AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Atlantoaxial instability (AAI) is characterized by excessive movement at the junction between the atlas (C1) and axis (C2) as a result of either a bony or ligamentous abnormality. Neurologic symptoms occur when the spinal cord is involved.

The causes of AAI are varied. AAI sometimes results from trauma. Other cases occur secondary to an upper respiratory infection or infection following head and neck surgery. Another cause is rheumatoid arthritis (RA), with its predilection for the upper cervical spine. In addition, congenital anomalies, syndromes, or metabolic diseases can increase the risk of AAI.

Related Medscape topics:
Resource Center: Back Pain
Resource Center: Exercise and Sports Medicine
Resource Center: Head and Neck Cancer
Resource Center: Joint Disorders
Resource Center: Rheumatoid Arthritis
Resource Center: Spinal Disorders
Resource Center: Trauma

Related eMedicine topics:
Idiopathic Scoliosis
Infantile Scoliosis
Juvenile Rheumatoid Arthritis
Neuromuscular Scoliosis
Rheumatoid Arthritis, Spine
Rheumatoid Spondylitis
Spinal Instability and Spinal Fusion Surgery

Pathophysiology

AAI may occur as a result of abnormalities or trauma associated with the C1-2 articulation, causing excessive movement around this joint. The 3 patterns of AAI are flexion-extension, distraction, and rotation (see Image 1, Image 2, Image 3). The most common abnormalities involve the transverse ligament or odontoid process.¹ The strong transverse ligament and the facet capsules maintain the integrity of the atlantoaxial articulation. The transverse ligament is the primary restraint against atlantoaxial anteroposterior (AP) translation. Cadaveric studies have demonstrated that the transverse ligament is stronger in resisting AP forces before failure versus lateral forces.

AAI is defined as an atlantodens interval (ADI, distance between odontoid process and the posterior border of the anterior arch of the atlas) of greater than 3 mm in adults and of greater than 5 mm in children as measured on plain radiography. Symptomatic AAI occurs when subluxation or dislocation causes the odontoid process, or posterior arch of the atlas, to impinge on the spinal cord and cause neurologic manifestations. No evidence exists that individuals with asymptomatic AAI are at a higher risk of developing symptomatic AAI. Vertical displacement of the atlas requires widening of the C1-2 facet joint. The underlying problem is the disruption of the alar ligament and tectorial membrane.

Traumatic rotatory displacement of the atlas can vary from subluxation to dislocation. One type is rotatory subluxation observed after upper respiratory infection or head and neck surgery. Grisel syndrome is the occurrence of atlantoaxial subluxation (AAS) in association with inflammation of adjacent soft tissues. The etiology and pathoanatomy are not totally understood, but Parke demonstrated direct connection between the periodontal venous plexus and the pharyngovertebral veins.² This may provide a route for exudates to be transported to the cervical spine, creating a local inflammatory reaction. In addition, children appear to be more susceptible secondary to their steeper dens-facet angle and rich vascular folds in the atlantoaxial and lateral atlantoaxial joint.

The cervical spine has multiple synovial lined articulations. Because it is a disease that affects synovial-lined joint, RA can manifest itself in the upper cervical spine.^{3, 4} In a person with AAI, the rheumatoid process affects the articular cartilage of the apophyseal joints, even the type II articular cartilage in the transverse ligament. In addition, the rheumatoid pannus and the associated inflammation can weaken the transverse ligaments, alar ligaments, and facet capsules early in the disease process. With the formation of the pannus, the large excursion of the C1 on C2 can cause further attenuation of the ligaments and destruction of the subchondral bone and erosion of the dens, which also contribute to the instability. While the predominant instability is in the AP plane, lateral and rotational instability also can occur.⁵

Certain congenital conditions can be associated with AAI. Associated conditions include Down syndrome, congenital scoliosis, osteogenesis imperfecta, neurofibromatosis, Morquio syndrome, Larsen syndrome, spondyloepiphyseal dysplasia congenita, chondrodysplasia punctata, metatropic dysplasia, and Kniest syndrome.

In individuals with Down syndrome, the primary cause of AAI is the laxity of the transverse ligament, which holds the dens against the posterior border of the anterior arch.

Other causes of AAI include odontoid anomalies such as aplasia, hypoplasia, duplication, third condyle, os terminale, and os odontoideum. Atlanto-occipital fusion also predisposes a patient to the development of AAI. A diagnosis of exclusion is laxity of the transverse atlantal ligament.

Frequency

United States

AAI is very rare in patients without predisposing factors. No data exist regarding prevalence. Among individuals with Down syndrome, frequency of asymptomatic AAI is 10-20%. Symptomatic AAI occurs in 1-2% of patients with Down syndrome.

In traumatic situations, approximately 10% of cervical fractures involve some injuries to the atlantoaxial level. Of injuries to the atlantoaxial complex, only 16% produce neurologic deficits secondary to the wide spinal canal at this level.

In persons with RA, the incidence of cervical involvement has been reported to be 25-30% to 60-80%.

Mortality/Morbidity

• Symptomatic patients are at risk for progressive neurologic symptoms. Paralysis and death are rare.
• Neurologic manifestations include clumsiness, lack of coordination, abnormal gait, difficulty walking, easy fatigability, neck pain, limited next mobility, torticollis, sensory deficits, neurogenic bladder, upper motor neuron signs (spasticity, hyperreflexia, clonus, Babinski sign), paraplegia, hemiplegia, and quadriplegia.
• Mikulowski reported on the postmortem study of 104 patients with RA.⁶ Cervicomedullary compression was noted in 11 patients, and 7 of these 11 died suddenly. Untreated AAI in individuals with RA can have severe consequences. In addition to cervicomedullary compression, vertebral artery insufficiency has been reported as a result of  the tortuous path of the artery at the atlantoaxial articulation. It has been reported that death is common in patients with RA once myelopathy develops in the patients with cervical spine involvement.

Race

No racial predilection is recognized.

Sex

No sex predilection is apparent.

Age

No strong preponderance of AAI exists in any one age group. A higher risk does exist in individuals with Down syndrome or RA. In addition, Grisel syndrome is more prevalent in the pediatric population, but AAS can occur after any oropharyngeal infection. Most reduce spontaneously and never present for treatment. In individuals with Down syndrome, this discrepancy is believed to be due to a strengthening of the transverse ligament with age.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• In some persons with Grisel syndrome, an antecedent illness or infection occurs.⁷
• In cases associated with trauma, head and facial injuries may be present. The head striking the windshield or the dashboard often leads to AAI.
• The cervical spine is involved more frequently in patients with RA. Cervical involvement tends to be asymptomatic in the scenario of systemic rheumatoid manifestations. In addition, the severity of the systemic manifestations should serve as a marker of the degree of cervical involvement.
• Two forms of spondyloepiphyseal dysplasia exist. The congenita form is associated with a 40% risk of AAI. The tarda form usually does not manifest AAI.
• In individuals with Morquio syndrome, AAI is usually secondary to odontoid hypoplasia or aplasia. These persons tend to present later in childhood and usually later than those with spondyloepiphyseal dysplasia congenita.
• The primary cause of disability and death is AAI in individuals with chondrodysplasia punctata. Death from spinal cord compression can occur at an early age.
• AAI also is observed in persons with the rare syndrome metatropic dysplasia. These children survive into young adulthood. This condition can be confused with Kniest syndrome in infancy. Children undergoing other procedures should have thorough neck examinations.
• Usually, persons with congenital anomalies do not become symptomatic before the third decade of life. The spine is assumed to be able to accommodate differing regions of hypermobility and fusions. With time, the degenerative changes occurring in the lower cervical spine increase rigidity and alter the balance. This gradual loss of motion places increasing loads on the atlantoaxial articulation.
• Predisposing factors for AAI are discussed in Causes.

Physical

• Neurologic examination
• • A careful neurologic examination should be conducted, especially for children at risk.
  • Assess sensory, motor, and other neurologic functions.
  • Upper motor neuron signs, including hyperreflexia, clonus, and extensor plantar reflexes, may be indicative of symptomatic AAI.
  • Somatosensory evoked response may reveal information regarding neurologic involvement.
• In individuals with rotatory displacement, a cock-robin deformity or torticollis can be the presenting symptom.
• Many patients with RA present with occipital pain. Others develop myelopathy, vertigo, brainstem signs, lower cranial nerve palsies, or myelopathy. The brainstem findings occur with either basilar invaginations or with the alteration of the path of the vertebral artery with changing of normal anatomy. Rana reported the subtle association of involvement of the fifth cranial nerve, which has a descending tract that extends to C2.⁸ Pyramidal signs, including hyperactive reflexes, a positive Babinski sign, and proprioceptive loss, should alert the physician for developing myelopathy.
• The most specific physical findings in patients with symptomatic AAI secondary to infections of the head and neck are torticollis, tenderness over the spinous process of the axis with palpation, and the Sudeck sign (displacement of spine of the axis in the direction of head tilt).
• A reduction in size of the nasopharynx and increased nasal resonance also may be present due to forward displacement of the arch of the atlas.
• Persons with AAI due to inflammatory processes less frequently exhibit signs of root or cord involvement.

Causes

• AAI associated with bony abnormalities can be caused by abnormal development or ossification of the odontoid or fracture with or without remodeling.
• Tumors can cause a pathologic fracture of the body of the axis, resulting in AAI.
• The cause of AAI associated with problems of the transverse ligament is not known. An abnormal protein structure in connective tissue may cause the ligamental laxity observed in individuals with Down syndrome. Inflammation of the ligament, as observed in persons with AAI secondary to infections or RA, can weaken the joint and predispose to subluxation.
• The following conditions can be associated with AAI:
• • Down syndrome⁹
  • Congenital scoliosis
  • Osteogenesis imperfecta
  • Neurofibromatosis
  • Morquio syndrome
  • Larsen syndrome
  • Spondyloepiphyseal dysplasia congenita
  • Chondrodysplasia punctata
  • Metatropic dysplasia (a rare syndrome that can present with AAI)
  • Kniest syndrome (also can present with AAI; a workup must be performed prior to any operative interventions)
  • Odontoid abnormalities
  • Os odontoideum
  • Ossiculum terminale
  • Third condyle
  • Hypoplasia or absence of the dens
  • Dwarfism¹⁰
  • Pseudoachondroplasia
  • Cartilage-hair hyperplasia
  • Rheumatoid arthritis
  • Ankylosing spondylitis
  • Scott syndrome
  • Infections of the head and neck
  • Tumors
  • Trauma
  • Cerebral palsy
  • Steroid therapy

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• No laboratory studies are relevant.

Imaging Studies

• Most injuries of the C1-2 articulation can be identified by radiography.¹¹
• • Standard views include open-mouth odontoid and lateral cervical spine radiograph. In certain circumstances, tomography may be indicated. On the open mouth odontoid view, the combined spread of the lateral masses of C1 on C2 should not exceed 6.9 mm. A number greater than 6.9 mm would indicate rupture of the transverse ligament. The presence of prevertebral swelling is an important finding for cervical spine trauma.
  • Occult instability can be identified on flexion-extension view.
  • Obtain radiographs of the cervical spine.
  • An atlantoaxial distance greater than 4-5 mm, as demonstrated by lateral radiographs, is indicative of AAI.
  • Measurements should be obtained in neutral, flexion, and extension positions for highest diagnostic accuracy. However, it has been demonstrated that these measurements are not always reliable or reproducible and are not predictive of existing neurologic deficits or later progression of asymptomatic AAI to symptomatic AAI.
  • Another marker of instability in the AP plane is displacement of 3.5 mm in flexion-extension films.
  • Another marker is the posterior atlantodental interval (PADI) measured from the posterior border of the dens to the anterior border of the posterior tubercle. This index may be more important because it more directly assesses the space available to the spinal cord. The degree of neurologic deficits has been demonstrated to correlate with the PADI.
  • The normal ADI in children is less than 4 mm on a neutral position lateral cervical spine radiograph.
• Computed tomography scan
• • Use of CT scan can provide additional information regarding the stability of the atlantoaxial joint.
  • Measuring displacement of defining rotation may be difficult on plain radiographs. Fine-cut CT with reformatting can be used for measuring the amount of displacement.
  • In addition, in a person in whom rotation deformity is suspected, patient-directed maximum rotation CT scan can delineate true rotational deformities.¹²
• Magnetic resonance imaging: MRI can provide additional information regarding the stability of the atlantoaxial joint.¹³

Other Tests

• In patients with RA in whom a thorough physical examination is difficult, somatosensory evoked potentials are being explored as a means of following myelopathy.

Staging

• In evaluating rotatory displacement, Fielding and Hawkins suggested a 4-part classification scheme, as follows:¹⁴
• • Type I is simple rotatory displacement with an intact transverse ligament.
  • Type II injuries involve anterior displacement of C1 on C2 of 3-5 mm with one lateral mass serving as a pivot point and a deficiency of the transverse ligament.
  • Type III injuries involve greater than 5 mm of anterior displacement.
  • Type IV injuries involve the posterior displacement of C1 on C2.
• Both Type III and IV are highly unstable injuries.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• Unless symptoms of spinal cord compression occur, AAI requires no treatment. Once symptoms arise, cervical spine stabilization is indicated until surgical stabilization is performed.
• In persons with rotatory displacement, the time of presentation dictates the treatment. Most of these patients' conditions resolve spontaneously, and additional care is not sought.
• • Patients presenting with subluxation of less than a week's duration are treated with a soft collar and rest for a week. If close follow-up fails to document reduction, a period of halter traction with analgesics and muscle relaxants is warranted. If this fails, halo bracing can be undertaken.
  • In patients with rotatory displacement for more than 1 month, a period of halo traction for 3 weeks is tried. Usually, 2 types of patients are in this group, those whose subluxation improves with bracing but recurs when bracing stops and those who usually present with a fixed deformity.

Surgical Care

The treatment goals for persons with AAI are to protect the spinal cord, stabilize the spinal column, decompress neural tissue, and reduce any deformity.

In C1-2 subluxation or dislocation, an ADI of greater than 3 mm indicates injury to the transverse ligament. In most cases, the injury is purely ligamentous and unlikely to heal. Therefore, these injuries usually are treated with posterior C1-2 fusion. If the CT scan revealed a bony avulsion injury as the source of failure, a trial of halo bracing may be tried.

In individuals with rotatory dislocation, the treatment for traumatic injuries is a collar for type I injuries that are regarded as stable subluxations. Type II injuries may be potentially unstable. Type III and IV rotatory displacements that are unstable are treated surgically with a reduction and C1-2 fusion. The techniques of fusion vary from sublaminar wiring techniques like Brooks or Gallie, Halifax clamp, or transarticular screw of Magerl.^{15, 16, 17, 18, 19} In situations of associated injuries, extending the fusion to the occiput may be required.

In rotatory displacement from nontraumatic causes, the pediatric population is most susceptible. In a patient with either a fixed deformity or recurrent deformity despite reduction in halo brace, a posterior C1-2 fusion is indicated.

• Posterior cervical spinal fusion can successfully treat symptomatic AAI in many cases.^{20, 21}  Surgery has been demonstrated to be most successful for treating patients with ligamentous instability but has demonstrated less success in patients with osseous instability. Best results have been obtained in patients with severe pain and mild myelopathy. Thus, detecting symptoms early is preferable for most successful treatment.
• It has been demonstrated that surgery is unlikely to reverse clinical symptoms when the spinal cord is compressed by more than 60%. However, surgery is not recommended for individuals without spinal cord involvement due to an unclear natural history of AAI.
• In individuals with RA, the goals of surgery are to relieve neural compression, relieve pain, and address instability. Indications for surgery include AAS of greater than 8 mm with evidence of cord compression on dynamic flexion-extension view, PADI of 14 mm or less, more than 3.5 mm of subaxial subluxation, or progressive neurologic deficit.²²
• • With atlantoaxial rotatory subluxation in patients with RA, treatment comprises gradual reduction in halo traction followed with an occiput to C2 fusion. The halo may be incorporated for postoperative bracing.
  • Usually, because of severe osteoporosis in patients with RA, multiple pins are used to improve fixation.
  • In addition, the nature of the subaxial cervical spine should be considered when planning the distal extent of the fusion.

Consultations

• Neurologist
• Neurosurgeon
• Orthopedic surgeon

Activity

• Before participation in sports, evaluations are recommended to detect neurologic involvement.
• Spinal cord compression can arise or worsen if susceptible patients are subjected to extreme ranges of motion. Special care should be taken to avoid excessive flexion or extension of the neck.
• Special Olympics, Inc., currently requires that all children with Down syndrome who compete in Special Olympics games have radiographic and neurologic examinations to exclude AAI. Individuals with AAI are restricted from participation in certain activities that may result in cervical spine injury. These include gymnastics, diving, pentathlon, butterfly stroke, diving starts in swimming, high jump, soccer, and certain warm-up exercises.
• • In 1983, the American Academy of Pediatrics Committee on Sports Medicine and Fitness issued a statement in agreement with the recommendations and requirements of the Special Olympics. However, a review of evidence in 1995 caused the committee to rescind their recommendations that all children with Down syndrome should be screened radiographically.²³
  • Although no indication exists that children with asymptomatic AAI are at increased risk of subluxation or progression to symptomatic AAI or that routine screening by radiographs is necessary, recommendations vary.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

No role currently exists for medications in the treatment of AAI. While nonsteroidal anti-inflammatory drugs (NSAIDs) are used in atlantoaxial rotary subluxation to control the inflammation, evidence to support this practice is lacking.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Special care should be taken to avoid excessive flexion or extension of the neck.
• Neutral positioning of the neck should be maintained during all surgeries, especially during otorhinolaryngologic procedures. Care also should be taken during anesthetic administration to avoid trauma to the atlantoaxial joint.
• Children should be monitored closely postoperatively for any signs of neurologic involvement.

Further Outpatient Care

• Individuals with Down syndrome, infections of the head and neck, or any other predisposing factors should be monitored carefully for neurologic symptoms indicative of symptomatic AAI.²⁴
• • In individuals with Down syndrome and an ADI of greater than 5 mm, the recommendation is to avoid contact sports or activities with high risk of flexion injury.
  • When the ADI is more than 10 mm or neurologic findings develop, a fusion is recommended.
• Regular assessments of the history and physical examinations, including evaluations before participation in sports, are recommended to detect neurologic involvement.
• Patients also should be monitored carefully for development of symptoms, though the association between AAI and neurologic symptoms is unclear.

Complications

• Spinal cord compression can arise or worsen if susceptible patients are subjected to extreme ranges of motion.

Prognosis

• Prognosis is good for patients with symptomatic AAI in whom posterior spinal fusion is successful and function returns.
• Surgery has been demonstrated to relieve pain in 95% of patients and decrease myelopathy in 74% of patients, depending on the severity of symptoms and the cause of instability.

Patient Education

• Family members should be aware of neurologic symptoms indicative of symptomatic AAI.
• For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education article Torticollis.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Extreme caution should be used when performing any procedure with sedation on an individual with Down syndrome or dwarfism. Keep the neck in a neutral position in these patients and others with risk factors for AAI. Documentation of this precautionary measure is important.

See also the Medscape topic Medical Malpractice and Legal Issues.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  The transverse ligament holds the dens against the anterior arch of the atlas.
	View Full Size Image
Media type:  Illustration

Media file 2:  A midsagittal section of the upper cervical spine. Note the landmarks for measuring the anterior atlantodens interval and the posterior atlantodens interval.
	View Full Size Image
Media type:  Illustration

Media file 3:  The 4 types of atlantoaxial rotatory subluxation.
	View Full Size Image
Media type:  Illustration

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Milz S, Schluter T, Putz R, et al. Fibrocartilage in the transverse ligament of the human atlas. Spine. Aug 15 2001;26(16):1765-71. [Medline].
2. Parke WW, Rothman RH, Brown MD. The pharyngovertebral veins: an anatomical rationale for Grisel''s syndrome. J Bone Joint Surg Am. Apr 1984;66(4):568-74. [Medline].
3. Boden SD, Dodge LD, Bohlman HH, Rechtine GR. Rheumatoid arthritis of the cervical spine. A long-term analysis with predictors of paralysis and recovery. J Bone Joint Surg Am. Sep 1993;75(9):1282-97. [Medline].
4. Clark CR, Goetz DD, Menezes AH. Arthrodesis of the cervical spine in rheumatoid arthritis. J Bone Joint Surg Am. Mar 1989;71(3):381-92. [Medline].
5. Babic-Naglic D, Potocki K, Curkovic B. Clinical and radiological features of atlantoaxial joints in rheumatoid arthritis. Z Rheumatol. Aug 1999;58(4):196-200. [Medline].
6. Mikulowski P, Wollheim FA, Rotmil P. Sudden death in rheumatoid arthritis with atlanto-axial dislocation. Acta Med Scand. Dec 1975;198(6):445-51. [Medline].
7. Yamazaki M, Someya Y, Aramomi M, Masaki Y, Okawa A, Koda M. Infection-related atlantoaxial subluxation (Grisel syndrome) in an adult with Down syndrome. Spine. Mar 1 2008;33(5):E156-60. [Medline].
8. Rana NA, Hancock DO, Taylor AR, Hill AG. Upward translocation of the dens in rheumatoid arthritis. J Bone Joint Surg Br. Aug 1973;55(3):471-7. [Medline].
9. Pueschel SM. Should children with Down syndrome be screened for atlantoaxial instability?. Arch Pediatr Adolesc Med. Feb 1998;152(2):123-5. [Medline].
10. Berkowitz ID, Raja SN, Bender KS, Kopits SE. Dwarfs: pathophysiology and anesthetic implications. Anesthesiology. Oct 1990;73(4):739-59. [Medline].
11. Kulkarni AG, Goel AH. Vertical atlantoaxial index: a new craniovertebral radiographic index. J Spinal Disord Tech. Feb 2008;21(1):4-10. [Medline].
12. Ilkko E, Tikkakoski T, Pyhtinen J. The helical three-dimensional CT in the diagnosis of torticollis with occipitocondylar hypoplasia. Eur J Radiol. Nov 1998;29(1):55-60. [Medline].
13. Yuksel M, Heiserman JE, Sonntag VK. Magnetic resonance imaging of the craniocervical junction at 3-T: observation of the accessory atlantoaxial ligaments. Neurosurgery. Oct 2006;59(4):888-92; discussion 892-3. [Medline].
14. Fielding JW, Hawkins RJ. Atlanto-axial rotatory fixation. (Fixed rotatory subluxation of the atlanto-axial joint). J Bone Joint Surg Am. Jan 1977;59(1):37-44. [Medline].
15. Haid RW Jr. C1-C2 transarticular screw fixation: technical aspects. Neurosurgery. Jul 2001;49(1):71-4. [Medline].
16. Naseer R, Bailey SI. Atlantoaxial instability treated with transarticular screw fixation. Int Orthop. 2001;25(4):268-71. [Medline].
17. Henriques T, Cunningham BW, Olerud C, et al. Biomechanical comparison of five different atlantoaxial posterior fixation techniques. Spine. Nov 15 2000;25(22):2877-83. [Medline].
18. Sugimoto Y, Tanaka M, Nakanishi K, Misawa H, Takigawa T, Ozaki T. Assessing the range of cervical rotation in patients with rheumatoid arthritis after atlantoaxial screw fixation using axial CT. Spine. Oct 1 2007;32(21):2318-21. [Medline].
19. Gunnarsson T, Massicotte EM, Govender PV, Raja Rampersaud Y, Fehlings MG. The use of C1 lateral mass screws in complex cervical spine surgery: indications, techniques, and outcome in a prospective consecutive series of 25 cases. J Spinal Disord Tech. Jun 2007;20(4):308-16. [Medline].
20. Ahmed R, Traynelis VC, Menezes AH. Fusions at the craniovertebral junction. Childs Nerv Syst. Apr 4 2008;[Medline].
21. Claybrooks R, Kayanja M, Milks R, Benzel E. Atlantoaxial fusion: a biomechanical analysis of two C1-C2 fusion techniques. Spine J. Nov-Dec 2007;7(6):682-8. [Medline].
22. Castel E, Benazet JP, Samaha C, et al. Delayed closed reduction of rotatory atlantoaxial dislocation in an adult. Eur Spine J. Oct 2001;10(5):449-53. [Medline].
23. American Academy of Pediatrics Committee on Sports Medicine & Fitness. Atlantoaxial instability in Down syndrome: subject review. Pediatrics. Jul 1995;96(1 Pt 1):151-4. [Medline].
24. Morton RE, Khan MA, Murray-Leslie C, Elliott S. Atlantoaxial instability in Down's syndrome: a five year follow up study. Arch Dis Child. Feb 1995;72(2):115-8; discussion 118-9. [Medline].

Article Last Updated: Jun 18, 2008