Atlantoaxial Instability 

Updated: May 13, 2020
Author: Daniel P Leas, MD; Chief Editor: Jeffrey A Goldstein, MD 



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.[1] Neurologic symptoms can occur when the spinal cord or adjacent nerve roots are involved.

This instability can originate from congenital conditions, but in adults, it is primarily seen in the setting of acute trauma or degenerative changes due to the inflammatory pannus of rheumatoid arthritis (RA). Infection has been found to be an additional cause of instability, with the rich arterial supply and venous plexus in this region of the body providing a route for infectious sequelae.

Congenital causes are multiple and include Down syndrome, osteogenesis imperfecta, neurofibromatosis, Morquio syndrome, Larsen syndrome, spondyloepiphyseal dysplasia (SED), chondrodysplasia punctata, metatropic dysplasia, and Kniest syndrome. Other formative characteristics include diseases that impact bone metabolism or structure and ligament characteristics.


AAI may occur as a result of abnormalities or trauma associated with the C1-2 articulation, causing excessive movement around this joint. This includes the articulation between the anterior arch of C1 and the odontoid process of C2, as well as the facet joints of the posterior elements. The following three patterns are noted:

  • Flexion-extension
  • Distraction
  • Rotation

The most common abnormalities involve the transverse ligament or odontoid process.[2] The strong transverse ligament and the facet capsules maintain the integrity of the atlantoaxial articulation. The transverse ligament is the primary restraint against anterior translation of the C1 on C2, whereas the odontoid is the primary restraint against posterior translation. (See the image below.) Cadaveric studies have demonstrated that the transverse ligament is stronger in resisting anteroposterior (AP) forces before failure as compared with lateral forces.

Transverse ligament holds dens against anterior ar Transverse ligament holds dens against anterior arch of atlas.

AAI is defined as an atlantodental (or atlantodens or atlas-dens) interval (ADI) of greater than 3 mm in adults and of greater than 5 mm in children as measured on plain radiography. The ADI is the distance between the odontoid process and the posterior border of the anterior arch of the atlas.

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. In addition, motion of the C1-2 segment can cause compression of adjacent or exiting nerve roots. No evidence exists that individuals with asymptomatic AAI are at higher risk for the development of 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, the superior longitudinal band of the cruciate ligament, the tectorial membrane, or a combination of these structures. (See the image below for anterior ADI [AADI] and posterior ADI [PADI] landmarks.)

Midsagittal section of upper cervical spine. Note Midsagittal section of upper cervical spine. Note landmarks for measuring anterior atlantodental interval (AADI) and posterior atlantodental interval (PADI).

Traumatic rotatory displacement of the atlas can vary from subluxation to dislocation. The four types of atlantoaxial rotatory subluxation are shown in the image below.

Shown are 4 types of atlantoaxial rotatory subluxa Shown are 4 types of atlantoaxial rotatory subluxation.

Because the cervical spine has multiple synovial-lined articulations, 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.[5] 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 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. Although the predominant instability is in the AP plane, lateral and rotational instability can also occur.[6]

Grisel syndrome is the occurrence of atlantoaxial subluxation (AAS) following inflammation of adjacent soft tissues after a pharyngeal infection or surgical intervention. Primarily seen in children aged 5-12 years (though possible in adults), its etiology and pathoanatomy are not totally understood. Parke demonstrated direct connection between the periodontal venous plexus and the pharyngovertebral veins.[7] 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.

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.

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

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 idiopathic laxity of the transverse atlantal ligament.


AAI or AAS associated with bony abnormalities can be caused by abnormal development or ossification of the odontoid or fracture with or without remodeling. In addition, tumors can be a source of bony destruction, causing a pathologic fracture of either C1 or C2 and 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 ligamentous 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 syndrome
  • Congenital scoliosis
  • Osteogenesis imperfecta
  • Neurofibromatosis
  • Morquio syndrome
  • Larsen syndrome
  • SED congenita
  • Chondrodysplasia punctata
  • Metatropic dysplasia
  • Kniest syndrome
  • Odontoid abnormalities
  • Os odontoideum
  • Ossiculum terminale
  • Third condyle
  • Hypoplasia or absence of the dens
  • Achondroplasia
  • Pseudoachondroplasia
  • Cartilage-hair hyperplasia
  • Rheumatoid arthritis
  • Scott syndrome
  • Infections of the head and neck
  • Tumors
  • Trauma
  • Steroid therapy


United States statistics

AAI is very rare in patients without predisposing factors. No data exist regarding prevalence in the absence of known risk factors. Among individuals with Down syndrome, the frequency of asymptomatic AAI was estimated to be 13.1% on the basis of a study by Pueschel et al that reviewed the radiographs of 404 patients with the syndrome.[8] Symptomatic AAI was found to be in 1.5% of these patients.

Approximately 14% of odontoid fractures have associated severe AAI, with a significant impact on patient morbidity and a twofold increase in mortality.[9]

In persons with RA, the rate of AAI or AAS has been found to be around 20%, but it has been reported to be as high as 49% in an older study population.[10, 11, 12, 13, 14, 15]

Although the introduction of biologic agents has changed the treatment of RA, the effect of such treatment on cervical lesions had not been studied until comparatively recently. In a small retrospective study of 38 patients receiving some form of biologic therapy, Kaito et al reported an 8% rate of de-novo development of cervical lesions.[16, 17] There was still a high rate of disease progression in patients that were already on the spectrum of cervical disease (81%).

Unfortunately, an intervention-versus-control trial is ethically impossible in view of the known benefits of biologic therapy in other targets of rheumatoid disease; consequently, the impact of these agents on development and cervical progression has yet to be truly determined. Long-term case studies compared to historical matched controls will be required to make any further comparison.

Takahashi et al completed one such review comparing patients to historical reports and found there to be a 10-30% reduction in the prevalence of cervical spine instability in the wake of approval of the use of biologic agents; however, because of the insufficiency of the numbers, the findings were not statistically significant.[18]

Age-, sex-, and race-related demographics

No strong preponderance of AAI exists in any one age group. A higher risk does exist in younger individuals with Down syndrome (probably because of a strengthening of the transverse ligament with age) or older patients with RA (secondary to prolonged exposure to the disease process). In addition, Grisel syndrome is more prevalent in the pediatric population, but AAS can occur after any oropharyngeal infection. Most of these cases resolve and reduce spontaneously without ever presenting for treatment.

Although no sex association has been noted with idiopathic AAI, other conditions that could lead to developing this instability may be considerably more common in one sex than in the other. For example, RA affects nearly five times as many women as it does men.

No racial predilection is recognized.


Prognosis is good for patients with symptomatic AAI in whom posterior spinal fusion is successful and function returns. Surgery may relieve pain, decrease myelopathy, or both in many patients, with results depending on the severity of symptoms and the cause of instability.

Morbidity and mortality

Pain is the most common presenting symptom for patients with AAI or AAS. This can be either a vague neck pain or a headache. However, this pain is an extremely nonspecific finding, and these patients will require further evaluation to determine its source. The proximity of the spinal cord and vascular supply to the posterior elements can lead to additional severe effects such as myelopathy or vascular occlusion. Exact frequencies for these effects are not available, but they are understood to increase as the disease and instability progresses.

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. Any patient with risk factors for development of AAI merits urgent radiographic and surgical evaluation.

Mikulowski reported on the postmortem study of 104 patients with RA.[19] Cervicomedullary compression was noted in 11 patients, and seven of the 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. Thirty-day mortality has been reported to be as high as 13% and 60% at 4 years in patients with advanced cervical disease.[20]

Patient Education

Family members of pediatric patients with conditions predisposing to AAI or AAS should be aware of neurologic symptoms indicative of symptomatic progression. Discussions with the treating physician are imperative for family and patient education.

For patient education resources, see the First Aid and Injuries Center, as well as Torticollis.




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.

The cervical spine is involved more frequently in patients with rheumatoid arthritis (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.[21]

In cases associated with trauma, head and facial injuries may be present. The flexion-extension moment exerted on the spine can cause ligamentous disruption with subsequent atlantoaxial instability (AAI).

In some persons with Grisel syndrome, an antecedent illness or infection occurs.[22]

For patients with genetic or metabolic syndromes with higher rates of AAI or atlantoaxial subluxation (AAS) as compared with a normal population, there are multiple additional details that are relevant to the clinician. A thorough cervical spine examination is warranted for patients presenting with the following conditions:

  • Down syndrome - Approximately 13% of patients with DS will have asymptomatic AAI, and 1.5% will have neurologic symptoms stemming from this instability [8]
  • Spondyloepiphyseal dysplasia (SED) - SED congenita is associated with a 40% risk of AAI; SED tarda usually does not manifest AAI [23]
  • Morquio syndrome - AAI is usually secondary to odontoid hypoplasia or aplasia; patients tend to present later in childhood and usually later than those with SED congenita; nearly all patients with Morquio syndrome will develop AAI, and some surgeons recommend prophylactic stabilization to combat the morbidity associated with spinal cord compression [24]
  • Chondrodysplasia punctata - AAI is the primary cause of disability and death in these patients; about 20% will present with weakness, and 20% will present with hyperreflexia; spinal cord compression can occur at an early age [25]
  • Metatropic dysplasia - Patients with this rare syndrome patients survive into young adulthood but develop AAI early; nearly all appear to have odontoid hypoplasia, and in a small series, 75% of these patients had associated instability [26]

Physical 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, or lower cranial nerve palsies. The brainstem findings occur either with 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.[27] 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 AAS due to inflammatory processes less frequently exhibit signs of root or cord involvement.


Spinal cord compression can arise or worsen if susceptible patients are subjected to extreme ranges of motion. Symptoms of progressive neurologic dysfunction can include upper motor neuron signs, including the following:

  • Spasticity
  • Myelopathy
  • Neck pain
  • Radicular symptoms


Diagnostic Considerations

The presence of previously defined radiographic findings (anterior atlantodental interval [AADI] >3 mm in adults or >5 mm in children) is diagnostic of atlantoaxial instability (AAI) or atlantoaxial subluxation (AAS). Patients who present with acute neurologic symptoms that raise concerns for cervical compression or neck pain but are without a known source should undergo a thorough physical examination and radiographic evaluation to determine the source.

Findings are generally nonspecific and can be representative of any number of related conditions, including the following:

  • Cervical strain
  • Cervical trauma or fracture
  • Occipital headaches
  • Degenerative disease of the spine
  • Previously undiagnosed syndrome

Children in particular should be screened for previously undiagnosed syndromes or conditions should they present with AAI or AAS without a definitive source (eg, trauma). Even with a recent history of oropharyngeal infection that could lead to Grisel syndrome, the child should be followed closely to ensure that neurologic symptoms do not develop and that the subluxation resolves.



Laboratory Studies

No laboratory studies are relevant. For children, referral to a geneticist or endocrinologist may be beneficial for special laboratory evaluation.

Plain Radiography

Most injuries of the C1-2 articulation can be identified by means of plain radiography.[28]  Standard views include open-mouth odontoid and lateral cervical spine radiograph. For the highest degree of diagnostic accuracy, measurements should be obtained in neutral, flexion, and extension positions. 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 atlantoaxial instability (AAI) to symptomatic AAI.

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 on the lateral film is an important finding for cervical spine trauma and should raise concerns about airway stability in the acute setting.

An atlantoaxial distance greater than 4-5 mm, as demonstrated by lateral radiographs, is indicative of AAI. Occult instability can be identified on the flexion-extension view. Another marker of instability in the anteroposterior (AP) plane is displacement of 3.5 mm in flexion-extension films. The normal atlantodental (or atlantodens or atlas-dens) interval (ADI) in children is less than 4 mm on a neutral-position lateral cervical spine radiograph.

Another marker is the posterior ADI (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.[29]

CT and MRI

Use of computed tomography (CT) 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 scanning can delineate true rotational deformities.[30]

Magnetic resonance imaging (MRI) can provide additional information regarding the stability of the atlantoaxial joint, as well as associated soft tissue changes not visible on conventional radiography.[31, 32]

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.


Fielding and Hawkins suggested a four-part classification scheme for evaluating rotatory displacement,[33]  as follows:

  • Type I - Simple rotatory displacement with an intact transverse ligament
  • Type II - 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 - Anterior displacement exceeding 5 mm
  • Type IV - Posterior displacement of C1 on C2

Both type III and type IV are highly unstable.



Medical Care

There are no pharmacologic interventions for atlantoaxial instability (AAI). Because of the chronicity of the instability at the time of presentation in most cases, corticosteroids have little, if any, impact on neurologic findings and may present many undesirable outcomes. In the acute traumatic setting, corticosteroids remain controversial in the literature. Guidelines provided by the American Academy of Neurological Surgeons (AANS) include level I evidence against the use of corticosteroids or gangliosides in the acute trauma patient.[34]

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 1 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 of more than 1 month's duration, a period of halo traction for 3 weeks is tried. Usually, two types of patients are in this group: (1) those whose subluxation resolves with bracing but recurs when bracing stops and (2) 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 most cases, the injury is purely ligamentous and unlikely to heal. Therefore, these injuries are typically treated with posterior C1-2 fusion. If computed tomography (CT) revealed a bony avulsion injury as the source of failure, a trial of halo bracing may be initiated.

On the basis of the Fielding and Hawkins grading scale, the following general treatment recommendations may be made:

  • Type I - Stable subluxations, treated conservatively in a collar
  • Type II - Potentially unstable, treated at the physician's discretion
  • Type III - Unstable, requires surgical stabilization
  • Type IV - Unstable, requires surgical stabilization

Potential surgical options for C1-2 fixation fusion include the following[35, 36, 37, 38, 39, 5, 40, 41, 42, 43, 44, 45, 46, 47, 48] :

  • Transarticular screws (TASs) along the posterior elements
  • Screw-rod constructs (SRCs) along the C1 lateral mass and C2 pedicle (or the C2 spinous process if the C2 pedicle is not accessible)
  • Posterior sublaminar wiring as described by Brookes or Gallie
  • Halifax clamp

The surgeon should always be wary of associated adjacent injuries or pathology so as to include potential fusion extension cranially to the occiput or to caudal vertebral segments. For example, rheumatoid arthritis (RA) can also have cranial settling or subaxial instability. In addition, possible poor bone quality should be considered in selecting the method of fixation.

In a 2014 meta-analysis of the literature, Elliot et al compiled 69 articles reviewing both TASs and SRCs.[49, 50, 51] Although there were some relevant differences in population characteristics (eg, age, graft source, and gender), outcomes were generally comparable and successful. Rates of fusion were 97.5% and 94.6%, favoring SRC; differences in the rates of vertebral artery injury (4.1% vs 2.0%) and malpositioned screws (7.1% vs 2.4%) were noted, also favoring SRC.

It is important to highlight an anatomic anomaly known as the arcuate foramen, through which the vertebral artery travels in approximately 15% of the population. The presence of this anomaly necessitates adapting the trajectory of the C1 lateral mass screw so as to prevent iatrogenic injury to the transiting artery.[52, 53]

C1 laminar hooks with C2 pedicle screw fixation appear to be an effective mode of treatment in the trauma population, though the limited evidence currently available does not support a change in practice.[54]

Pediatric patients account for the majority of cases of nontraumatic rotatory displacement. Initially, these patients are treated with a halo brace; however, if this treatment is unsuccessful because of a fixed deformity or recurrent deformity, posterior fusion of C1-2 is required.

Posterior cervical spinal fusion can successfully treat symptomatic AAI in many cases.[55, 56] Surgery is most successful for treating patients with ligamentous instability and less successful in treating patients with osseous instability. Optimal results have been obtained in patients with severe pain and mild myelopathy. Thus, detecting symptoms early is preferable for the most successful treatment.

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 the following[57] :

  • Atlantoaxial subluxation (AAS) of greater than 8 mm with evidence of cord compression on dynamic flexion-extension view
  • Posterior atlantodental (or atlanto-dens or atlas-dens) interval (ADI) of 14 mm or less
  • More than 3.5 mm of subaxial subluxation
  • Progressive neurologic deficit

Additional concerns

Special care should be taken to avoid excessive flexion or extension of the neck.

Extreme caution should be used in performing any procedure with sedation or neck manipulation on patients with known risk factors for, or a previous diagnosis of, AAI. Neutral positioning of the neck should be maintained during these procedures and all surgical procedures, especially 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.


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 undergo 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 warmup exercises.[58]

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.[59]

Although no indication exists that children with asymptomatic AAI are at increased risk for subluxation or progression to symptomatic AAI or that routine screening by radiographs is necessary, recommendations vary.


Consultations that may be considered include the following:

  • Neurologist
  • Neurosurgeon or orthopedic spine surgeon
  • In children without a preexisting diagnosis, a geneticist or endocrinologist

Long-Term Monitoring

Individuals with predisposing factors should be monitored carefully for neurologic symptoms indicative of symptomatic AAI.[60] 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.



Medication Summary

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

Kaito et al found a de novo rate of cervical lesions of 8% in a small retrospective study of 38 RA patients receiving some form of biologic therapy. There was still a high disease progression rate in patients that were already on the spectrum of cervical disease (81%).[16, 17]

Unfortunately, an intervention-versus-control trial is ethically impossible, given the known benefits of biologic therapy in other targets of rheumatoid disease. Thus, the impact of these agents on development and cervical progression has yet to be truly determined. Long-term case studies compared to historical matched controls will be required to make any further comparison.


Questions & Answers


What is atlantoaxial instability (AAI)?

What are the patterns of atlantoaxial instability (AAI)?

What abnormalities are involved in atlantoaxial instability (AAI)?

What is the definition of atlantoaxial instability (AAI)?

What pathophysiology is involved in symptomatic atlantoaxial instability (AAI)?

How does rheumatoid arthritis (RA) manifest in the pathophysiology of atlantoaxial instability (AAI)?

What is Grisel syndrome in atlantoaxial instability (AAI)?

Which congenital conditions are associated with atlantoaxial instability (AAI)?

What causes atlantoaxial instability (AAI)?

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How common is atlantoaxial instability (AAI) in the US?

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What is the clinical presentation of atlantoaxial instability (AAI)?

When is a thorough spine exam indicated in suspected atlantoaxial instability (AAI)?

What are the clinical findings in atlantoaxial instability (AAI)?

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What are the diagnostic considerations in the workup of atlantoaxial instability (AAI)?


Which lab studies are indicated in the workup of atlantoaxial instability (AAI)?

When is plain radiography indicated in the workup of atlantoaxial instability (AAI)?

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When is MRI indicated in the workup of atlantoaxial instability (AAI)?

What other tests are indicated in the workup of atlantoaxial instability (AAI)?

How are rotatory displacements classified in atlantoaxial instability (AAI)?


What is the medical care for atlantoaxial instability (AAI)?

What are the treatment goals for atlantoaxial instability (AAI)?

What are the Fielding and Hawkins treatment recommendations for atlantoaxial instability (AAI)?

What are the surgical options for C1-2 fixation fusion in atlantoaxial instability (AAI)?

Which anatomic anomalies should be noted in the surgical treatment of atlantoaxial instability (AAI)?

When is surgery indicated in pediatric patients with atlantoaxial instability (AAI)?

When is surgery most successful in the treatment of atlantoaxial instability (AAI)?

When is surgery contraindicated in the treatment of atlantoaxial instability (AAI)?

When is surgery indicated for the treatment of atlantoaxial instability (AAI) in individuals with rheumatoid arthritis (RA)?

What special considerations are indicated in the surgical care of atlantoaxial instability (AAI)?

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What is the medical therapy for atlantoaxial instability (AAI)?