A pseudotumor behind dens is known to be a factor associated with cervical myelopathy at the atlantoaxial region. The pathogenesis of pseudotumor is thought to be a granulation around transverse ligament of atlas (TLA). There have been only four reports about ossification of TLA so far, and the present condition could be a rare cause of cervical myelopathy at upper cervical spine [¹–⁴]. We experienced a case of ossification of TLA. We report details of radiological findings and inference of mechanism of the ossification of TLA from current and previously reported cases.

A 76-year-old woman had been suffered from numbness and clumsiness in both upper limbs and gait disturbance for six months before presentation.

There have been only four reports concerning ossification of TLA [¹–⁴]. Characteristic features of patients with ossification of TLA were elderly population, AAS, and hypertrophied dens. AAS were recognized in three cases, and hypertrophied dens were recognized in two cases. Hayashi and colleagues described that a trauma of 12 years ago led to ossification of TLA, but they did not describe a mechanism of this ossification in detail [¹]. The mechanism of this ossification is still unclear from the previous literatures.

Irreducible AAS and osteoarthritis at atlantoaxial joints with hypertrophied dens were seen in the current case similar to the previously reported cases. A coalition of atlantooccipital joints was also recognized only in the current case. Remnants of the atlantooccipital joints were seen in a coronal reconstructed CT, and so we diagnosed not as an assimilation of atlas but as a coalition caused by degeneration. According to Detlef and Walter, an assimilation of the atlas caused AAS [⁵]. Greenberg, Hagiwara, and colleagues suggested a mechanism that atlantoaxial joint compensated the function of stabilized atlantooccipital joint and a greater stress on TLA results in stretching and leading to AAS [⁶, ⁷]. Coalition of atlantooccipital joints is different from an assimilation of atlas, but it may cause AAS as the adjacent segment degeneration by similar mechanism. On the basis of these findings, we suggested mechanism of ossification of TLA as follows: hypertrophied dens and coalition of atlantooccipital joints make forward shift of the atlas leading to irreducible AAS. Continuous stress given to TLA by irreducible AAS would result in hypertrophied and ossification of TLA leading to spinal cord compression.

The posterior decompression was performed for current case, because there was no instability at occipito-atlantoaxial complex. We adopted the same procedure with previous reports and had no instability and complaint postoperatively.