Hindawi Publishing Corporation
Case Reports in Medicine
Volume 2011, Article ID 238748, 5 pages
doi:10.1155/2011/238748

Case Report
Ossification of Transverse Ligament of Atlas Causing Cervical
Myelopathy: A Case Report and Review of the Literature
Tatsuro Sasaji, Chikashi Kawahara, and Fujio Matsumoto
Department of Orthopaedic Surgery, Tohoku Rosai Hospital, 4-3-21 Dainohara, Aoba-ku, Sendai 981-8563, Japan
Correspondence should be addressed to Tatsuro Sasaji, taturosasaji@hotmail.com
Received 13 October 2010; Accepted 5 June 2011
Academic Editor: John Kortbeek
Copyright © 2011 Tatsuro Sasaji et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
A case of ossification of transverse ligament of atlas (TLA) is reported. A 76-year-old female suﬀered from a transverse
type myelopathy was successfully treated by posterior decompression. Dynamic lateral plain radiographs showed irreducible
atlantoaxial subluxation (AAS). A computed tomogram revealed ossified mass compatible to ossification of TLA. Coalition ofthe atlantooccipital joints and osteoarthritis of the atlantoaxial joints with degenerated dens was also revealed. Magnetic resonanceimaging showed compressed spinal cord at C1 level by the ossification of TLA and AAS. We suggest a mechanism of ossificationof TLA as follows: hypertrophied dens and stress to the atlantoaxial joints caused by coalition of atlantooccipital joints could
make forward shift of atlas leading to irreducible AAS, and continuous tension given to TLA from irreducible AAS would result in
hypertrophied and ossification of TLA.

1. Introduction
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, andthe present condition could be a rare cause of cervicalmyelopathy at upper cervical spine [1–4]. We experienced acase of ossification of TLA. We report details of radiologicalfindings and inference of mechanism of the ossification ofTLA from current and previously reported cases.

2. Case Report
A 76-year-old woman had been suﬀered from numbness andclumsiness in both upper limbs and gait disturbance for six
months before presentation.
2.1. Neurological Examination. She was diagnosed as atransverse type cervical myelopathy without neck pain. Herneck motion was severely restricted especially in rotation. Allof the laboratory findings were within normal limits.

2.2. Radiological Findings. Dynamic lateral plain radiographs of cervical spine revealed irreducible atlantoaxial subluxation (AAS) (Figure 1). A sagittal reconstructed computedtomogram (CT) revealed the ossified mass behind dens
and osteophyte continuing to dens. Dens and anterior archof atlas were sclerotic, and dens itself was hypertrophied.
There was no ossification of posterior longitudinal ligament(Figure 2(a)). CT also revealed ossified mass compatible toossification of TLA. A space between dens and posterior archdecreased (Figure 2(b)). Dens and lateral masses of atlas weresclerotic and space around dens decreased in a coronal reconstructed CT. Coalition of bilateral atlantooccipital joints wasseen (Figure 2(c)). A sagittal planes of magnetic resonanceimaging (MRI) showed compressed spinal cord with highintensities within the spinal cord by the mass behind dens.
The mass showed high intensities on T2-weighted images.
The spinal cord was compressed between the mass andposterior arch of atlas, and there was no subarachnoid spacearound the spinal cord. The spinal cord was also compressedat the level of C3-4 and C4-5 (Figure 3(a)). Axial planes of
MRI also showed compressed spinal cord at the level of C1
between the mass and posterior arch of atlas (Figure 3(b)).

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(a)

(b)

Figure 1: Preoperative dynamic lateral plain radiographs. Flexion view (a) and extension (b) view. Preoperative plain radiographs in flexed
position (a) and in extended position (b) showed ossified mass behind dens and irreducible atlantoaxial subluxation. The atlantodental
interval is 6 mm and the space available for the spinal cord is 7 mm in each positions.

(a)

(b)

(c)

Figure 2: Reconstructed computed tomogram (CT). (a) Sagittal reconstructed CT. Ossified mass behind dens (arrow) and osteophyte
continuing from the dens (arrowhead) can be seen. The dens itself is degenerated and hypertrophied. (b) Axial CT. Most of the spinal canal
is occupied by ossification of transverse ligament of atlas. (c) Coronal reconstructed CT. The joint space of atlantoaxial joint and the spaces
between dens and lateral masses of atlas were narrowed. Coalition of bilateral atlantooccipital joints can be seen (arrow).

Case Reports in Medicine

3(a)

(b)

Figure 3: Preoperative MRI on T2-weighted image. (a) Sagittal plane. The spinal cord is compressed at the level of C1, C3-4, and C4-5, withhigh intensities within the spinal cord at C1 level. (b) Axial plane. The spinal cord is compressed by the mass behind dens and posterior archof the atlas.

(a)

(b)

Figure 4: Postoperative dynamic lateral plain radiographs. Flexion (a) and extension (b) view. Atlantoaxial subluxation had not progressed.

2.3. Operation. Posterior arch of the atlas, C3, and C4 lamina
were explored through a posterior approach. Resection of theposterior arch of atlas and laminectomy of C3 and C4 were
performed using burr. After the decompression, the duramater became pulsant and the decompression was confirmedby an ultrasonography.
2.4. Postoperative Course. Her numbness and clumsiness ofboth upper limbs and gait disturbance were improved soonafter the operation. At eighteen months after surgery, shereturned to a normal daily life without neck pain. Followup plain lateral radiographs showed no deterioration of AAS

after surgery (Figures 4(a) and 4(b)). The follow-up MRI
revealed an adequate decompressed spinal cord (Figures 5(a)and 5(b)).

3. Discussion
There have been only four reports concerning ossificationof TLA [1–4]. Characteristic features of patients withossification of TLA were elderly population, AAS, andhypertrophied dens. AAS were recognized in three cases, andhypertrophied dens were recognized in two cases. Hayashi
and colleagues described that a trauma of 12 years ago led to4

Case Reports in Medicine(a)(b)

Figure 5: Postoperative MRI on T2-weighted image. Sagittal (a) and axial (b) plane. The spinal cord had been decompressed.

ossification of TLA, but they did not describe a mechanismof this ossification in detail [1]. The mechanism of thisossification 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 coronalreconstructed CT, and so we diagnosed not as an assimilationof 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 amechanism that atlantoaxial joint compensated the functionof stabilized atlantooccipital joint and a greater stress on TLA
results in stretching and leading to AAS [6, 7]. Coalitionof atlantooccipital joints is diﬀerent from an assimilationof atlas, but it may cause AAS as the adjacent segmentdegeneration by similar mechanism. On the basis of thesefindings, 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-atlantoaxialcomplex. We adopted the same procedure with previous
reports and had no instability and complaint postoperatively.

References[1] T. Hayashi, Y. Hirose, M. Sagoh, and H. Murakami, “Ossification of transverse ligament of the atlas associated with atlantoaxial dislocation—case report,” Neurologia Medico-Chirurgica,
vol. 38, no. 7, pp. 425–428, 1998.
[2] M. Nobukiyo, K. Ichimura, K. Sainou, and T. Kawaguchi, “A
case of cervical myelopathy caused by the ossified lesion behindthe dens,” Chubu Seikei Saigai Geka Gakkai Zasshi, vol. 51, pp.
609–610, 2008 (Japanese).
[3] S. Perera, C. H. G. Davis, and R. C. Gupta, “Spinal cord
compression caused by ossification of the transverse ligamentof the atlas,” British Journal of Neurosurgery, vol. 9, no. 6, pp.
787–788, 1995.
[4] W. Tsuruta, K. Yanaka, M. Okazaki, A. Matsumura, andT. Nose, “Cervical myelopathy caused by hypoplasia of theatlas and ossification of the transverse ligament—case report,”
Neurologia Medico-Chirurgica, vol. 43, no. 1, pp. 55–59, 2003.
[5] T. Detlef and G. Walter, The Upper Cervical Spine, Butterworth,London, UK, 1972.
[6] A. D. Greenberg, “Atlanto-axial dislocations,” Brain, vol. 91, no.
4, pp. 655–684, 1968.

Case Reports in Medicine[7] M. Hagiwara, Y. Kanbara, Y. Nishibayashi, T. Shou, and O.
Kataoka, “A case report of surgically treated congenital atlantoaxial dislocation associated with atlas assimilation,” Orthopaedic Surgery and Traumatology, vol. 29, pp. 1847–1850, 1986
(Japanese).

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