• Yoshiro Musha and Kazuhiro Mizutani.
• Department of Orthopaedic Surgery, Toho University School of Medicine, Meguro-ku, Tokyo, Japan. yoshiro2006musha@yahoo.co.jp
• J Spinal Disord Tech. 2009 May 1;22(3):228-32.

Study DesignCase reports of 2 patients having cervical myelopathy accompanied with idiopathic hypoplasia of the posterior arch of the atlas.ObjectiveA standard for the sagittal inside diameter (SID) of the vertebral foramen of the atlas was determined for use in the diagnosis of hypoplasia. From the point of view of short SID, the etiologies of myelopathy in patients with this disease were analyzed.Summary Of Background DataThere is no established definition of hypoplasia of the atlantal vertebral foramen. The mechanism underlying the occurrence of this myelopathy in adulthood is unknown.MethodsLateral x-ray views of the cervical vertebrae of 150 Japanese men and 150 Japanese women were investigated, and the standard values of the SID were obtained. The features of myelopathy associated with this disease were analyzed in 2 cases managed at our facility and in the literature.ResultsThe mean standard value was 34.4 mm in women and 37.1 mm in men, showing a significant sex difference (P<0.0001). When a case with a value -2 SD below the standard was regarded as having hypoplasia, case 1 (female) showed 25 mm, that is, -3.9 SD, and case 2 (male) showed 30 mm, that is, -2.7 SD. The space available for the spinal cord of the atlas was 8.0 mm in case 1 and 9.5 mm in case 2. Both patients showed atlantoaxial subluxation on images, but atlantodental interval on flexion in cases 1 and 2 was 3.8 and 4.5 mm, respectively, showing the degree to be mild.ConclusionsIn the presence of congenital hypoplasia of the posterior arch of the atlas, the spinal cord is highly susceptible to injury because congenital spinal canal stenosis is present. Therefore, the presence of even a mild mechanical compressive lesion leads to myelopathy. Acquired mild atlantoaxial subluxation was associated with this hypoplasia, and the association was considered to be the mechanism underlying the occurrence of myelopathy in adulthood.

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