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Spinal Cord Injuries Clinical Presentation

  • Author: Lawrence S Chin, MD, FACS; Chief Editor: Brian H Kopell, MD  more...
 
Updated: May 12, 2016
 

History and Physical Examination

As with all trauma patients, initial clinical evaluation of a patient with suspected spinal cord injury (SCI) begins with a primary survey. The primary survey focuses on life-threatening conditions. Assessment of airway, breathing, and circulation (ABCs) takes precedence. A spinal cord injury must be considered concurrently.[31, 32, 6]

Perform careful history taking, focusing on symptoms related to the vertebral column (most commonly pain) and any motor or sensory deficits. Ascertaining the mechanism of injury is also important in identifying the potential for spinal injury.

The axial skeleton should be examined to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. The posterior cervical spine and paraspinal tissues should be evaluated for pain, swelling, bruising, or possible malalignment. Logrolling the patient to systematically examine each spinous process of the entire axial skeleton from the occiput to the sacrum can help identify and localize injury. The skeletal level of injury is the level of the greatest vertebral damage on radiograph.

Complete bilateral loss of sensation or motor function below a certain level indicates a complete spinal cord injury.

Pulmonary evaluation

The clinical assessment of pulmonary function in acute spinal cord injury begins with careful history taking regarding respiratory symptoms and a review of underlying cardiopulmonary comorbidity such as chronic obstructive pulmonary disease (COPD) or heart failure.

Carefully evaluate respiratory rate, chest wall expansion, abdominal wall movement, cough, and chest wall and/or pulmonary injuries. Arterial blood gas (ABG) analysis and pulse oximetry are especially useful, because the bedside diagnosis of hypoxia or carbon dioxide retention may be difficult.

The degree of respiratory dysfunction is ultimately dependent on preexisting pulmonary comorbidity, the level of the spinal cord injury, and any associated chest wall or lung injury. Any or all of the following determinants of pulmonary function may be impaired in the setting of spinal cord injury:

  • Loss of ventilatory muscle function from denervation and/or associated chest wall injury
  • Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion
  • Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs

A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction, as follows:

  • With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent
  • With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective
  • With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak
  • With lower cord injuries, respiratory function improves
  • With injuries at T11, respiratory dysfunction is minimal; vital capacity is essentially normal, and cough is strong.

Other findings of respiratory disfunction include the following:

  • Agitation, anxiety, or restlessness
  • Poor chest wall expansion
  • Decreased air entry
  • Rales, rhonchi
  • Pallor, cyanosis
  • Increased heart rate
  • Paradoxic movement of the chest wall
  • Increased accessory muscle use
  • Moist cough

Hemorrhage, hypotension, and hemorrhagic and neurogenic shock

Hemorrhagic shock may be difficult to diagnose, because the clinical findings may be affected by autonomic dysfunction. Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure. In addition, occult internal injuries with associated hemorrhage may be missed.

In a study showing a high incidence of autonomic dysfunction, including orthostatic hypotension and impaired cardiovascular control, following spinal cord injury, it was recommended that an assessment of autonomic function be routinely used, along with American Spinal Injury Association (ASIA) assessment, in the neurologic evaluation of patients with spinal cord injury.[33]

In all patients with spinal cord injury and hypotension, a diligent search for sources of hemorrhage must be made before hypotension is attributed to neurogenic shock. In acute spinal cord injury, shock may be neurogenic, hemorrhagic, or both.

The following are clinical "pearls" useful in distinguishing hemorrhagic shock from neurogenic shock:

  • Neurogenic shock occurs only in the presence of acute spinal cord injury above T6; hypotension and/or shock with acute spinal cord injury at or below T6 is caused by hemorrhage
  • Hypotension with a spinal fracture alone, without any neurologic deficit or apparent spinal cord injury, is invariably due to hemorrhage
  • Patients with a spinal cord injury above T6 may not have the classic physical findings associated with hemorrhage (eg, tachycardia, peripheral vasoconstriction); this vital sign confusion attributed to autonomic dysfunction is common in spinal cord injury
  • The presence of vital sign confusion in acute spinal cord injury and a high incidence of associated injuries requires a diligent search for occult sources of hemorrhage

Cord syndromes and nerve root injury

A careful neurologic assessment, including motor function, sensory evaluation, deep tendon reflexes, and perineal evaluation, is critical and required to establish the presence or absence of spinal cord injury and to classify the lesion according to a specific cord syndrome.

The presence or absence of sacral sparing is a key prognostic indicator. Sacral-sparing is evidence of the physiologic continuity of spinal cord long tract fibers (with the sacral fibers located more at the periphery of the cord). Indication of the presence of sacral fibers is of significance in defining the completeness of the injury and the potential for some motor recovery. This finding tends to be repeated and better defined after the period of spinal shock.

Determine the level of injury and try to differentiate nerve root injury from spinal cord injury, but recognize that both may be present. Differentiating a nerve root injury from spinal cord injury can be difficult. The presence of neurologic deficits that indicate multilevel involvement suggests spinal cord injury rather than a nerve root injury. In the absence of spinal shock, motor weakness with intact reflexes indicates spinal cord injury, whereas motor weakness with absent reflexes indicates a nerve root lesion.

ASIA has established pertinent definitions (see the following image). The neurologic level of injury is the lowest (most caudal) level with normal sensory and motor function. For example, a patient with C5 quadriplegia has, by definition, abnormal motor and sensory function from C6 down.

American Spinal Injury Association (ASIA) method f American Spinal Injury Association (ASIA) method for classifying spinal cord injury (SCI) by neurologic level.

Sensory function testing

Assessment of sensory function helps to identify the different pathways for light touch, proprioception, vibration, and pain. Use a pinprick to evaluate pain sensation.

Sensory level is the most caudal dermatome with a normal score of 2/2 for pinprick and light touch.

Sensory index scoring is the total score from adding each dermatomal score with a possible total score of 112 each for pinprick and light touch.

Sensory testing is performed at the following levels:

  • C2: Occipital protuberance
  • C3: Supraclavicular fossa
  • C4: Top of the acromioclavicular joint
  • C5: Lateral side of antecubital fossa
  • C6: Thumb
  • C7: Middle finger
  • C8: Little finger
  • T1: Medial side of antecubital fossa
  • T2: Apex of axilla
  • T3: Third intercostal space
  • T4: Fourth intercostal space at nipple line
  • T5: Fifth intercostal space (midway between T4 and T6)
  • T6: Sixth intercostal space at the level of the xiphisternum
  • T7: Seventh intercostal space (midway between T6 and T8)
  • T8: Eighth intercostal space (midway between T6 and T10)
  • T9: Ninth intercostal space (midway between T8 and T10)
  • T10: 10th intercostal space or umbilicus
  • T11: 11th intercostal space (midway between T10 and T12)
  • T12: Midpoint of inguinal ligament
  • L1: Half the distance between T12 and L2
  • L2: Midanterior thigh
  • L3: Medial femoral condyle
  • L4: Medial malleolus
  • L5: Dorsum of the foot at third metatarsophalangeal joint
  • S1: Lateral heel
  • S2: Popliteal fossa in the midline
  • S3: Ischial tuberosity
  • S4-5: Perianal area (taken as 1 level)

Sensory scoring is for light touch and pinprick, as follows:

  • 0: Absent; a score of zero is given if the patient cannot differentiate between the point of a sharp pin and the dull edge
  • 1: Impaired or hyperesthesia
  • 2: Intact

Motor strength testing

Muscle strength always should be graded according to the maximum strength attained, no matter how briefly that strength is maintained during the examination. The muscles are tested with the patient supine.

Motor level is determined by the most caudal key muscles that have muscle strength of 3 or above while the segment above is normal (= 5).

Motor index scoring uses the 0-5 scoring of each key muscle, with total points being 25 per extremity and with the total possible score being 100.

Lower extremities motor score (LEMS) uses the ASIA key muscles in both lower extremities, with a total possible score of 50 (ie, maximum score of 5 for each key muscle [L2, L3, L4, L5, and S1] per extremity). A LEMS of 20 or less indicates that the patient is likely to be a limited ambulator. A LEMS of 30 or more suggests that the individual is likely to be a community ambulator.

ASIA recommends use of the following scale of findings for the assessment of motor strength in spinal cord injury:

  • 0: No contraction or movement
  • 1: Minimal movement
  • 2: Active movement, but not against gravity
  • 3: Active movement against gravity
  • 4: Active movement against resistance
  • 5: Active movement against full resistance

Neurologic level and extent of injury

Neurologic level of injury is the most caudal level at which motor and sensory levels are intact, with motor level as defined above and sensory level defined by a sensory score of 2.

Zone of partial preservation is all segments below the neurologic level of injury with preservation of motor or sensory findings. This index is used only when the injury is complete.

The key muscles that need to be tested to establish neurologic level are as follows:

  • C5: Elbow flexors (biceps, brachialis)
  • C6: Wrist extensors (extensor carpi radialis longus and brevis)
  • C7: Elbow extensors (triceps)
  • C8: Long finger flexors (flexor digitorum profundus)
  • T1: Small finger abductors (abductor digiti minimi)
  • L2: Hip flexors (iliopsoas)
  • L3: Knee extensors (quadriceps)
  • L4: Ankle dorsiflexors (tibialis anterior)
  • L5: Long toe extensors (extensor hallucis longus)
  • S1: Ankle plantar flexors (gastrocnemius, soleus)

Perform a rectal examination to check motor function or sensation at the anal mucocutaneous junction. The presence of either is considered sacral-sparing.

The sacral roots may be evaluated by documenting the following:

  • Perineal sensation to light touch and pinprick
  • Bulbocavernous reflex, S3 or S4
  • Anal wink, S5
  • Rectal tone
  • Urine retention or incontinence
  • Priapism

The extent of injury is defined by the ASIA Impairment Scale (modified from the Frankel classification), using the following categories[3, 4] :

  • A = Complete: No sensory or motor function is preserved in sacral segments S4-S5 [5]
  • B = Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5
  • C = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade less than 3
  • D = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade greater than or equal to 3
  • E = Normal: Sensory and motor functions are normal

Thus, definitions of complete and incomplete spinal cord injury, as based on the above ASIA definition, with sacral-sparing, are as follows[3, 4, 5] :

  • Complete: Absence of sensory and motor functions in the lowest sacral segments
  • Incomplete: Preservation of sensory or motor function below the level of injury, including the lowest sacral segments

With the ASIA classification system, the terms paraparesis and quadriparesis have become obsolete. Instead, the ASIA classification uses the description of the neurologic level of injury in defining the type of spinal cord injury (eg, "C8 ASIA A with zone of partial preservation of pinprick to T2").

 
 
Contributor Information and Disclosures
Author

Lawrence S Chin, MD, FACS Robert B and Molly G King Endowed Professor and Chair, Department of Neurosurgery, State University of New York Upstate Medical University

Lawrence S Chin, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association for Cancer Research, Children's Oncology Group, Society for Neuro-Oncology, Congress of Neurological Surgeons, American Association of Neurological Surgeons, American College of Surgeons, Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM Attending Interventional Physiatrist, Wellspan Health

Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM is a member of the following medical societies: American College of Sports Medicine, American Academy of Physical Medicine and Rehabilitation, Royal College of Surgeons of England, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Medical Informatics Association, Association of Academic Physiatrists, International Society of Physical and Rehabilitation Medicine

Disclosure: Nothing to disclose.

Fassil B Mesfin, MD, PhD Assistant Professor of Neurosurgery, Director of Complex Spine and Spine Oncology Program, University of Missouri-Columbia School of Medicine

Fassil B Mesfin, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Association for Cancer Research, American Association of Neurological Surgeons, American Medical Association, National Medical Association, Congress of Neurological Surgeons, American Academy of Neurological Surgery

Disclosure: Nothing to disclose.

Chief Editor

Brian H Kopell, MD Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai

Brian H Kopell, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neurological Surgeons, International Parkinson and Movement Disorder Society, Congress of Neurological Surgeons, American Society for Stereotactic and Functional Neurosurgery, North American Neuromodulation Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from St Jude Neuromodulation for consulting; Received consulting fee from MRI Interventions for consulting.

Acknowledgements

Denise I Campagnolo, MD, MS Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers

Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Milton J Klein, DO, MBA Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Richard Salcido, MD Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Tom Scaletta, MD Chair, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine

Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Donald Schreiber, MD, CM Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine

Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Abbott Point of Care Inc Research Grant and Speakers Bureau Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research; Abbott Diagnostics Inc Grant/research funds None

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Hand L. FDA OKs device to help people with some spinal injuries walk. Medscape Medical News. June 26, 2014. [Full Text].

  2. FDA news release. FDA allows marketing of first wearable, motorized device that helps people with certain spinal cord injuries to walk. US Food and Drug Administration. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm402970.htm. Accessed: June 29, 2014.

  3. American Spinal Injury Association. International Standards for Neurological Classifications of Spinal Cord Injury. revised ed. Chicago, Ill: American Spinal Injury Association; 2000. 1-23.

  4. Ditunno JF Jr, Young W, Donovan WH, Creasey G. The international standards booklet for neurological and functional classification of spinal cord injury. American Spinal Injury Association. Paraplegia. 1994 Feb. 32(2):70-80. [Medline].

  5. Waters RL, Adkins RH, Yakura JS. Definition of complete spinal cord injury. Paraplegia. 1991 Nov. 29(9):573-81. [Medline].

  6. Wuermser LA, Ho CH, Chiodo AE, Priebe MM, Kirshblum SC, Scelza WM. Spinal cord injury medicine. 2. Acute care management of traumatic and nontraumatic injury. Arch Phys Med Rehabil. 2007 Mar. 88(3 Suppl 1):S55-61. [Medline].

  7. Congress of Neurologic Surgeons. Blood pressure management after acute spinal cord injury. Neurosurgery. 2002 Mar. 50(3 Suppl):S58-62. [Medline].

  8. Westgren N, Levi R. Quality of life and traumatic spinal cord injury. Arch Phys Med Rehabil. 1998 Nov. 79(11):1433-9. [Medline].

  9. Kriss VM, Kriss TC. SCIWORA (spinal cord injury without radiographic abnormality) in infants and children. Clin Pediatr (Phila). 1996 Mar. 35(3):119-24. [Medline].

  10. Pang D. Spinal cord injury without radiographic abnormality in children, 2 decades later. Neurosurgery. 2004 Dec. 55(6):1325-42; discussion 1342-3. [Medline].

  11. Yucesoy K, Yuksel KZ. SCIWORA in MRI era. Clin Neurol Neurosurg. 2008 May. 110(5):429-33. [Medline].

  12. Rhee P, Kuncir EJ, Johnson L, Brown C, Velmahos G, Martin M, et al. Cervical spine injury is highly dependent on the mechanism of injury following blunt and penetrating assault. J Trauma. 2006 Nov. 61(5):1166-70. [Medline].

  13. National Spinal Cord Injury Statistical Center (NSCIS). Spinal cord injury facts and figures at a glance. February 2011. [Full Text].

  14. Krause JS, Sternberg M, Lottes S, Maides J. Mortality after spinal cord injury: an 11-year prospective study. Arch Phys Med Rehabil. 1997 Aug. 78(8):815-21. [Medline].

  15. DeVivo MJ. Epidemiology of traumatic spinal cord injury. Kirshblum S, Campagnolo DI, DeLisa JA, eds. Spinal Cord Medicine. Baltimore, Md: Lippincott Williams & Wilkins; 2002. 69-81.

  16. Go BK, DeVivo MJ, Richards JS. The epidemiology of spinal cord injury. Stover SL, DeLisa JA, Whiteneck GG, eds. Spinal Cord Injury. Gaithersburg, Md: Aspen; 1995. 21-55.

  17. Avery JD, Avery JA. Malignant spinal cord compression: a hospice emergency. Home Healthc Nurse. 2008 Sep. 26(8):457-61; quiz 462-3. [Medline].

  18. Vitale MG, Goss JM, Matsumoto H, Roye DP Jr. Epidemiology of pediatric spinal cord injury in the United States: years 1997 and 2000. J Pediatr Orthop. 2006 Nov-Dec. 26(6):745-9. [Medline].

  19. Krause JS. Years to employment after spinal cord injury. Arch Phys Med Rehabil. 2003 Sep. 84(9):1282-9. [Medline].

  20. Morse LR, Stolzmann K, Nguyen HP, Jain NB, Zayac C, Gagnon DR, et al. Association between mobility mode and C-reactive protein levels in men with chronic spinal cord injury. Arch Phys Med Rehabil. 2008 Apr. 89(4):726-31. [Medline]. [Full Text].

  21. Furlan JC, Fehlings MG. Cardiovascular complications after acute spinal cord injury: pathophysiology, diagnosis, and management. Neurosurg Focus. 2008. 25(5):E13. [Medline].

  22. Turner AP, Bombardier CH, Rimmele CT. A typology of alcohol use patterns among persons with recent traumatic brain injury or spinal cord injury: implications for treatment matching. Arch Phys Med Rehabil. 2003 Mar. 84(3):358-64. [Medline].

  23. Frisbie JH, Tun CG. Drinking and spinal cord injury. J Am Paraplegia Soc. 1984 Oct. 7(4):71-3. [Medline].

  24. Strauss DJ, Devivo MJ, Paculdo DR, Shavelle RM. Trends in life expectancy after spinal cord injury. Arch Phys Med Rehabil. 2006 Aug. 87(8):1079-85. [Medline].

  25. Budh CN, Osteråker AL. Life satisfaction in individuals with a spinal cord injury and pain. Clin Rehabil. 2007 Jan. 21(1):89-96. [Medline].

  26. Widerström-Noga E, Biering-Sørensen F, Bryce T, Cardenas DD, Finnerup NB, Jensen MP, et al. The international spinal cord injury pain basic data set. Spinal Cord. 2008 Dec. 46(12):818-23. [Medline].

  27. van Middendorp JJ, Hosman AJ, Donders AR, Pouw MH, Ditunno JF Jr, Curt A, et al. A clinical prediction rule for ambulation outcomes after traumatic spinal cord injury: a longitudinal cohort study. Lancet. 2011 Mar 19. 377(9770):1004-10. [Medline].

  28. Wolpaw JR, McFarland DJ. Control of a two-dimensional movement signal by a noninvasive brain-computer interface in humans. Proc Natl Acad Sci U S A. 2004 Dec 21. 101(51):17849-54. [Medline].

  29. Birbaumer N, Ghanayim N, Hinterberger T, Iversen I, Kotchoubey B, Kubler A. A spelling device for the paralysed. Nature. 1999 Mar 25. 398(6725):297-8. [Medline].

  30. Pfurtscheller G, Muller GR, Pfurtscheller J, Gerner HJ, Rupp R. Thought'--control of functional electrical stimulation to restore hand grasp in a patient with tetraplegia. Neurosci Lett. 2003 Nov 6. 351(1):33-6. [Medline].

  31. Harris MB, Sethi RK. The initial assessment and management of the multiple-trauma patient with an associated spine injury. Spine. 2006 May 15. 31(11 Suppl):S9-15; discussion S36. [Medline].

  32. Ho CH, Wuermser LA, Priebe MM, Chiodo AE, Scelza WM, Kirshblum SC. Spinal cord injury medicine. 1. Epidemiology and classification. Arch Phys Med Rehabil. 2007 Mar. 88(3 Suppl 1):S49-54. [Medline].

  33. Claydon VE, Krassioukov AV. Orthostatic hypotension and autonomic pathways after spinal cord injury. J Neurotrauma. 2006 Dec. 23(12):1713-25. [Medline].

  34. Brown CV, Antevil JL, Sise MJ, Sack DI. Spiral computed tomography for the diagnosis of cervical, thoracic, and lumbar spine fractures: its time has come. J Trauma. 2005 May. 58(5):890-5; discussion 895-6. [Medline].

  35. Grogan EL, Morris JA Jr, Dittus RS, et al. Cervical spine evaluation in urban trauma centers: lowering institutional costs and complications through helical CT scan. J Am Coll Surg. 2005 Feb. 200(2):160-5. [Medline].

  36. Keenen TL, Antony J, Benson DR. Non-contiguous spinal fractures. J Trauma. 1990 Apr. 30(4):489-91. [Medline].

  37. Powell JN, Waddell JP, Tucker WS, Transfeldt EE. Multiple-level noncontiguous spinal fractures. J Trauma. 1989 Aug. 29(8):1146-50; discussion 1150-1. [Medline].

  38. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. 2000 Jul 13. 343(2):94-9. [Medline].

  39. Stiell IG, Clement CM, McKnight RD, et al. The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med. 2003 Dec 25. 349(26):2510-8. [Medline].

  40. Stiell IG, Wells GA, Vandemheen KL. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA. 2001 Oct 17. 286(15):1841-8. [Medline].

  41. Acheson MB, Livingston RR, Richardson ML, Stimac GK. High-resolution CT scanning in the evaluation of cervical spine fractures: comparison with plain film examinations. AJR Am J Roentgenol. 1987 Jun. 148(6):1179-85. [Medline].

  42. Bracken MB, Shepard MJ, Hellenbrand KG, et al. Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. J Neurosurg. 1985 Nov. 63(5):704-13. [Medline].

  43. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997 May 28. 277(20):1597-604. [Medline].

  44. Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev. 2002. CD001046. [Medline].

  45. Nesathurai S. Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma. 1998 Dec. 45(6):1088-93. [Medline].

  46. Hurlbert RJ, Hamilton MG. Methylprednisolone for acute spinal cord injury: 5-year practice reversal. Can J Neurol Sci. 2008 Mar. 35(1):41-5. [Medline].

  47. Sansam KA. Controversies in the management of traumatic spinal cord injury. Clin Med. 2006 Mar-Apr. 6(2):202-4. [Medline].

  48. Hadley MN, Walters BC, Grabb PA, et al. Pharmacological therapy after acute spinal cord injury. Neurosurgery. 2002. 50 Suppl:63-72.

  49. Eck JC, Nachtigall D, Humphreys SC, Hodges SD. Questionnaire survey of spine surgeons on the use of methylprednisolone for acute spinal cord injury. Spine. 2006 Apr 20. 31(9):E250-3. [Medline].

  50. Anderson P. New CNS/AANS Guidelines Discourage Steroids in Spinal Injury. Medscape Medical News. Mar 28 2013. Available at http://www.medscape.com/viewarticle/781669. Accessed: April 7 2013.

  51. Hadley MN, Walters BC. Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries. Neurosurgery. Mar 2013;72(Suppl 2):1-259. Available at http://journals.lww.com/neurosurgery/toc/2013/03002. Accessed: Apr 9 2013.

  52. Geisler FH, Dorsey FC, Coleman WP. Recovery of motor function after spinal-cord injury--a randomized, placebo-controlled trial with GM-1 ganglioside. N Engl J Med. 1991 Jun 27. 324(26):1829-38. [Medline].

  53. Bagnall AM, Jones L, Duffy S, Riemsma RP. Spinal fixation surgery for acute traumatic spinal cord injury. Cochrane Database Syst Rev. 2008 Jan 23. CD004725. [Medline].

  54. Gaebler C, Maier R, Kutscha-Lissberg F, Mrkonjic L, Vecsei V. Results of spinal cord decompression and thoracolumbar pedicle stabilisation in relation to the time of operation. Spinal Cord. 1999 Jan. 37(1):33-9. [Medline].

  55. Mirza SK, Krengel WF 3rd, Chapman JR, Anderson PA, Bailey JC, Grady MS. Early versus delayed surgery for acute cervical spinal cord injury. Clin Orthop Relat Res. 1999 Feb. (359):104-14. [Medline].

  56. Vaccaro AR, Daugherty RJ, Sheehan TP, et al. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine. 1997 Nov 15. 22(22):2609-13. [Medline].

  57. Lyrica (pregabalin) [package insert]. New York, NY: Pfizer. June 2012. Available at [Full Text].

  58. Sanin L, Parsons B, et al. Weekly Assessments of Pain and Sleep During a 17-week, Double-blind, Placebo-controlled Trial of Pregabalin for the Treatment of Chronic Neuropathic Pain After Spinal Cord Injury. American Academy of Neurology 64th Annual Meeting. Emerging Science Poster #005. Presented April 25, 2012. New Orleans, LA.

  59. Annual Report for the Model Spinal Cord Injury Care Systems. December 2007;

  60. Fehlings MG, Perrin RG. The role and timing of early decompression for cervical spinal cord injury: update with a review of recent clinical evidence. Injury. 2005 Jul. 36 Suppl 2:B13-26. [Medline].

  61. Fisher CG, Noonan VK, Dvorak MF. Changing face of spine trauma care in North America. Spine (Phila Pa 1976). 2006 May 15. 31(11 Suppl):S2-8; discussion S36. [Medline].

  62. Goodman A. Pregabalin Rapidly Relieves Neuropathic Pain in Spinal Cord Injury. Medscape Medical News. Available at http://www.medscape.com/viewarticle/804197. Accessed: May 18, 2013.

  63. Hurlbert RJ. Strategies of medical intervention in the management of acute spinal cord injury. Spine (Phila Pa 1976). 2006 May 15. 31(11 Suppl):S16-21; discussion S36. [Medline].

  64. Parsons B, Emir B. Examining the time-to-improvement of pain in patients with chronic neuropathic pain due to spinal cord injury. J Pain. April 2013. 14(4, Supplement):S60.

 
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American Spinal Injury Association (ASIA) method for classifying spinal cord injury (SCI) by neurologic level.
 
 
 
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