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


Vertebral Fracture Treatment & Management

  • Author: George M Ghobrial, MD; Chief Editor: Brian H Kopell, MD  more...
Updated: Feb 22, 2016

Medical Therapy

Prehospital care

Paramedics and first responders ascribe to the basic tenet of "do no harm." Their routine protocol is to use spinal immobilization for patients with major traumatic injuries, patients whose mechanism of injury is not clear, and patients who may have experienced some trauma. Of course, the initial focus is on cervical spine injuries, and they routinely apply a cervical spine immobilization device, typically a rigid plastic cervical collar. They use a logroll technique when transferring the patient onto a long spine board or rescue board, which avoids unnecessary movement. Once on a spine board, the patient is secured and prepared for transport. Even patients with no spinal tenderness or neurologic deficits are transported in this fashion. The goal of routine spinal immobilization protocols is to avoid injuries during transport and during the prehospital phase.

Once in the hospital, remove the patient from the board as soon as practical. Prolonged use may be uncomfortable and even counterproductive because uncomfortable patients may start moving on the board. Some patients develop skin breakdown and decubitus ulcers, even after 1 hour of use. Controlled transfer, use of a sliding board or scoop system, and the logroll technique can prevent further injury. Adequate personnel are needed to facilitate these transfers.

Emergency department management

Focus the initial assessment and stabilization of patients with spine injuries on the ABCs and patient immobilization. As part of the initial assessment and stabilization, the airway may need to be secured using rapid-sequence intubation and spinal stabilization. Once the ABCs algorithm is satisfied, focus attention on the secondary survey. Quite often, these patients are victims of multiple traumas. Associated injuries, such as brain, thoracic, or abdominal injuries, take precedence. The neurologic examination helps determine the presence of deficits. In the presence of neurologic deficits, hypotension and bradycardia may indicate neurogenic shock.

The treatment goal for patients in neurogenic shock is to maintain hemodynamic stability. Maintain the systolic blood pressure at a value of at least 90 mm Hg with a heart rate of 60-100 beats per minute. Initial treatment of hypotension is fluid resuscitation; typical adults may require up to 2 liters of crystalloids. Bradycardia may be titrated by the use of atropine. Attempt to maintain urine output at a minimum of 30 mL/h. If all of the above parameters are difficult to maintain, consider support with inotropic agents. These patients are also at risk for hypothermia and should be warmed to maintain a core temperature of at least 96°F. Place a Foley catheter to help with voiding. A nasogastric tube can help with ileus, which is common in the setting of spinal injury. Priapism is not usually treated.

Paramedics and rescue personnel often transport patients on a spinal board with complete spinal immobilization. The objective is to minimize the possibility of injury during transport. Traditionally, patients have been kept on the spinal board until all radiographic studies were completed and no fractures were identified. A more practical approach is to logroll patients off the board, even prior to obtaining radiographs. A cervical collar can be kept in place until the cervical spine is cleared. The objective is to provide maximal patient comfort while minimizing iatrogenic injury. Early clearance from the spinal board can prevent formation of pressure sores and necrosis. Ensure that patients are turned every 1-2 hours to prevent decubitus ulcer formation. Administer pain medication to maintain patient comfort.

For patients with blunt trauma injuries and neurologic deficits, consider the administration of high-dose intravenous steroids to help minimize deficits. Begin steroid therapy within 8 hours of the injury. The initial dose of methylprednisolone is 30 mg/kg administered over 15 minutes. Start an infusion for the maintenance dose of 5.4 mg/kg/h at the beginning of the first hour and continue it through the 23rd hour. Recent studies have shown that steroid use may result in complications and inconsistent results. Whether steroid use will continue to be the standard of care for these injuries remains unclear.[10, 11, 12, 13]

Nonsurgical management of fractures

Fractures may be managed operatively or nonoperatively depending on the extent of spinal cord injury and the overall health of the patient. Minor fractures or those with column stability are managed nonoperatively. Major fractures or those with significant instability can be managed operatively. Operative management is used for stabilization of the spinal column and prevention of spinal deformity, although major factors in nonsurgical candidates can be treated conservatively with nonoperative treatment.

Nonoperative management of unstable spinal fractures involves the use of a spinal orthotic vest or brace. The objective of the brace is to prevent rotational movement and bending. Give consideration to the stabilization of patients with spinal cord injuries and paraplegia. These patients need to be stabilized sufficiently so that their upper body and axial skeleton are appropriately supported, which allows for effective rehabilitation. Stabilization allows patients to use their upper body strength to help with mobility and rehabilitation.

Spinal orthoses are somewhat uncomfortable and only partially effective in providing full stabilization of the thoracic and lumbar spine. The thoracolumbar junction is especially difficult to immobilize externally. As with cervical collar immobilization of the neck, the patient can exhibit an almost complete range of motion with minimal effort. External braces and orthoses primarily serve as a reminder to the patient to minimize movement. A more effective means of immobilization is the body cast, although the body cast is very uncomfortable and may not be well tolerated.

High-dose steroids

Results from the National Acute Spinal Cord Injury Study (NASCIS) demonstrated the benefit of high-dose steroid administration after blunt spinal cord trauma. Methylprednisolone administration resulted in improved motor and sensory function in subjects with moderate or severe spinal cord injuries. The conclusion of the study was that high-dose methylprednisolone administered within 8 hours of injury resulted in improved motor and sensory function. In the first hour of the protocol, a bolus of 30 mg/kg was administered. For the following 23 hours, subjects were given a steroid infusion of 5.4 mg/kg/h. Because researchers noted that subjects improved significantly, the clinical trial was halted with the assumption that high-dose steroids were a viable treatment for acute spinal cord injury. The treatment was not targeted at patients with penetrating trauma injuries.

Later studies showed inconsistent results. Some studies did not demonstrate an improvement of the neurologic deficit. Other studies showed long-term detrimental effects, such as increased rates of infection, including pneumonia. The current standard of care is to use the high-dose steroid protocol until conclusive studies are conducted.


Surgical Therapy

Operative approaches

The goals of operative treatment are to decompress the spinal cord canal and to stabilize the disrupted vertebral column. Three basic approaches are used for surgical management of the thoracolumbar spine: (1) the posterior approach, (2) the posterolateral approach, and (3) the anterior approach. Selection of the best approach is guided by the anatomy of the fracture and the location of spinal canal encroachment. Also consider the need for stabilization procedures.

The posterior approach with a midline incision and a laminectomy allows for access to the posterior elements, although it does not permit access to the vertebral bodies and, as a result, is not commonly used. Spinal cord compression as a result of isolated fractures of the posterior elements is not very common. Spinal canal compromise is more frequent when the vertebral bodies and anterior elements are involved. The posterior approach is useful for stabilization procedures that involve fixation of the posterior bony elements. The posterior approach is used when early mobilization is considered and decompression of the spinal canal is not a major consideration.

The posterolateral technique improves access to the vertebral bodies, although access is still limited. Decompression of ventral impingement of the canal is technically difficult using this approach. It is useful when only a limited exposure of the ventral elements is required. It may be combined with a posterior stabilization procedure when limited ventral exposure is needed. The approach to the high thoracic segments is technically difficult. This technique is often used for high thoracic fractures such as T1 through T4.

The anterior approach allows access to the vertebral bodies at multiple levels. Transthoracic exposure is required in order to access the vertebral bodies down to L2. Lower fractures require a transabdominal-retroperitoneal exposure. It is most useful for decompression of injuries and spinal canal compromise caused by vertebral body fractures. Examples of significant vertebral body fractures include a burst fracture, sagittal slice fracture, and severe compression fractures. Sometimes, a modified combined approach is used to maximize exposure and access. When an anterior approach is used, the vertebral bodies are often resected and replaced with autologous bone or bone from the bone bank. This technique, unlike the posterior stabilization procedures, does not result in early stability.


Preoperative Details

Positioning of the patient and anesthesia considerations

Depending on the surgical approach, the patient must be properly positioned. For a posterior approach, place the patient in the prone position with either horizontal or flexed positioning at the hips. For a lateral approach, the surgeon can use either the prone position or a modified lateral decubitus position. For the ventral approach, position the patient supine. Ensure that the anesthesiologist has proper intravenous access and access to the extremities and chest for intraoperative monitoring. Exercise the usual precautions of positioning and avoidance of pressure on peripheral nerves, eyes, and other organs. Surgery is usually performed with the patient under general anesthesia with endotracheal intubation. Prophylactic antibiotics are routine. To obtain maximum pain control, the incision is infiltrated with a local anesthetic. During surgery, implement prophylaxis for deep venous thrombosis with use of pneumatic sequential compression devices or thromboembolic disease(TED) stockings.


Intraoperative Details

Surgical exposure

Proper exposure of the affected area is necessary. Often, going several segments above and below the affected area is necessary in order to ensure optimal exposure and proper placement of stabilizing hardware. The skin and soft tissue incision may be 10 cm or more in depth, and the incision requires retractors for optimal exposure. Meticulous attention to hemostasis is required because even minimal bleeding may cause the operative area to eventually fill with blood. If at all possible, keep the thecal sack intact. Evacuate epidural or subdural hematomas.

Categories of procedures for spine stabilization

The 4 basic types of stabilization procedures are (1) posterior lumbar interspinous fusion, (2) posterior rods, (3) cage, and (4) the Z-plate anterior thoracolumbar plating system. Each has different advantages and disadvantages.

Posterior lumbar interspinous fusion is the least-invasive method and involves the use of screws to obtain stability and promote fusion. Most patients have good results with this technique. It can be used effectively for isolated or relatively stable fractures.[14]

Posterior rods require extensive exposure and are effective in stabilizing multiple fractures or unstable fractures. The use of rods prevents further deformity and deterioration. The rods are attached with pedicle screws, stainless steel wires, clips, and clamps to achieve a stable construct. Also, in the case of spinal tuberculosis, use of posterior stabilization using long rods prevents further deterioration and deformity.[15]

The Z-plate anterior thoracolumbar plating system has been used for the treatment of burst fractures. Surgery is performed for neurologic deficits, deformity, progressive kyphosis, and late pain. Ghanayem and Zdeblick reported good success with this form of anterior arthrodesis.


Postoperative Details

Postoperative care of the surgical incision

The incision is usually closed in a layered fashion, and the skin is either stapled or sutured. A dressing is applied and taped in place. Some surgeons keep the dressing in place postoperatively for 24-48 hours. Other surgeons elect to inspect the incision the next day and subsequently place a fresh dressing. Postoperative antibiotics may be given for up to a total of 3 doses. If a significant amount of stabilizing hardware was implanted, continuation of antibiotics is appropriate.

Prevention of complications

Patients are susceptible to postoperative cardiac complications such as myocardial infarction. Place patients with risk factors in an intensive care unit or monitored setting. Pulmonary complications, which cause pain and decreased tidal volume, can occur as a result of stabilizing procedures. Use incentive spirometry to help patients with deep breathing and early ambulation. The patient's hematocrit value should be monitored, especially for those patients with significant blood loss during surgery. Similarly, monitor renal function and electrolyte values, especially for susceptible patients. Patients are at risk for deep vein thrombosis after any surgery or prolonged immobilization. Precautions include the use of pneumatic compression devices, TED stockings, or subcutaneous heparin injections.

Remove the Foley catheter after 24-48 hours or once the patient is ambulatory. This decreases the risk of urinary tract infections and possible hematogenous spread to the spine and implanted hardware.

Length of hospitalization

Patients with isolated vertebral fractures that are stable and have no neurologic deficits may be observed for a short period and discharged home. An example is a patient with a vertebral compression fracture.

Patients who have more than one traumatic injury may require prolonged hospitalization secondary to associated injuries and complications.

Patients who have undergone a vertebral fracture stabilization procedure must attempt ambulation as soon as tolerable. Ensure they are properly medicated for pain so that pulmonary function is not compromised.

Refer patients with moderate or severe neurologic deficits to a rehabilitation facility as soon as feasible.



The operating surgeon reevaluates the patient within 1-2 weeks of surgery. Of course, if patients experience postoperative complications or complicated surgeries, they are seen within 2-3 days after discharge.

Rehabilitation and physical therapy

Early ambulation is recommended for patients who are neurologically intact or those who have limited neurologic impairment. Pain control is important to facilitate early ambulation. Patients with significant neurologic impairment or those who are paraplegic should also have active recovery and early mobilization. Full stabilization may take up to 2 years. The rate of improvement depends on the ongoing maturation of the fused vertebrae and the conditioning of the muscles. Recommend that patients refrain from smoking because this impairs the healing process.

Rehabilitation facilities

Patients with significant neurologic impairment or those who are paraplegic may need to spend time at a rehabilitation facility until they have been trained to adapt and to cope with their disability. The focus of rehabilitation is on bowel and bladder management and on transfer techniques. Psychological counseling is essential to help patients cope with their injury. Some patients may require antidepressant or antianxiety medications. Proper pain management is also important for successful rehabilitation.



Complications of vertebral fractures may include mechanical complications from the fracture itself, neurologic deficits, and resultant comorbid conditions. Surgical stabilization procedures also have associated complications.

A study by Dimar et al identified factors predictive of complications after surgery to stabilize thoracolumbar spinal injuries.[16] The study determined that severity of neurologic injury, quantity of associated morbidities, and high-dose steroid use independently increase the risk for major complications after stabilization.

Mechanical complications

Vertebral fractures of the thoracic and lumbar spine that are somewhat mechanically unstable and have not been stabilized with instrumentation may develop progressive deformity despite the use of an orthotic brace. Such a deformity may hamper rehabilitation. Unstable fractures may result in further deterioration of a partial neurologic lesion.

Neurologic deficits

In the acute phase, patients with partial spinal cord injuries may experience an increase of the neurologic deficit. The initial flaccid paralysis may turn into spasticity.

Resultant comorbid conditions

A major complication of thoracic or lumbar spinal cord injury and the resultant paraplegia is the development of pressure sores. Prevention starts in the emergency department; patients need to be removed from spinal cord immobilization as soon as possible. During hospitalization, decubitus precautions should be implemented; the patient should be turned frequently. Use of egg-crate foam mattresses or air mattresses is also protective. Educating the patient and any caregivers is another important component of prevention.

Pulmonary complications may occur in patients with high thoracic injuries. In the acute phase, associated rib fractures and pulmonary contusions may occur. This predisposes the patient to hypoxemia and other complications. Also, the diaphragm, the major muscle of respiration, is supplied by the phrenic nerve at cervical spine levels C3 through C5; the diaphragm is also supplemented by the intercostal muscles from thoracic segmental levels. This could result in a decrease in the tidal volume of respiration, thus predisposing the patient to atelectasis and pneumonia.

Patients with spinal cord injuries are predisposed to the development of ileus and constipation. They should be treated to prevent impaction and associated complications. In the acute phase, a nasogastric tube may be placed for the first 24-48 hours. Early enteral feeding via a feeding tube at a slow rate may be tolerated. The feeding rate should be advanced slowly until complete nutritional support is provided and is adequately tolerated.


Future and Controversies

The initial multicenter clinical trials that used methylprednisolone for the treatment of spinal cord injury, the NASCIS II trial, were promising and methylprednisolone quickly turned into the standard of care. Patients showed significant improvement of neurologic function at 6 months after injury, provided they were treated within 8 hours of injury. In some individuals who had spinal cord epidural hematomas with neurologic deficits, significant improvement was observed after high-dose methylprednisolone treatment.

At the molecular level, some benefit appears to be gained with the use of high-dose methylprednisolone. Animal studies show a decrease in the production of deleterious compounds and molecules by the cell, such as the expression of p75 neurotrophin receptor. Likewise, methylprednisolone reduces spinal cord injury in rats by decreasing lipid peroxidation; however, a decrease in production of protective tumor necrosis factor-alpha also occurs.

The NASCIS III trial compared the use of methylprednisolone over 48 hours with 24-hour control subjects, which was the recommended treatment of the NASCIS II trial. Subjects who began treatment within 3 hours of injury improved regardless of the length of treatment (24 or 48 h). Subjects who began therapy 3-8 hours after injury showed better long-term recovery if they received methylprednisolone for 48 hours.

In 2001, Bracken performed a meta-analysis of several studies on the topic. He concluded that high-dose methylprednisolone given within 8 hours is a safe and relatively effective therapy in some patients. A meta-analysis by Hulbert (and other studies) failed to show that high-dose steroids improved patient outcomes. Controversy exists because methylprednisolone is not a completely benign drug and adverse effects can occur. High-dose steroids may have detrimental effects, such as immunosuppression and adrenal suppression. From an evidence-based approach, methylprednisolone should not be recommended for routine use. Many centers have continued to use high-dose steroids until definitive studies are completed.

Contributor Information and Disclosures

George M Ghobrial, MD Resident Physician, Department of Neurological Surgery, Thomas Jefferson University Hospital

Disclosure: Nothing to disclose.


James S Harrop, MD Associate Professor, Departments of Neurological and Orthopedic Surgery, Jefferson Medical College of Thomas Jefferson University

James S Harrop, MD is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, American Spinal Injury Association, North American Spine Society, Congress of Neurological Surgeons, Cervical Spine Research Society

Disclosure: Received consulting fee from Depuy spine for consulting; Received none from Geron for none; Received none from Neural Stem for none; Received ownership interest from Axiomed for none; Received honoraria from Stryker Spine for none.

Zachary J Senders, MD Resident Physician, Department of General Surgery, Case Western/UH Case Medical Center, Case Western Reserve University School of Medicine

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.

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.

Additional Contributors

Michael G Nosko, MD, PhD Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School

Michael G Nosko, MD, PhD is a member of the following medical societies: Academy of Medicine of New Jersey, Congress of Neurological Surgeons, Canadian Neurological Sciences Federation, Alpha Omega Alpha, American Association of Neurological Surgeons, American College of Surgeons, American Heart Association, American Medical Association, New York Academy of Sciences, Society of Critical Care Medicine

Disclosure: Nothing to disclose.


Joseph T Alexander, MD, FACS Director of Spine Research, Assistant Professor, Department of Neurosurgery, Division of Surgical Science, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.

Gary Godorov, MD Staff Physician, Department of Emergency Medicine, Bellflower Medical Center

Disclosure: Nothing to disclose.

George Timothy Reiter, MD Associate Professor, Department of Neurosurgery, Pennsylvania State University College of Medicine; Director of Spinal Neurosurgery, Associate Director, Penn State Spine Center, Milton S Hershey Medical Center; Active Staff, Hershey Outpatient Surgery Center; Active Staff, Wilkes-Barre General Hospital; Hospital Appointment, Penn State Rehabilitation Hospital

George Timothy Reiter, MD is a member of the following medical societies: American Association of Neurological Surgeons and Congress of Neurological Surgeons

Disclosure: Synthes Spine Consulting fee Consulting; Integra Grant/research funds None; Integra Consulting fee Consulting

Amiram Shneiderman , MD Assistant Program Director, Co-Director of Quality Assurance, Department of Emergency Medicine, Martin Luther King-Charles Drew Medical Center

Disclosure: Nothing to disclose.

  1. Winkler EA, Yue JK, Birk H, Robinson CK, Manley GT, Dhall SS, et al. Perioperative morbidity and mortality after lumbar trauma in the elderly. Neurosurg Focus. 2015 Oct. 39 (4):E2. [Medline].

  2. Ghanayem AJ, Zdeblick TA. Anterior instrumentation in the management of thoracolumbar burst fractures. Clin Orthop. 1997 Feb. (335):89-100. [Medline].

  3. McAfee PC, Yuan HA, Fredrickson BE, Lubicky JP. The value of computed tomography in thoracolumbar fractures. An analysis of one hundred consecutive cases and a new classification. J Bone Joint Surg Am. 1983 Apr. 65(4):461-73. [Medline].

  4. Denis F. The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine. 1983 Nov-Dec. 8(8):817-31. [Medline].

  5. Haczynski J, Jakimiuk A. Vertebral fractures: a hidden problem of osteoporosis. Med Sci Monit. 2001 Sep-Oct. 7(5):1108-17. [Medline].

  6. Qaseem A, Snow V, Shekelle P, Hopkins R Jr, Forciea MA, Owens DK. Pharmacologic treatment of low bone density or osteoporosis to prevent fractures: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2008 Sep 16. 149(6):404-15. [Medline]. [Full Text].

  7. Baldwin KM, Ryb GE, Miller D, Counihan TC, Brotman S. Is spine consultation needed for all thoracolumbar fractures? Evaluation of a subspecialist-sparing protocol for screening and management of stable fractures. J Trauma. 2010 Dec. 69(6):1491-5; discussion 1495-6. [Medline].

  8. Guarnieri G, Izzo R, Muto M. The role of emergency radiology in spinal trauma. Br J Radiol. 2015 Nov 27. 20150833. [Medline].

  9. Inaba K, Nosanov L, Menaker J, Bosarge P, Williams L, Turay D, et al. Prospective derivation of a clinical decision rule for thoracolumbar spine evaluation after blunt trauma: An American Association for the Surgery of Trauma Multi-Institutional Trials Group Study. J Trauma Acute Care Surg. 2015 Mar. 78 (3):459-65; discussion 465-7. [Medline].

  10. Bracken MB. Methylprednisolone and acute spinal cord injury: an update of the randomized evidence. Spine. 2001 Dec 15. 26(24 Suppl):S47-54. [Medline].

  11. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. 1990 May 17. 322(20):1405-11. [Medline].

  12. Bracken MB, Shepard MJ, Collins WF Jr, et al. Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. Results of the second National Acute Spinal Cord Injury Study. J Neurosurg. 1992 Jan. 76(1):23-31. [Medline].

  13. Ghaly RF. Recovery after high-dose methylprednisolone and delayed evacuation: a case of spinal epidural hematoma. J Neurosurg Anesthesiol. 2001 Oct. 13(4):323-8. [Medline].

  14. Goel VK, Pope MH. Biomechanics of fusion and stabilization. Spine. 1995 Dec 15. 20(24 Suppl):85S-99S. [Medline].

  15. Al-Sebai MW, Al-Khawashki H, Al-Arabi K, Khan F. Operative treatment of progressive deformity in spinal tuberculosis. Int Orthop. 2001. 25(5):322-5. [Medline].

  16. Dimar JR, Fisher C, Vaccaro AR, et al. Predictors of complications after spinal stabilization of thoracolumbar spine injuries. J Trauma. 2010 Dec. 69(6):1497-500. [Medline].

  17. Anderson DK, Hall ED, Braughler JM, et al. Effect of delayed administration of U74006F (tirilazad mesylate) on recovery of locomotor function after experimental spinal cord injury. J Neurotrauma. 1991 Fall. 8(3):187-92. [Medline].

  18. Baron BJ, Scalea TM. Spinal cord injuries. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 5th ed. New York, NY: McGraw-Hill. 2000: 1645-61.

  19. Belaval E, Roy S. Fractures, Cervical Spine. Medscape Reference Journal [serial online]. 2002. Available at:. [Full Text].

  20. Benz RJ, Garfin SR. Current techniques of decompression of the lumbar spine. Clin Orthop. 2001 Mar. (384):75-81. [Medline].

  21. Bergman TA, Seljeskog EL. Management of thoracolumbar and lumbar spine injuries. In: Youmans JR, ed. Neurological Surgery: A Comprehensive Reference Guide to the Diagnosis and Management of Neurosurgical Problems. 3rd ed. Philadelphia, Pa: WB Saunders. 1990: 2411-22.

  22. Brandoli C, Shi B, Pflug B, et al. Dexamethasone reduces the expression of p75 neurotrophin receptor and apoptosis in contused spinal cord. Brain Res Mol Brain Res. 2001 Feb 19. 87(1):61-70. [Medline].

  23. Braughler JM, Hall ED. Current application of "high-dose" steroid therapy for CNS injury. A pharmacological perspective. J Neurosurg. 1985 Jun. 62(6):806-10. [Medline].

  24. Brockmeyer D. Pediatric Spinal Cord and Spinal Column Trauma. Neurosurgery://On-Call [serial online]. 2000. Available at: [Full Text].

  25. Bruecker KA. Principles of vertebral fracture management. Semin Vet Med Surg (Small Anim). 1996 Nov. 11(4):259-72. [Medline].

  26. Collins WF. Surgery in the acute treatment of spinal cord injury: a review of the past forty years. J Spinal Cord Med. 1995 Jan. 18(1):3-8. [Medline].

  27. d'Hemecourt PA, Gerbino PG 2nd, Micheli LJ. Back injuries in the young athlete. Clin Sports Med. 2000 Oct. 19(4):663-79. [Medline].

  28. Dunn ME, Seljeskog EL. Management of thoracic spine fractures. In: Youmans JR, ed. Neurological Surgery: A Comprehensive Reference Guide to the Diagnosis and Management of Neurosurgical Problems. 3rd ed. Philadelphia, Pa: WB Saunders. 1990: 2403-10.

  29. Gamble CL. Osteoporosis: drug and nondrug therapies for the patient at risk. Geriatrics. 1995 Aug. 50(8):39-43. [Medline].

  30. Gerszten PC, Welch WC. Current surgical management of metastatic spinal disease. Oncology (Huntingt). 2000 Jul. 14(7):1013-24; discussion 1024, 1029-30. [Medline].

  31. Gray H. Joints and ligaments. In: Goss CM, ed. Anatomy of the Human Body. 29th ed. Philadelphia, Pa: Lea & Febiger. 1973: 109-13.

  32. Gray H. Osteology. In: Goss CM, ed. Anatomy of the Human Body. 29th ed. Philadelphia, Pa: Lea & Febiger. 1973: 100-4.

  33. Hall ED. Pharmacological treatment of acute spinal cord injury: how do we build on past success?. J Spinal Cord Med. 2001 Fall. 24(3):142-6. [Medline].

  34. Hall ED. The neuroprotective pharmacology of methylprednisolone. J Neurosurg. 1992 Jan. 76(1):13-22. [Medline].

  35. Hall ED, Wolf DL. A pharmacological analysis of the pathophysiological mechanisms of posttraumatic spinal cord ischemia. J Neurosurg. 1986 Jun. 64(6):951-61. [Medline].

  36. Harrington KD. Orthopedic surgical management of skeletal complications of malignancy. Cancer. 1997 Oct 15. 80(8 Suppl):1614-27. [Medline].

  37. Hee HT, Majd ME, Holt RT, Pienkowski D. Better treatment of vertebral osteomyelitis using posterior stabilization and titanium mesh cages. J Spinal Disord Tech. 2002 Apr. 15(2):149-56. [Medline].

  38. Hilton G, Frei J. High-dose methylprednisolone in the treatment of spinal cord injuries. Heart Lung. 1991 Nov. 20(6):675-80. [Medline].

  39. Hsiang JNK. Spinal Stenosis. Medscape Reference Journal [serial online]. 2001. [Full Text].

  40. Hurlbert RJ. The role of steroids in acute spinal cord injury: an evidence-based analysis. Spine. 2001 Dec 15. 26(24 Suppl):S39-46. [Medline].

  41. Hurlbert RJ, Hadley MN, Walters BC, Aarabi B, Dhall SS, Gelb DE, et al. Pharmacological therapy for acute spinal cord injury. Neurosurgery. 2013 Mar. 72 Suppl 2:93-105. [Medline].

  42. Inaoka M, Tada K, Yonenobu K. Problems of posterior lumbar interbody fusion (PLIF) for the rheumatoid spondylitis of the lumbar spine. Arch Orthop Trauma Surg. 2002 Feb. 122(2):73-9. [Medline].

  43. Janssen ME, Lam C, Beckham R. Outcomes of allogenic cages in anterior and posterior lumbar interbody fusion. Eur Spine J. 2001 Oct. 10 Suppl 2:S158-68. [Medline].

  44. Laheri VJ, Badhe NP, Dewnany GT. Single stage decompression, anterior interbody fusion and posterior instrumentation for tuberculous kyphosis of the dorso-lumbar spine. Spinal Cord. 2001 Aug. 39(8):429-36. [Medline].

  45. Larson JL. Injuries to the spine. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 5th ed. New York, NY: McGraw-Hill. 2000: 1792-1800.

  46. Lowe TG, Tahernia AD. Unilateral transforaminal posterior lumbar interbody fusion. Clin Orthop. 2002 Jan. (394):64-72. [Medline].

  47. Mehta JS, Bhojraj SY. Tuberculosis of the thoracic spine. A classification based on the selection of surgical strategies. J Bone Joint Surg Br. 2001 Aug. 83(6):859-63. [Medline].

  48. Moon MS. Tuberculosis of the spine. Controversies and a new challenge. Spine. 1997 Aug 1. 22(15):1791-7. [Medline].

  49. National Institute of Neurological Disorders and Stroke. Spinal Cord Injury: Emerging Concepts. 2001. Available at: [Full Text].

  50. Nobunaga AI, Go BK, Karunas RB. Recent demographic and injury trends in people served by the Model Spinal Cord Injury Care Systems. Arch Phys Med Rehabil. 1999 Nov. 80(11):1372-82. [Medline].

  51. Oxland TR, Lund T. Biomechanics of stand-alone cages and cages in combination with posterior fixation: a literature review. Eur Spine J. 2000 Feb. 9 Suppl 1:S95-101. [Medline].

  52. Papadopoulos SM, Selden NR, Quint DJ, et al. Immediate spinal cord decompression for cervical spinal cord injury: feasibility and outcome. J Trauma. 2002 Feb. 52(2):323-32. [Medline].

  53. Rotter R, Martin H, Fuerderer S, Gabl M, Roeder C, Heini P, et al. Vertebral body stenting: a new method for vertebral augmentation versus kyphoplasty. Eur Spine J. 2010 Jun. 19(6):916-23. [Medline]. [Full Text].

  54. Schreiber D. Spinal Cord Injuries. Medscape Reference Journal [serial online]. 2003. [Full Text].

  55. Spinal Cord Injury Information Network. Spinal Cord Injury: Facts and Figures at a Glance. 2001. Available at: [Full Text].

  56. Stambough JL. Posterior instrumentation for thoracolumbar trauma. Clin Orthop. 1997 Feb. (335):73-88. [Medline].

  57. Tan SC, Harwant S, Selvakumar K, Kareem BA. Predictive factors in the evolution of neural deficit in tuberculosis of the spine. Med J Malaysia. 2001 Jun. 56 Suppl C:46-51. [Medline].

  58. Taoka Y, Okajima K, Uchiba M, Johno M. Methylprednisolone reduces spinal cord injury in rats without affecting tumor necrosis factor-alpha production. J Neurotrauma. 2001 May. 18(5):533-43. [Medline].

  59. Ullrich PF. Spine Topics. 2001. Available at: [Full Text].

  60. Vaccaro AR, Silber JS. Post-traumatic spinal deformity. Spine. 2001 Dec 15. 26(24 Suppl):S111-8. [Medline].

  61. Wetzel FT, Phillips FM. Management of metastatic disease of the spine. Orthop Clin North Am. 2000 Oct. 31(4):611-21. [Medline].

  62. Wilson DJ, Owen S, Corkill RA. Coblation vertebroplasty for complex vertebral insufficiency fractures. Eur Radiol. 2013 Feb 27. [Medline].

Anteroposterior and lateral radiographs of an L1 osteoporotic wedge compression fracture.
Fluoroscopic view of a kyphoplasty procedure.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.