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Spinal Cord Injuries Treatment & Management

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

Approach Considerations

Admit all patients with an acute spinal cord injury (SCI). Depending on the level of neurologic deficit and associated injuries, the patient may require admission to the intensive care unit (ICU), neurosurgical observation unit, or general ward.

The most common levels of injury on admission are C4, C5 (the most common), and C6, whereas the level for paraplegia is the thoracolumbar junction (T12). The most common type of injury on admission is American Spinal Injury Association (ASIA) level A (see Neurologic level and extent of injury under Clinical).


Depending on local policy, patients with acute spinal cord injury are best treated at a regional spinal cord injury center. Therefore, once stabilized, early referral to a regional spinal cord injury center is best. The center should be organized to provide ongoing definitive care.

Other reasons to transfer the patient include the lack of appropriate diagnostic imaging (computed tomography [CT] scanning or magnetic resonance imaging [MRI]) and/or inadequate spine consultant support (orthopedist or neurosurgeon).


Consultation with a neurosurgeon and/or an orthopedist is required, depending on local preferences. Because most patients with spinal cord injury have multiple associated injuries, consultation with a general surgeon or a trauma specialist as well as other specialists may also be required.


Prehospital Management

Most prehospital care providers recognize the need to stabilize and immobilize the spine on the basis of mechanism of injury, pain in the vertebral column, or neurologic symptoms. Patients are usually transported to the emergency department (ED) with a cervical hard collar on a hard backboard. Commercial devices are available to secure the patient to the board.

The patient should be secured so that in the event of emesis, the backboard may be rapidly rotated 90° while the patient remains fully immobilized in a neutral position. Spinal immobilization protocols should be standard in all prehospital care systems.


Emergency Department Management

Most patients with spinal cord injuries (SCIs) have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation (ABCs) takes precedence.

The patient is best treated initially in the supine position. Occasionally, the patient may have been transported prone by the prehospital care providers. Logrolling the patient to the supine position is safe to facilitate diagnostic evaluation and treatment. Use analgesics appropriately and aggressively to maintain the patient's comfort if he or she has been lying on a hard backboard for an extended period.

Airway management

Airway management in the setting of spinal cord injury, with or without a cervical spine injury, is complex and difficult. The cervical spine must be maintained in neutral alignment at all times. Clearing of oral secretions and/or debris is essential to maintain airway patency and to prevent aspiration. The modified jaw thrust and insertion of an oral airway may be all that is required to maintain an airway in some cases. However, intubation may be required in others. Failure to intubate emergently when indicated because of concerns regarding the instability of the patient's cervical spine is a potential pitfall.

Hypotension, hemorrhage, and shock

Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury. Because of the vital sign confusion in acute spinal cord injury and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made.

The most common sources of occult hemorrhage are injuries to the chest, abdomen, and retroperitoneum and fractures of the pelvis or long-bones. Appropriate investigations, including radiography or computed tomography (CT) scanning, are required. In the unstable patient, diagnostic peritoneal lavage or bedside FAST (focused abdominal sonography for trauma) ultrasonographic study may be required to detect intra-abdominal hemorrhage.

Neurogenic shock management and treatment goals

Once occult sources of hemorrhage have been excluded, initial treatment of neurogenic shock focuses on fluid resuscitation. Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 L is the initial treatment of choice. Overzealous crystalloid administration may cause pulmonary edema, because these patients are at risk for the acute respiratory distress syndrome (ARDS).

The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters:

  • A systolic blood pressure (BP) of 90-100 mm Hg should be achieved; systolic BPs in this range are typical for patients with complete cord lesions. Compelling animal and human studies recommend maintenance of systolic BP above 90 mm Hg and to avoid any hypotensive episodes [6, 7]
  • The most important treatment consideration is to maintain adequate oxygenation and perfusion of the injured spinal cord; supplemental oxygenation and/or mechanical ventilation may be required [6, 7]
  • Heart rate should be 60-100 beats per minute (bpm) in normal sinus rhythm
  • Hemodynamically significant bradycardia may be treated with atropine
  • Urine output should be more than 30 mL/h; placement of a Foley catheter to monitor urine output and to decompress the neurogenic bladder is essential
  • Rarely, inotropic support with dopamine or norepinephrine is required; this should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation; usually, low doses of dopamine in the 2- to 5-mcg/kg/min range are sufficient
  • Prevent hypothermia

Head injuries and neurologic evaluation

Associated head injury occurs in about 25% of patients with spinal cord injury. A careful neurologic assessment for associated head injury is compulsory. The presence of amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, and a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning.


Ileus is common. Placement of a nasogastric (NG) tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function (see Treatment of Pulmonary Complications and Injury). Antiemetics should be used aggressively.

Pressure sores

Prevent pressure sores. Denervated skin is particularly prone to pressure necrosis. Turn the patient every 1-2 hours. Pad all extensor surfaces. Undress the patient to remove belts and back pocket keys or wallets. Remove the spine board as soon as possible.


Steroid Therapy in SCI and Controversies

The National Acute Spinal Cord Injury Studies (NASCIS) II and III,[42, 43] a Cochrane Database of Systematic Reviews article of all randomized clinical trials,[44] and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete spinal cord injuries (SCIs) who were treated with high doses of methylprednisolone within 8 hours of injury.

NASCIS II and III trials

High doses of steroids or tirilazad are thought to minimize the secondary effects of acute SCI. The NASCIS II study evaluated a 30-mg/kg bolus of methylprednisolone administered within 8 hours of injury, whereas the NASCIS III study evaluated methylprednisolone 5.4 mg/kg/h for 24 or 48 hours versus tirilazad 2.5 mg/kg q6h for 48 hours. (Tirilazad is a potent lipid preoxidation inhibitor.)

Between the 2 studies, it was determined that: (1) in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 hours was best; (2) in patients treated 3-8 hours after injury, the use of methylprednisolone for 48 hours was best; (3) Tirilazad was equivalent to methylprednisolone for 24 hours.[43]

Both NASCIS studies evaluated the patients' neurologic status at baseline on enrollment into the study, at 6 weeks, and at 6 months and found absolutely no evidence suggests that giving the medication earlier (eg, in the first hour) provides more benefit than giving it later (eg, between hours 7 and 8). The authors concluded that there was only a benefit if methylprednisolone or tirilazad were given within 8 hours of injury.[43]

Controversy re results of NASCIS studies

Following the NASCIS trials, the use of high-dose methylprednisolone in nonpenetrating acute SCI had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned the validity of the results.[45] These authors cited concerns about the statistical analysis, randomization, and clinical endpoints used in the study. In addition, the investigators noted that even if the benefits of steroid therapy were valid, the clinical gains were questionable. Other reports have also cited flaws in the study designs, trial conduct, and final presentation of the data.

The risks of steroid therapy are not inconsequential. An increased incidence of infection and avascular necrosis has been documented.

Revised recommendations

As a result of the controversy over the NACSIS II and III studies, a number of professional organizations have revised their recommendations pertaining to steroid therapy in SCI.[46, 47]

The Congress of Neurological Surgeons (CNS) has stated that steroid therapy "should only be undertaken with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit."[48] The American College of Surgeons (ACS) has modified their advanced trauma life support (ACLS) guidelines to state that methylprednisolone is "a recommended treatment" rather than "the recommended treatment." The Canadian Association of Emergency Physicians (CAEP) is no longer recommending high-dose methylprednisolone as the standard of care.

In a survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids in SCI, but only 24% believed that they were of any clinical benefit.[49] Note that the investigators not only discovered that approximately 7% of spine surgeons do not recommend or use steroids at all in acute SCI, but that most centers were following the NASCIS II trial protocol.

Updated guidelines issued in 2013 by the CNS and the American Association of Neurological Surgeons (AANS) recommend against the use of steroids early after an acute SCI. The guidelines recommend that methylprednisolone not be used for the treatment of acute SCI within the first 24-48 hours following injury. The previous standard was revised because of a lack of medical evidence supporting the benefits of steroids in clinical settings and evidence that high-dose steroids are associated with harmful adverse effects.[50, 51]


Two North American studies have addressed the administration of monosialotetrahexosyl ganglioside (GM-1) following acute spinal cord injury. The available medical evidence does not support a significant clinical benefit. It was evaluated as a treatment adjunct after the administration of methylprednisolone.[7, 52]


Overall, the benefit from steroids is considered modest at best, but for patients with complete or incomplete quadriplegia, a small improvement in motor strength in one or more muscles can provide important functional gains.

The administration of steroids remains an institutional and physician preference in spinal cord injury. Nevertheless, the administration of high-dose steroids within 8 hours of injury for all patients with acute spinal cord injury is practiced by most physicians.

The current recommendation is to treat all patients with spinal cord injury according to the local/regional protocol. If steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus.

Local policy will also determine if the NASCIS II or NASCIS III protocol is to be followed.


Treatment of Pulmonary Complications and Injury

Treatment of pulmonary complications and/or injury in patients with spinal cord injury (SCI) includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax.

The ideal technique for emergent intubation in the setting of spinal cord injury is fiberoptic intubation with cervical spine control. This, however, has not been proven better than orotracheal with in-line immobilization. Furthermore, no definite reports of worsening neurologic injury with properly performed orotracheal intubation and in-line immobilization exist. If the necessary experience or equipment is lacking, blind nasotracheal or oral intubation with in-line immobilization is acceptable.

Indications for intubation in spinal cord injury are acute respiratory failure, decreased level of consciousness (Glasgow score < 9), increased respiratory rate with hypoxia, partial pressure of carbon dioxide (PCO2) greater than 50 mm Hg, and vital capacity less than 10 mL/kg.

In the presence of autonomic disruption from cervical or high thoracic spinal cord injury, intubation may cause severe bradyarrhythmias from unopposed vagal stimulation. Simple oral suctioning can also cause significant bradycardia. Preoxygenation with 100% oxygen may be preventive. Atropine may be required as an adjunct. Topical lidocaine spray can minimize or prevent this reaction.


Surgical Intervention

Spine service consultants should determine the need for and timing of any surgical intervention. Currently, there are no defined standards existing regarding the timing of decompression and stabilization in spinal cord injury. The role of immediate surgical intervention is limited. Emergent 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. Emergent decompression is also suggested in the setting of spinal nerve impingement with progressive radiculopathy and in those select patients with extradural lesions such as epidural hematomas or abscesses or in the setting of the cauda equina syndrome.

A prospective surgical trial, the Surgical Treatment for Acute Spinal Cord Injury Study (STASCIS) conducted by the Spine Trauma Study Group, is ongoing. Preliminary data from this study are showing that 24% of patients who receive decompressive surgery within 24 hours of their injury experience a 2-grade or better improvement on the ASIA scale, compared with 4% of those in the delayed-treatment group. Furthermore, the study found that cardiopulmonary and urinary tract complications were found to be 37% in the early surgery group compared with the delayed group rate of 48.6%. The hope is that the final data from STASCIS will better define the benefits and timing of early surgical decompression and stabilization.

A review article of spinal fixation surgery for acute traumatic spinal cord injury concluded that, in the absence of any randomized controlled studies, no recommendations regarding risks or benefits could be made.[53]

Previous studies from the 1960s and 1970s showed that the patients experienced no improvement with emergent surgical decompression, although 2 studies in the late 1990s appeared to show improved neurologic outcomes with early stabilization. Gaebler et al reported that early decompression and stabilization procedures within 8 hours of injury allowed for a higher rate of neurologic recovery.[54] Mirza et al reported that stabilization within 72 hours of injury in cervical spinal cord injury improved neurologic outcomes.[55]

Unfortunately, both the above studies and others were not prospectively controlled or randomized. In the only prospective, randomized, controlled study to determine whether functional outcome is improved in patients with cervical spinal cord injury, Vaccaro et al reported no significant difference between early (< 3 d, mean 1.8 d) or late (>5 d, mean 16.8 d) surgery.[56]



Neurologic deterioration, pressure sores, aspiration and pulmonary complications, and other complications following spinal cord injury (SCI) are briefly discussed in this section.

Neurologic deterioration

The neurologic deficit of spinal cord injury (SCI) often increases during the hours to days following acute injury, despite optimal treatment.

One of the first signs of neurologic deterioration is the extension of the sensory deficit cephalad. Careful repeat neurologic examination may reveal that the sensory level has risen 1 or 2 segments. Repeat neurologic examinations to check for progression are essential.

Pressure sores

Careful and frequent turning of the patient is required to prevent pressure sores. Denervated skin is particularly prone to this complication. Remove belts and objects from back pockets, such as keys and wallets.

Try to remove the patient from the backboard as soon as possible. Some patients may require spinal immobilization in a halo vest or a Stryker frame. Many patients with acute spinal cord injury have stable vertebral fractures yet needlessly spend hours on a hard backboard.

Aspiration and pulmonary complications

Patients with spinal cord injury are at high risk for aspiration. Nasogastric decompression of the stomach is mandatory.

Pulmonary complications in spinal cord injury are common. Such complications are directly correlated with mortality, and both are related to the level of neurologic injury. Pulmonary complications of spinal cord injury include the following:

  • Atelectasis secondary to decreased vital capacity and decreased functional residual capacity
  • Ventilation-perfusion (V/Q) mismatch due to sympathectomy and/or adrenergic blockade
  • Increased work of breathing because of decreased compliance
  • Decreased coughing, which increases the risk of retained secretions, atelectasis, and pneumonia
  • Muscle fatigue

Other complications

Severe sepsis or pneumonia frequently follows treatment with high-dose methylprednisolone that is frequently used in spinal cord injury.

Prevent hypothermia by using external rewarming techniques and/or warm humidified oxygen.

Contributor Information and Disclosures

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.


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.


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

  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 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 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 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 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.

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