Study Design. Case report.
Objective. We report on a patient with thoracic myelopathy caused by ossification of the posterior longitudinal ligament (OPLL) of the spine.
Summary of Background Data. Surgery for thoracic OPLL (T-OPLL) is associated with a high rate of complications. Posterior spinal instrumentation (PSI) with decompression is a relatively safe procedure with satisfactory results. However, the mechanisms by which PSI with decompression produces neurological recovery in patients who undergo T-OPLL have not been elucidated fully, and no reports have described the radiographical progress after PSI.
Methods. The patient was a 78-year-old female with a 4-month history of gait disturbance and paresthesia of the lower extremities who had continuous OPLL at T1–T4. The spinal cord was impinged by beak-type OPLL with a nonossified area at T3–T4. PSI without decompression of C7–T6 was performed.
Results. After surgery, the patient showed clear improvement in neurological symptoms. She recovered fully after 2 years, by which time, the point of the beak-type OPLL at T3–T4 had become a mild protuberance and the nonossified area was fused through the remodeling process. This reduced the size of the ossified lesion that had caused severe compression of the spinal cord before surgery.
Conclusion. The remaining mobility at the nonossified lesion, where the point of the beak-type OPLL compressed the spinal cord, might have caused the myelopathy in this patient. We propose that stabilization with PSI stimulates bone remodeling of nonossified lesions, leading to a reduction of OPLL. This finding provides a clue about the mechanisms responsible for neurological improvement after PSI for T-OPLL.
Level of Evidence: N/A
We report on a patient with thoracic myelopathy caused by beak-type ossification of the posterior longitudinal ligament of the thoracic spine, in which the symptoms improved markedly after posterior spinal instrumentation without decompression, and computed tomography revealed that the size of the ossified lesion was reduced through remodeling.
From the Department of Orthopedic Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Address correspondence and reprint requests to Hiroaki Kimura, MD, PhD, Department of Orthopedic Surgery, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan; E-mail: firstname.lastname@example.org
Acknowledgment date: October 30, 2013. First revision date: December 13, 2013. Acceptance date: December 16, 2013.
The manuscript submitted does not contain information about medical device(s)/drug(s).
No funds were received in support of this work.
Relevant financial activities outside the submitted work: grants/grants pending.