Medscape is available in 5 Language Editions – Choose your Edition here.


Lower Cervical Spine Fractures and Dislocations Treatment & Management

  • Author: J Allan Goodrich, MD; Chief Editor: Jeffrey A Goldstein, MD  more...
Updated: Mar 03, 2014

Medical Therapy

Medical management involves treating the multiple traumas and, more specifically, treating concomitant neurologic injury. The use of steroids for neurologic injury has become standard to prevent secondary causes of spinal cord damage, such as release of toxic peroxidases, and to minimize associated local edema. Steroids are thought to help stabilize neural membranes, to prevent uncontrolled intracellular calcium influx, to decrease lysosomal enzyme action, and to diminish swelling and inflammation.

According to 3 National Acute Spinal Cord Injury Study (NASCIS) reports, the recommended management for patients with spinal cord injury presenting within 3 hours of injury is a loading dose of methylprednisolone of 30 mg/kg over an hour intravenously, followed by 5.4 mg/kg/h for the next 23 hours. If the patient presents more than 3 hours but less than 8 hours postinjury, the 5.4 mg/kg/h is extended for 48 hours following the same loading dose. Steroid treatment does not seem to be beneficial if begun more than 8 hours postinjury or after nerve root trauma.[15, 16, 17, 18, 19]

The Spine Focus Panel, in a recent review of the literature, continues to recommend the steroid protocol based on its modest neuroprotective effects, favorable risk-to-benefit ratio, and lack of alternative therapies. However, the use of steroids in penetrating injuries, especially gunshot wounds, has not proven to be beneficial.[20]

More recently, the use of steroids has been questioned because of its risk-to-benefit ratio. Complications, including increased risk of infection, stress ulcers, hyperglycemia, and compromised healing of surgical and other wounds, have prompted many clinicians to avoid steroids in the case of spinal cord injuries. A committee of neurosurgeons, orthopedic surgeons, emergency physicians, and physiatrists, at the request of the Canadian Spine Society and the Canadian Neurosurgical Society, concluded the following[21, 22] :

  • There is insufficient evidence to support the use of high-dose methylprednisolone within 8 hours following acute closed spinal cord injury as a standard or as a guideline for treatment.
  • Methylprednisolone prescribed as a bolus intravenous infusion of 30 mg/kg of body weight over 15 minutes within 8 hours of acute closed spinal cord injury, followed 45 minutes later by an infusion of 5.4 mg/kg of body weight per hour for 23 hours, is a treatment option for which there is weak clinical evidence.(level II, III).
  • There is insufficient evidence to support extending methylprednisolone infusion beyond 23 hours if chosen as a treatment option.

These recommendations were presented to the 2 sponsoring societies and adopted.

Prospective studies also have assessed the effect of lazaroids and gangliosides on ultimate neurologic outcome, and no significant lasting effects have been documented. Their effectiveness has been shown in the mild and partial injury groups and not in complete cord injury.[23] Other modalities of treatment have included hypothermia, calcium-channel blockers, and naloxone, but these treatments have failed to show helpful effects.

The use of histamine 2 (H2) blockers (eg, famotidine [Pepcid], ranitidine [Zantac]) generally is recommended, to prevent stress ulceration from spinal cord injury and for prophylaxis when following the steroid protocols.

Prophylaxis for deep vein thrombosis (DVT) and pulmonary embolism is of particular concern in the neurologically compromised patient. Rates for DVT in complete injuries range from 30-90%; DVT warrants medical and/or mechanical treatment. This may include low-molecular-weight heparin, oral warfarin (Coumadin), intermittent compression devices for the lower extremities, or vena cava filters.


Surgical Therapy

The initial surgical management focuses on the specific injury encountered, which can be classified as involving (1) the anterior column or vertebral body primarily; (2) the posterior column with pedicle, facet, or lamina injury; or (3) both columns. Spinal realignment generally is emphasized. This begins with application of cervical tongs and serially increasing traction until normal spinal alignment is achieved and bony compression is reduced. Gardner-Wells tongs have been the criterion standard for years because they are easy to apply and can withstand great weight until reduction is obtained. MRI-compatible tongs or halos can also be used and have the advantage of allowing urgent MRI when appropriate. See the image below.

Reduction of C5 burst fracture after tongs tractio Reduction of C5 burst fracture after tongs traction.

If the injury primarily involves the anterior column, a Smith-Robinson or standard anterior approach to the spine is used to allow anterior decompression and reconstruction with either allograft or autograft iliac crest or fibula, followed by stabilization with anterior locking plates.

The posterior approach is indicated when the pathoanatomy involves the posterior elements and is the basic midline approach with muscle retraction off the cervical spine to the lateral aspect of the facet joints bilaterally.

Occasionally, a dual approach is necessary to remove an offending disk fragment anteriorly prior to reduction, followed by posterior stabilization with anterior reconstruction. These global injuries are usually quite unstable, and they benefit from both anterior and posterior reconstruction.


Preoperative Details

In-hospital care of the patient with a cervical spine injury should be meticulous in the preoperative period. These patients are at risk for pulmonary problems secondary to concomitant injuries and to immobilization. Gastrointestinal bleeding has been reported in up to 40% of patients and is most common around 10 days following injury. This can be aggravated by corticosteroid use and can be treated with H2 blockers and early enteral feedings. These patients are also at risk for developing DVT secondary to immobilization. Incidence of DVT has been reported to be as high as 95%, and DVTs are clinically relevant in up to 35% of people. Some form of anticoagulation and compression boots should be used. Skin breakdown due to immobilization is also a problem and should be treated aggressively with pressure relief and wound care.

The above preoperative problems and their association with immobilization have contributed to controversy in the timing of surgical intervention. Proponents exist for both early and late surgical intervention.[24] Studies exist showing worsening after surgical intervention within the first 5 days after injury. These studies reported increased mortality rates and neurologic deterioration, concluding that a 1-2 week delay in operative intervention is best. However, other studies have shown that neurologic damage is affected not only by the degree of cord compression but also by its duration. These studies have led to recommendations for urgent decompression.

Most surgeons now advocate early intervention, recognizing that patients are better candidates for surgery in this early window of opportunity before other complications occur. The best reasons for early surgical intervention are to avoid preoperative systemic problems, to provide rapid decompression of the injured cord, and to return to mobilization. One other important scenario is in the patient who exhibits progressive neurologic worsening: prompt surgical decompression is generally agreed to be absolutely necessary.


Intraoperative Details

When the patient is taken to the operating room, certain issues must be addressed. If the patient has been in traction or a halo for reduction of the spine, this must be maintained in the transfer to the operating table and while on the operating table. This sometimes requires an awake patient and/or nasal intubation, with meticulous handling of the cervical spine during the entire process. Thus, the surgeon, anesthesiologist, and nursing staff must all be working in concert to ensure the patient's safety.

The operative approach obviously dictates whether the patient is prone or supine, and in some instances, both are needed for the combined approach. Whatever the position of the patient, the hips, knees, shoulders, hands, and feet should all be well padded to prevent pressure sores and peripheral nerve palsies. The Stryker frame and Jackson frame are operating beds designed with a pulley to facilitate traction of the cervical spine. They also are designed with removable pads for patient positioning, and some are equipped with a turning frame to allow the patient to be spun safely from the supine to the prone position and back.

The indications for spinal cord monitoring are also somewhat controversial among surgeons. Somatosensory evoked potentials (SSEPs) offer a safe, noninvasive, and continuous technique for assessing the functional integrity of the spinal cord. Several reports suggest that changes in evoked potentials are predictive of neurologic change in the patient. When a signal deformity is detected, it can be checked with a wake-up test to ensure its accuracy. However, the delayed nature of the change makes these tests of limited efficacy in preventing intraoperative injury. A major problem with the technique is that multiple false-positive and false-negative results have been reported. In addition, monitoring is only as good as the skill of the personnel performing it. In summary, SSEPs and motor-evoked potentials (MEPs) may have some benefit in the neurologically intact patient in whom significant intraoperative manipulation of the spinal column is anticipated.


Postoperative Details

Postoperatively, patients usually are maintained in some sort of cervical orthosis, depending on the quality of fixation obtained. Fixation techniques have improved dramatically in recent years. Before, most patients were placed in a halo postoperatively; now, patients are placed in only a rigid or soft collar for comfort. The patient should be mobilized out of bed as soon as possible to prevent pulmonary and DVT complications. A return to independence should be approached aggressively, with the help of a comprehensive team that includes a physical therapist, social service personnel, and family. In patients with spinal cord injury and neurologic deficit, extensive physical and emotional rehabilitation should be instituted immediately following surgery to ensure the best physical and psychological outcome for the future.[25] See the images below.

Postoperative image of C5 burst fracture; note ant Postoperative image of C5 burst fracture; note anterior and posterior fixation.
Postoperative image of C5 burst fracture. Postoperative image of C5 burst fracture.
Postoperative anteroposterior view of C7-T1 fractu Postoperative anteroposterior view of C7-T1 fracture/dislocation.
Postoperative lateral view of C7-T1 fracture/dislo Postoperative lateral view of C7-T1 fracture/dislocation.

Postoperative management of bowel and bladder dysfunction should include instruction in intermittent catheterizations, as well as the use of alternate-day suppositories and a high-fiber diet to assist with bowel function and avoid impaction.

Close attention to skin breakdown should include frequent turning of the patient and, as mentioned above, prompt mobilization.



Patients must be monitored closely for the first 4 weeks postoperatively to ensure maintenance of spinal alignment and the absence of evidence of neurologic deterioration. Independence should be encouraged, and attempts to regain preinjury activity levels should begin. Between 2 and 3 months of healing usually is expected, and radiographic signs of osseous healing should be noted in this time frame. Some patients may require up to 6 months to achieve preinjury activity levels; others, based on concomitant injuries and age, may never reach this status. Aggressive therapy should continue during this entire period. Once the injury is healed and the patient is functioning at maximal levels, return to full activity is begun.

During the follow-up period, any deterioration in neurologic function should prompt further investigation, including MRI for posttraumatic syrinx or other intrinsic or extrinsic compressive lesions.



Complications secondary to lower cervical spine fractures and dislocations can be divided into 2 major categories: (1) fracture/dislocation-associated problems and (2) spinal cord injury or medical-related problems, including pulmonary problems (eg, pneumonia, atelectasis, pulmonary embolus), gastrointestinal problems (eg, stress ulcers), urologic problems, skin problems (eg, decubiti), DVT, and psychological problems (eg, depression).

Autonomic dysreflexia is a syndrome of generalized sympathetic discharge resulting in severe headache, nausea, chills, anxiety, and sweating. Blood pressure may become dangerously high, usually as a result of bladder distention or fecal impaction. Prompt removal of the inciting stimulus and treatment of the high blood pressure are emergency measures necessary to avoid catastrophic stroke. This is a potentially lethal condition if unrecognized.

Failure to achieve realignment of the spine is among the first problems that can be encountered in dealing with this group of injuries. While reduction of bilateral facet dislocations tends to be accomplished easily with cervical tongs and traction, unilateral jumped facets may be more problematic. If a reasonable attempt at reduction has been performed (50 lb) or neurologic deficit is persistent or worsening, open reduction and stabilization usually can be accomplished through a posterior approach.

A unilateral root injury is more typical with these injuries. Simple inline traction does not address the rotational component of this injury, and a manipulative reduction with the patient awake can be performed once sufficient traction and flexion have disengaged the locked facet. Closed reductions are successful in about 50% of cases; the remainder require open reduction, which can be achieved easily by grasping the spinous processes and lifting and rotating the facet into place.

Because unreduced dislocations are associated with a high incidence of instability, pain, and stiffness, reduction should be performed by either closed or open means. Simple wiring or lateral mass plate fixation can maintain stability while healing occurs. Supplementing the fixation with bone grafting for arthrodesis does not always seem to be necessary, as pointed out by Levine and Roy-Camille, with plating techniques.[26]


Outcome and Prognosis

The clinical outcome after lower cervical spinal injury generally is related to the level and severity of associated spinal cord injury. Incomplete spinal cord injuries, as defined by objective motor or sensory preservation below the level of trauma, have the potential for recovery. In general, the sooner the evidence of return, the better the overall prognosis, although recovery may continue for a year or more.

The level of injury also determines the overall functional status of the patient.

  • The patient with C3-4 cord level injury must use a sip-and-puff (mouth) or chin/head control for mobilization in a wheelchair.
  • Patients with C5 level injuries, as defined by greater than three-fifths strength in the respective muscle group, are able to assist with upper body dressing, can feed themselves with assistive devices, and can operate a power wheelchair.
  • Some grooming and assistance with bowel and bladder programs are within the realm of capabilities of the quadriplegic patient with C6 level injuries. These patients are able to feed themselves with hand or tenodesis splints and can transfer to and from wheelchairs or toilets with some assistance.
  • Patients with injuries at the C7 level can transfer independently to the bed, car, or toilet; can use manual or power wheelchairs; and can dress independently using assistive devices.
  • Patients with injuries at the C8 level or below should be independent in all transfers and be able to use a manual wheelchair and assist in some homemaking activities.

The life expectancy of patients with cervical spinal cord injuries has increased with better management of urinary complications. Urinary complications are no longer among the most common causes of death after the first year after injury.


Future and Controversies

Restoration of spinal cord function after injury remains a major challenge to those treating paralyzed victims. While prevention and treatment of secondary cord damage continues to be a primary objective, the ability to reverse established cord dysfunction is a major goal. Attempts to reestablish neural recovery have focused on modification of the injured tissue through implantation of acellular guiding prosthesis, fetal tissue, and glial cells.

The activation of intrinsic neural capacities through gene therapy or by delivering a host of neurotropic substances such as nerve growth factor or brain-derived neurotrophic factors is being explored experimentally. The use of stem cells and trials using olfactory glial cells remain on the horizon. Olfactory glial cells are the only neurons able to replicate in adult life. They are capable of crossing scar tissue as well as bridging the gap between the peripheral nervous system and the central nervous system.

Potassium channel blockade has been used in the clinical arena and has been successful in helping up to one third of patients with chronic spinal cord injuries. The drug 4-aminopyridine has been most effective in patients with incomplete cord injuries.[27] It is believed to work through blockage of the fast A-type potassium channels that increase the safety factor of conduction across demyelinated or thinly remyelinated internodes or by increasing influx of calcium at presynaptic terminals, which improves neural transmission.

The timing of surgical interventions remains controversial, with advocates of emergent decompression and stabilization versus those contending that delaying surgical management by 5 days can minimize neurologic deterioration. Controlled prospective studies are needed to resolve this ongoing controversy. However, it is generally accepted that abrupt neurologic deterioration in the face of persistent compression warrants immediate surgical intervention.

A recent critical review of the literature regarding preclinical and clinical evidence on the potential impact of timing of surgical decompression after traumatic spinal cord injury included 153 abstracts of which 22 fulfilled the inclusion and exclusion criteria. The vast majority were level 4 evidence with 2 level 2b. The most common definition of early surgery was 24-72 hours following spinal cord injury. An expert panel recommended that early surgical intervention be considered from 8-24 hours following acute spinal cord injury. Using a modified Delphi process, the following recommendations were made[28, 29] :

  • There is strong preclinical evidence for the biological benefits of early surgical decompression in animal spinal cord injury models.
  • Decompression should be performed within 24 hours when medically feasible. The optimal timing of surgical decompression or whether surgery is indicated at all in patients with central cord syndrome injury remains unclear.
  • There are clinical, neurological, and functional benefits of early spinal cord decompression.
Contributor Information and Disclosures

J Allan Goodrich, MD Staff Physician, Orthopaedic Spine Surgeon, Doctor's Hospital

J Allan Goodrich, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, North American Spine Society, Society of Lateral Access Surgery

Disclosure: Received consulting fee from Nuvasive for speaking and teaching; Received royalty from Globus for consulting.


Thad Andrew Riddle, MD Orthopedic Surgeon and Partner, Georgia Bone and Joint Surgeons

Thad Andrew Riddle, MD is a member of the following medical societies: AO Foundation, American Academy of Orthopaedic Surgeons, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

William O Shaffer, MD Orthopedic Spine Surgeon, Northwest Iowa Bone, Joint, and Sports Surgeons

William O Shaffer, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Association, Kentucky Medical Association, North American Spine Society, Kentucky Orthopaedic Society, International Society for the Study of the Lumbar Spine, Southern Medical Association, Southern Orthopaedic Association

Disclosure: Received royalty from DePuySpine 1997-2007 (not presently) for consulting; Received grant/research funds from DePuySpine 2002-2007 (closed) for sacropelvic instrumentation biomechanical study; Received grant/research funds from DePuyBiologics 2005-2008 (closed) for healos study just closed; Received consulting fee from DePuySpine 2009 for design of offset modification of expedium.

Chief Editor

Jeffrey A Goldstein, MD Clinical Professor of Orthopedic Surgery, New York University School of Medicine; Director of Spine Service, Director of Spine Fellowship, Department of Orthopedic Surgery, NYU Hospital for Joint Diseases, NYU Langone Medical Center

Jeffrey A Goldstein, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Orthopaedic Association, North American Spine Society, Scoliosis Research Society, Cervical Spine Research Society, International Society for the Study of the Lumbar Spine, AOSpine, Society of Lateral Access Surgery, International Society for the Advancement of Spine Surgery, Lumbar Spine Research Society

Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from NuVasive for consulting; Received royalty from Nuvasive for consulting; Received consulting fee from K2M for consulting; Received ownership interest from NuVasive for none.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Samuel Hu, MD, to the development and writing of this article.

  1. Uhrenholt L, Charles AV, Hauge E, Gregersen M. Pathoanatomy of the lower cervical spine facet joints in motor vehicle crash fatalities. J Forensic Leg Med. 2009 Jul. 16(5):253-60. [Medline].

  2. Kouyoumdjian P, Guerin P, Schaelderle C, Asencio G, Gille O. Fracture of the lower cervical spine in patients with ankylosing spondylitis: Retrospective study of 19 cases. Orthop Traumatol Surg Res. 2012 Sep. 98(5):543-51. [Medline].

  3. Hubbard ME, Jewell RP, Dumont TM, Rughani AI. Spinal injury patterns among skiers and snowboarders. Neurosurg Focus. 2011 Nov. 31(5):E8. [Medline].

  4. Allen BL, Ferguson RL, Lehmann TR et al. A mechanistic classification of closed, indirect fractures and dislocations of the lower cervical spine. Spine. 1982. 7:1-27.

  5. Zehnder SW, Lenarz CJ, Place HM. Teachability and reliability of a new classification system for lower cervical spinal injuries. Spine (Phila Pa 1976). 2009 Sep 1. 34(19):2039-43. [Medline].

  6. Toh E, Nomura T, Watanabe M, Mochida J. Surgical treatment for injuries of the middle and lower cervical spine. Int Orthop. 2006 Feb. 30(1):54-8. [Medline].

  7. Marco RA, Meyer BC, Kushwaha VP. Thoracolumbar burst fractures treated with posterior decompression and pedicle screw instrumentation supplemented with balloon-assisted vertebroplasty and calcium phosphate reconstruction. Surgical technique. J Bone Joint Surg Am. 2010 Mar. 92 Suppl 1 Pt 1:67-76. [Medline].

  8. Kim HJ, Lee KY, Kim WC. Treatment outcome of cervical tear drop fracture. Asian Spine J. 2009 Dec. 3(2):73-9. [Medline]. [Full Text].

  9. Dvorak MF, Fisher CG, Aarabi B, Harris MB, Hurbert RJ, Rampersaud YR, et al. Clinical outcomes of 90 isolated unilateral facet fractures, subluxations, and dislocations treated surgically and nonoperatively. Spine. 2007 Dec 15. 32(26):3007-13. [Medline].

  10. Milligram MA, Rand N. Cervical Spine Anatomy. Spine State of the Art Reviews. 2000. 14(3):521-532.

  11. Platzer P, Hauswirth N, Jaindl M, Chatwani S, Vecsei V, Gaebler C. Delayed or missed diagnosis of cervical spine injuries. J Trauma. 2006 Jul. 61(1):150-5. [Medline].

  12. Silva CT, Doria AS, Traubici J, Moineddin R, Davila J, Shroff M. Do additional views improve the diagnostic performance of cervical spine radiography in pediatric trauma?. AJR Am J Roentgenol. 2010 Feb. 194(2):500-8. [Medline].

  13. Antevil JL, Sise MJ, Sack DI, Kidder B, Hopper A, Brown CV. Spiral computed tomography for the initial evaluation of spine trauma: A new standard of care?. J Trauma. 2006 Aug. 61(2):382-7. [Medline].

  14. Eismont FJ, Arena MJ, Green BA. Extrusion of an Intervertebral Disc associated with Traumatic Subluxation or Dislocation of Cervical Facets. J Bone Joint Surg AM. 1991. 73:1555-1560.

  15. Tsutsumi S, Ueta T, Shiba K, Yamamoto S, Takagishi K. Effects of the Second National Acute Spinal Cord Injury Study of high-dose methylprednisolone therapy on acute cervical spinal cord injury-results in spinal injuries center. Spine. 2006 Dec 15. 31(26):2992-6; discussion 2997. [Medline].

  16. Bracken MB, Holford TR. Neurological and functional status 1 year after acute spinal cord injury: estimates of functional recovery in National Acute Spinal Cord Injury Study II from results modeled in National Acute Spinal Cord Injury Study III. J Neurosurg. 2002 Apr. 96(3 Suppl):259-66. [Medline].

  17. Young W, Bracken MB. The Second National Acute Spinal Cord Injury Study. J Neurotrauma. 1992 Mar. 9 Suppl 1:S397-405. [Medline].

  18. Young W, Bracken MB. The Second National Acute Spinal Cord Injury Study. J Neurotrauma. 1992 Mar. 9 Suppl 1:S397-405. [Medline].

  19. Bracken MB, Shepard MJ, Hellenbrand KG, Collins WF, Leo LS, Freeman DF, 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].

  20. Fehlings MG. Summary statement: the use of methylprednisolone in acute spinal cord injury. Spine. 2001 Dec 15. 26(24 Suppl):S55. [Medline].

  21. Hugenholtz H, Cass DE, Dvorak MF, et al. High-dose methylprednisolone for acute closed spinal cord injury--only a treatment option. Can J Neurol Sci. 2002 Aug. 29(3):227-35. [Medline].

  22. Hurlbert RJ, Hadley MN, Walters BC, et al. Pharmacological therapy for acute spinal cord injury. Neurosurgery. 2013 Mar. 72 Suppl 2:93-105. [Medline].

  23. Fehlings MG, Bracken MB. Summary Statement: The Sygen(R) (GM-1 Ganglioside) Clinical Trial in Acute Spinal Cord Injury. Spine. 2001 Dec 15. 26(24 Suppl):S99-S100. [Medline].

  24. Sapkas GS, Papadakis SA. Neurological outcome following early versus delayed lower cervical spine surgery. J Orthop Surg (Hong Kong). 2007 Aug. 15(2):183-6. [Medline].

  25. Apple DF. Spinal cord injury rehabilitation. In: Garfin SR, Vaccaro AR, eds. Orthopaedic Knowledge Update: Spine. Vol 2. American Academy of Orthopaedic Surgeons. 2002:239-244.

  26. Levine AM. Facet fractures and dislocations. In: Lampert R, ed. Spine Trauma. WB Saunders Co. 1998:331-365.

  27. Segal JL, Pathak MS, Hernandez JP, et al. Safety and efficacy of 4-aminopyridine in humans with spinal cord injury: a long-term, controlled trial. Pharmacotherapy. 1999 Jun. 19(6):713-23. [Medline].

  28. Furlan JC, Noonan V, Cadotte DW, Fehlings MG. Timing of decompressive surgery of spinal cord after traumatic spinal cord injury: an evidence-based examination of pre-clinical and clinical studies. J Neurotrauma. 2011 Aug. 28(8):1371-99. [Medline]. [Full Text].

  29. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012. 7(2):e32037. [Medline]. [Full Text].

  30. Fehlings MG, Sekhon LHS. Restoration of spinal cord function. In: Garfin SR, Vaccaro AR, eds. Orthopaedic Knowledge Update: Spine. Vol 2. American Academy of Orthopaedic Surgeons. 2002:483-488.

  31. Rang M. Spine Fractures and Traumatic Paraplegia. The Story of Orthopaedics. 2000. 411-422.

  32. Vaccaro AR, Zlotolow DA, Blam OG. The Lower Cervical Spine in Spinal Cord Injury. Spine State of the Art Reviews. 1999. 13(3):489-506.

Cross-sectional anatomy of the cervical cord.
Normal anatomy of the lower cervical spine.
Lateral film of a C5 burst/teardrop fracture.
Sagittal CT scan of C5 burst fracture.
Axial CT scan of C5 burst fracture.
Reduction of C5 burst fracture after tongs traction.
Postoperative image of C5 burst fracture; note anterior and posterior fixation.
Postoperative image of C5 burst fracture.
Standard lateral cervical spine of an 80-year-old patient after a motor vehicle accident; patient has no neurologic deficits and no neck pain.
Swimmer's view of the same 80-year-old patient as in Image 9; note the C7-T1 fracture/dislocation.
Axial CT scan of C7-T1 fracture/dislocation.
Sagittal CT of C7-T1 fracture/dislocation.
MRI of C7-T1 fracture/dislocation.
Reduction of C7-T1 fracture/dislocation.
Postoperative anteroposterior view of C7-T1 fracture/dislocation.
Postoperative lateral view of C7-T1 fracture/dislocation.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.