Atlantoaxial Instability
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Direct answer
Half of all head rotation happens at the atlantoaxial articulation, which is why instability at C1-C2 threatens the cord with every turn of the neck. The transverse ligament is the primary restraint holding the dens against the anterior arch of the atlas, and its competence is measured on the lateral radiograph as the atlantodental interval — normally 3 mm or less in adults and 5 mm or less in children; widening beyond these numbers defines instability. Rheumatoid arthritis, Down syndrome, trauma, and Grisel syndrome after ENT infection make up the classical cause list, with rotary subluxation classified by Fielding and Hawkins into four types. Reducible instability is treated by C1-C2 fusion, while irreducible anterior compression from the dens needs transoral decompression before fusion.
What you must remember
- The ADI numbers: anterior atlantodental interval of 3 mm or less in adults and 5 mm or less in children is normal; widening to 3-5 mm in the adult implies transverse ligament insufficiency, and intervals approaching 8-10 mm mean the alar ligaments too have failed, with cord compression increasingly likely.
- Ligament hierarchy: transverse ligament (the horizontal band of the cruciate ligament) is the primary check; alar ligaments and the apical ligament are secondary — tested together on flexion-extension lateral films.
- Adult cause number one: rheumatoid arthritis, through pannus erosion and ligamentous laxity — neck pain plus myelopathy in a long-standing RA patient is C1-C2 until excluded.
- Paediatric angles: Down syndrome (instability in a significant minority, screened before contact sport), Grisel syndrome — rotatory subluxation after pharyngeal infection or ENT surgery — and post-traumatic ligament injury.
- Fielding-Hawkins rotary types: type I, pure rotatory fixation without anterior displacement (the commonest); type II, rotation with 3-5 mm anterior shift; type III, over 5 mm; type IV, posterior displacement — progressively more dangerous.
- Clinical tells: torticollis with the cock-robin posture in children, neck pain worse on rotation, Lhermitte phenomena on turning, and upper motor neuron signs in the limbs.
- Treatment logic: reducible instability → halo or traction then C1-C2 fusion (Gallie or Brooks wiring, Harms-Goel screw-rod, Magerl transarticular screws); irreducible anterior compression → transoral odontoidectomy first, then fusion; rheumatoid instability with cord compression or ADI beyond roughly 8-10 mm is fused on indication.
Measuring, then deciding
A 45-year-old woman with twenty years of rheumatoid arthritis reports neck pain and electric shocks down her arms on looking up. Flexion-extension films show the ADI opening from 4 mm in extension to 8 mm in flexion — the transverse ligament has failed — and MRI adds pannus behind the dens flattening the cord where it has the least room. She is a fusion candidate: a Harms-type C1-C2 screw-rod construct stabilises the segment, and because her compression is reduceable in extension, no anterior decompression is needed.
The child next door presents differently: a sore throat two weeks ago, now a fixed, tilted head held rotated to one side and flexed — the cock-robin posture of atlantoaxial rotatory fixation, Grisel syndrome by mechanism. Dynamic CT in rotated positions maps the fixed rotation; Fielding-Hawkins type I without anterior translation. Early cases yield to traction or a Philadelphia collar with anti-inflammatories, and the head recentres as the inflammation settles; only chronic, fixed cases proceed to fusion. Two patients, one interval: the adult measured by ADI widening, the child by lost rotation symmetry.
How the exam frames it
The numbers come first: 3 mm and 5 mm — examiners ask the ADI norms for adults and children as a pair, then the meaning of progressive widening through the ligament hierarchy. The names come second: Grisel for the post-ENT rotatory subluxation of children, Fielding-Hawkins for its four types (type I both the commonest and the safest), Gallie, Brooks and Harms for the fusion options in ascending order of rigidity. The cause question is generational — rheumatoid arthritis in the adult, Down syndrome and infection in the child. An Indian addendum worth voicing: atlantoaxial tuberculosis occurs in endemic practice as a destructive, unstable C1-C2 presentation, and a child with persistent torticollis after adenoidectomy deserves atlantoaxial imaging, not reassurance.
Frequently asked questions
What are the normal atlantodental interval values?
Three millimetres or less in adults and five millimetres or less in children on the lateral view; widening beyond these defines atlantoaxial instability.
Which ligament is the primary stabiliser of the atlantoaxial joint?
The transverse ligament, holding the dens against the anterior arch of C1; the alar ligaments provide secondary restraint.
What is Grisel syndrome?
Rotatory atlantoaxial subluxation following pharyngeal infection or ENT surgery, presenting in children with painful torticollis and the cock-robin posture.
Which Fielding-Hawkins type is the commonest rotatory injury?
Type I — rotatory fixation without anterior displacement — which is also the most stable and the most likely to settle without fusion.
When is transoral odontoidectomy required?
When an irreducible dens or pannus compresses the cord anteriorly: the decompression precedes a posterior C1-C2 fusion, since fusing over unrelieved compression seals the deficit in.