterior columns. This occurs as a result of a flexion injury that damages the anterior two-thirds of the spinal cord, most commonly caused by vascular insult to the anterior vertebral artery, leaving the two posterior vertebral arteries intact.Motor recovery is less common in these patients compared with other incomplete lesions. [12][15]

Posterior Cord Lesion: Presents with preservation of motor function, pain and temperature pathways but with loss of light touch, proprioception and vibration secondary to damage to posterior column. This presentation is very rare and individuals will display profound ataxia due to loss of proprioception.

Conus Medullaris Lesion: An injury located around T12 - L2, Conus Medullaris can present as either an upper motor neuron lesion, lower motor neuron lesion or mixed pattern, with or without the sacral reflexes (anal/bulbocavernus), displaying variable symmetrical lower-limb deficits with bladder and bowel dysfunctions, depending on the level of injury. Can also cause disruption to bowel, bladder, and some sexual function. Commonly occurs as a result of avulsion of the lumbar or sacral roots from the terminal part of the cord from trauma or tumor.[16]

Cauda Equina Syndrome: An injury located below the level at which the spinal cord splits into the Cauda Equine, around Levels L2 - S5 below the Conus Medullaris, most commonly caused by compression. While not a true spinal cord injury as it impacts on the nerve roots rather than the spinal cord, it presents as a lower motor neuron lesion with flaccid paralysis secondary to peripheral nerve damage at this level of the spine, usually affecting several levels with variable sacral root interruption and loss of spinal cord mediated reflexes. It can cause low back pain, weakness or paralysis in the lower limbs, loss of sensation, bowel and bladder dysfunction, and loss of reflexes, and more commonly occur on one side of the body. This type of injury has better prognosis for recovery of function if managed early as the peripheral nervous system has a greater capacity for healing than the central nervous system.[16][17]

Differential Diagnosis

Diagnostic Procedures

Imaging technology is an important part of the diagnostic process of acute or chronic spinal cord injuries. Spinal cord injuries can be detected using different types of imaging, which depends on the type of underlying pathology. Antero-posterior, lateral, and special-view Radiographs (odontoid, neural foramina views) can define integrity and alignment of bony structures. However, radiographs can miss fractures, especially facet fractures therefore absence of fracture on radiographs does not ensure spinal-column stability. Additional information can be provided with dynamic views eg, in flexion-extension movement of the spine, but these views are contraindicated in acute neurological dysfunction. 

Spinal fractures and bony lesions are well characterized by Computed Tomography (CT), which can also detect soft-tissue changes with cord oedema, infarction, demyelination, cysts, or abscesses producing reduced signal density, while haemorrhages and calcifications increase signal density. Combination of computed tomography and myelography better defines abnormalities in the spinal canal than computed tomography alone, with combination especially useful when spinal hardware in situ makes MRI difficult. Canal compromise and extradural lesions (tumour, arteriovenous malformations) are especially well defined in computed tomography myelograms. [18]

Magnetic Resonance Imaging (MRI) has become the golden standard for imaging neurological tissues such as the spinal cord, ligaments, discs and other soft tissues and can provide better definition of bony structures than radiography, especially when radiographs suggest injury or include poorly visualised areas. Only MRI sequences of sagittal T2 were found to be useful for prognosticative purposes. [19]

Medical Management

An holistic approach, in which all team members work towards common goals, are necessary throughout the acute and rehabilitation phase of spinal cord injury management. All medical intervention at the time of injury is directed at minimising further spinal cord damage while managing other injuries, associated impairments and optimising neurological recovery. Traumatic spinal cord injuries can be associated with structural damage and instability or the vertebral column, withspinal fractures classified as stable, unstable or quasistable (i.e. currently stable but possibility for instability in the course of everyday activity), based on the three column principles. 

Individuals are generally mobilized within a few days of injury provided they are medically stable, if there is no vertebral instability or damage, as often can occur following ischaemic injuries. However, when there is instability of the vertebral column, the management is quite different, and depending on severity and type of injury can include conservative or surgical management.

Conservative Management

Individuals managed conservatively are generally confined to bed rest with the spine immobilized for a period of 6 - 12 weeks. Depending on the degree of instability, they may have to be maintained in spinal alignment by skull traction (cervical lesions), or some type of pillow wedge (for thoracic, lumbar and sacral lesions) with tight restrictions placed on therapies, which may cause movement at the injury site, and patients are turned and moved only under strict medical supervision. Post this period of immobilization the individual is mobilized in a wheelchair, often with a spinal orthosis, that is worn for a further few months. In some cases this immobilization may be done with extensive bracing e.g. halo-thoracic brace that may allow for earlier mobilization in a wheelchair.

Surgical Management

The more common approach in the management of vertebral damage and instability is surgical, which aims to minimize neurological deterioration, restore alignment and stabilization, facilitate early mobilization, reduce pain, minimize hospital stay and prevent secondary complications. [13] Currently, there are no defined standards existing regarding the timing of decompression and stabilization in spinal cord injury. Decompression of the spinal cord is suggested in the setting of acute spinal cord injury with progressive neurologic deterioration, facet dislocation, or bilateral locked facets or in spinal nerve impingement with progressive radiculopathy and in those select patients with extradural lesions such as epidural hematomas or abscesses or cauda equina syndrome. There are many different surgical approaches but typically vertebrae are realigned and surgical stabilization is achieved by anterior or posterior fixation, or a combination of the two, with or without spinal decompression. [1][2][20] 

Patients managed surgically are often permitted to mobilize much more rapidly than those managed conservatively, sometimes within 7 - 10 days post surgery. They may or may not require some type of bracing once mobilized. The main implication of this approach for physiotherapy management is that patients are confined to bed for a shorter period, and so experience fewer complications associated with immobilization and often result in a shorter inpatient stay. On the other hand, anaesthesia depresses respiratory function, increasing risk of respiratory compromise in the days after surgery. [1][2] 

Pharmocological Management

There is still no commonly accepted pharmacological agent.[21] The most important candidates currently in use include:

  • Glucocorticoids (Methylprednisolone), which suppress many of the ‘secondary’ events of spinal cord injury. These are inflammation, lipid peroxidation and excitotoxity. Randomised clinical trials are contradictory in their results and so are the opinions of experts.[22]
  • Thyrotropin-releasing Hormone (TRH) shows antagonistic effects against the secondary injury mediators. [21]
    For more information, see article.
  • Polyunsaturated Fatty Acids (PUFA) such as Docosahexanoic Acid (DHA) has recently been explored for spinal cord injury management. It is said to improve neurological recovery through increased neuronal and oligodendrocyte survival and decreased microglia/macrophage responses, which reduces axonal accumulation of B-Amyloid Precursor Protein (b-APP) and increase synaptic connectivity.
  • Eicosapentaenoic Acid (EPA) is also thought to increase synaptic connectivity, to restore neuro-plasticity. [23]

Read more about Pharmacological Management of Spinal Cord Injuries

Cellular Therapy Interventions

Cellular therapies have been quite controversial in the management of spinal cord injury with the aim of cellular therapies to provide functional recovery of deficit through axonal regeneration and restoration. Much of these cellular therapy interventions are still only in use in clinical trials and research but may in the future play a larger role in the management of spinal cord injury.

  • Schwann Cell is one of the most widely used cell types for repair of the spinal cord.
  • Olfactory Ensheating Cells are capable of promoting axonal regeneration and remyelination after injury.
  • Bone Marrow derived Mononuclear Cells (BM-MNC’s) transplantation is feasible, safe and have a good degree of outcome improvement.
  • Stimulated Macrophages invade the impaired tissue. [21]

Physiotherapy Management

The rehabilitation of patients who had a spinal cord injury depends on the level of the spine injured, and whether it is a complete or an incomplete spinal cord injury. In case of an incomplete spinal cord injury approximatley 25% will not become independent ambulators. The therapies differ according to where the lesion happened, cervical, thoracic or lumbar. The management of an individual with spinal cord injury is complex and lifelong requiring a multidisciplinary approach. A functional, goal-oriented, interdisciplinary, rehabilitation programme should enable the individual with a spinal cord injury to live as full and independent a life as possible.[24][25]

In the early post injury phase, physical management will mainly involve prevention and management of respiratory and circulatory complications, care of pressure areas and minimize the impact of immobilization such as contractures (Chartered Society of Physiotherapy Standards, 1997).

Treatment objectives in the acute phase include:

  • to institute a prophylactic respiratory regimen and treat any complications
  • to achieve independent respiratory status where possible
  • to maintain full ROM of all joints within the limitations determined by fracture stability
  • to monitor and manage neurological status as appropriate
  • to maintain/strengthen all innervated muscle groups and facilitate functional patterns of activity
  • to support/educate the patient, carers, family and staff.

While the aims and objectives of the rehabilitation phase include:

  • to establish an interdisciplinary process which is patient-focused, comprehensive and co-ordinated 

  • physical motor functional activities with early intervention and prophylaxis to prevent further 
complications 

  • to learn new information to equip the individual 
with knowledge to achieve independence 

  • to achieve functional independence, whether physical or verbal, and equipment provision in order to 
facilitate this independence 

  • to achieve and maintain successful reintegration 
into the community. 

Clinical Bottom Line

Spinal cord injuries are a serious, widespread health issue resulting in a large amount of disfunction and as such have a big socio-economic impact. Therapy is multidisciplinary and focus should be on regaining of function (relevant to the patient!), as tissue recovery is often impossible.

References

  1. 1.0 1.1 1.2 1.3 1.4 Stack E, Stokes M, editors. Physical Management for Neurological Conditions. Elsevier Churchill Livingstone; 2012.
  2. 2.0 2.1 2.2 2.3 Harvey L. Management of Spinal Cord Injuries: A Guide for Physiotherapists. Elsevier Health Sciences; 2008 Jan 10.
  3. Tymianski, D., Sarro, A. Green, T. (2012). Navigating Neuroscience Nursing: A Canadian Perspective. 1st Ed. Pappin Communications, Pembroke, Ontario
  4. 4.0 4.1 Kirshblum SC, Burns SP, Biering-Sorensen F, Donovan W, Graves DE, Jha A et al. International standards for neurological classification of spinal cord injury (revised 2011). J Spinal Cord Med 2011; 34: 535-546
  5. 5.0 5.1 Moore KL, Agur AM, Dalley AF. Essential Clinical Anatomy. Philadelphia: Lippincott Williams & Wilkins; 2002 Mar.
  6. 6.0 6.1 Francisco de Assis Aquino Gondim et al., Topographic and Functional Anatomy of the Spinal Cord, Medshape, 2015
  7. Designed by Freepik at http://www.freepik.com
  8. Spinal CordBlausen Medical. Retrieved on 26 January 2016.
  9. 9.0 9.1 9.2 9.3 Singh A, Tetreault L, Kalsi-Ryan S, Nouri A, Fehlings MG. Global Prevalence and Incidence of Traumatic Spinal Cord Injury. Clinical Epidemiology. 2014;6:309.
  10. 10.0 10.1 Furlan, J.C. et al. “Global incidence and prevalence of traumatic spinal cord injury.” Can J Neurol Sci. 2013 Jul;40(4):456-64
  11. 11.0 11.1 J.W. McDonald et al. Spinal-Cord Injury. Lancet 2002 Fed2;359 (9304):417-25
  12. 12.0 12.1 Foo D. Spinal cord injury in forty four patients with cervical spondylosis. Paraplegia 1986, 24:301–306.
  13. 13.0 13.1 Johnston L. Human spinal cord injury: new and emerging approaches to treatment. Spinal Cord 2001, 39:609–613.
  14. Little JW, Habur E. Temporal course of motor recovery after Brown Séquard spinal cord injury. Paraplegia 1985,23:39–46.
  15. Crozier KS, Groziani V, Ditunno JF et al. Spinal cord injury, prognosis for ambulation based on sensory examination in patients who are initially motor complete. Arch Phys Med Rehab 1991, 72:119–121.
  16. 16.0 16.1 Field-Fote, E. Spinal Cord Injury: An Overview. In Spinal Cord Injury Rehabilitation. FA Davis. 2009
  17. Marx, J.; Walls, R.; Hockberger, R. Rosen's Emergency Medicine: Concepts and Clinical Practice. Elsevier Health Sciences. (2013)
  18. Andrew L G. et al., Advances in Imaging of Vertebral and Spinal Cord Injury, J Spinal Cord Med. 2010 Apr; 33(2): 105–116
  19. Anthony B. et al., The Role of Magnetic Resonance Imaging in the Management of Acute Spi-nal Cord Injury, J Neurotrauma. 2011 Aug; 28(8): 1401–1411
  20. Collins W. Surgery in the acute treatment of spinal cord injury: a review of the past forty years. J Spinal Cord Med1995, 18:3–8.
  21. 21.0 21.1 21.2 Yilmaz T., et al., Current and future medical therapeutic strategies for the functional repair of spinal cord injury, 2015, World J Orthop. 2015 Jan 18;6(1):42-55
  22. V. Cheung et al., Methylprednisolone in the management of spinal cord injuries: Lessons from randomized, controlled trials Surg Neurol Int. 2015; 6: 142
  23. W.-Y. Yu et al., Current trends in spinal cord injury repair. Eur Rev Med Pharmacol Sci 2015; 19 (18): 3340-3344
  24. Mehrholz J, Kugler J, Pohl M. Locomotor Training for Walking after Spinal Cord Injury. Cochrane Database of Systematic Reviews. 2012 (11).
  25. Lu X, Battistuzzo CR, Zoghi M, Galea MP. Effects of Training on Upper Limb Function after Cervical Spinal Cord Injury: A Systematic Review. Clinical Rehabilitation. 2015 Jan;29(1):3-13.