Relationship between developmental canal stenosis and surgical results of anterior decompression and fusion in patients with cervical spondylotic myelopathy

Cervical spondylotic myelopathy (CSM) is a common disease in older people. Its etiology is multifactorial and includes degenerative changes and/or instability of cervical spine. CSM patients have a high incidence of developmental canal stenosis (DCS), and DCS alone may predispose CSM patients to myelopathy. Anterior cervical decompression and fusion (ACDF) can decompress the spinal cord anteriorly and preserve the stability of the spinal column. However, few studies have investigated the incidence of DCS and surgical outcome of CSM in patients with DCS [ 1– 3]. The purpose of the present study was to investigate morbidity from DCS among CSM patients who underwent ACDF in our hospital. Furthermore, we compared the surgical outcomes of ACDF between CSM patients with and those without DCS to determine whether cervical spine DCS, as a static factor of the cervical spine, influenced surgical outcomes.

The aging process causes degenerative changes in the cervical spine. Osteophytes and narrowed intervertebral discs are common degenerative changes in the cervical spines of elderly people. Cervical myelopathy is a serious form of cervical spondylosis among those aged over 55 years [ 8]. Although the exact pathophysiology of cervical myelopathy remains unclear, it is widely accepted that this disorder involves compressive forces on the cervical spine, likely caused by multiple factors. As a static mechanical factor, developmental spinal canal stenosis places a patient at increased risk for developing cervical cord compression and myelopathy. Numerous authors have identified the normal AP diameter of the cervical spinal canal to be approximately 17–18 mm from C3 to C7 [ 9– 11]. However, patients with a sagittal diameter <13 mm are at increased risk for developing signs and symptoms of cervical myelopathy [ 12]. To avoid magnification variables, Pavlov described the canal-to-body ratio as a reliable determinant of cervical spinal stenosis. A value > 1 is regarded as normal; a value < 0.82 indicates DCS [ 4].

In this study, the diameters of the spinal canal and vertebral body were measured using plain radiographs because the posterior longitudinal ligament could not be distinguished from the vertebral body on MRI. Although spinal canal size is an important predisposing factor for myelopathy, DCS is not always correlated with neurologic deficit [ 13]. Hayashi et al. [ 13] reported that 10 % of subjects over 60 years of age with critical static canal stenosis measuring < 13 mm displayed no neurological deficits. These results suggest that the development of cervical myelopathy may be dependent on other factors in addition to the narrowed spinal canal.

Mechanically, myelopathy has been directly attributed to morbid processes such as spondylotic encroachment on the cervical spinal canal. Nevertheless, a narrowed spinal canal, as a second etiological factor, is thought to allow insufficient space to accommodate an average amount of spondylotic encroachment. In our study, DCS was recognized in 41.0 % of all the enrolled patients. Although DCS is a very important factor influencing the development of cervical myelopathy, it did not affect the clinical results in the current study, and there was no difference in the pre- and postoperative JOA scores or in the recovery rate between DCS and non-DCS groups.

Cervical myelopathy patients with a developmentally narrow canal may have either DCS with no significant evidence of spondylosis or DCS with clear evidence of spondylosis causing pressure on the cervical spinal cord. Epstein et al. [ 14] felt that in the former situation, decompressive laminectomy should be performed. However, according to Kadoya et al. [ 15], few cases of myelopathy are caused by the narrowed spinal canal itself; instead, they are attributed primarily to spondylotic changes with advancing age. Therefore, Kadoya et al. [ 15] emphasized that in the latter case, ACDF should be performed and laminectomy will consequently not be required. Several authors argue that the enlargement of the spinal canal by anterior decompression is limited to surgically repaired segments [ 16– 18], and postoperative deterioration of myelopathy due to the development of instability and/or bone spurs at adjacent levels may be more likely to occur in a narrowed spinal canal [ 16, 18]. Baba et al. [ 19] observed that 25 % of patients undergoing anterior cervical fusion subsequently developed new spinal canal stenosis above the fused segments over an average of 8.5 years of follow-up. Bohlman et al. [ 20] reviewed 122 patients after ACDF with an average of 6 years of follow-up and observed that 9 % of all patients developed ASD-S. Morishita et al. [ 21] found that a congenitally narrow canal had different effects on cervical kinematics. In other words, subjects with a congenitally narrow cervical canal may be exposed to large mechanical loading at the cervical spine. Their results suggested that a cervical spinal canal diameter of <13 mm may be a risk factor for degenerative disc disease as measured on MRI studies. Eubanks et al. [ 22] found that although congenital stenosis increases the incidence of radiographic ASD, it does not appear to predict symptomatic ASD. In the present study, the incidence of ASD after ACDF was significantly higher in the DCS group, but the incidence of ASD-S did not differ between groups.

The achievement of optimal alignment is a major goal of cervical spine surgery. Generally, kyphosis might be a contraindication for laminoplasty decompression in CSM patients because kyphosis cases might be insufficient for the posterior shift of the spinal cord. However, ACDF can achieve good release and distraction, so an improvement of cervical alignment can be achieved and maintained. Our radiological outcomes support previous results [ 23, 24], which show a significant improvement of cervical lordosis.

It is well known that failure of fusion remains a major limitation of multilevel ACDF. In our study, 4 patients in the DCS group and 5 in the non-DCS group exhibited non-fusion 6 months after operation. This finding is consistent with prior reports. In 2002, Barnes et al. [ 25] reported satisfactory outcomes in only 65 % of patients who had undergone multilevel ACDF, with an overall fusion rate of only 90 %.

In summary, we evaluated the clinical significance of DCS in CSM patients treated with ACDF. DCS was observed in 41.0 % of our CSM patients. DCS can greatly influence CSM, but it did not affect neurologic improvement postoperatively at the short-term follow-up. Although DCS increased the incidence of ASD after anterior fusion, it did not predict ASD-S. Therefore, patients with DCS must receive close follow-up.