We present the case of a 68-year-old female with a past medical history significant for a Type II odontoid fracture sustained 25 years previously. This presented originally with neck pain and was detected on spinal radiographs, with conservative management in a soft cervical orthosis implemented. There was no further clinical or radiological follow-up for her condition. She presented with 6 months of progressive cervical myelopathy that manifests as upper extremity weakness and hand incoordination, extremity paresthesiae, and gait instability. Her modified Japanese Orthopedic Association score (mJOA) was 13. On physical examination, she exhibited increased tone and diffused hyperreflexia, unsteady broad-based and hesitant gait, and bilateral Hoffman and Babinski signs. Computed tomography (CT) [], demonstrates a chronic odontoid pseudoarthrosis with anterior subluxation, a significant posterior osteophyte narrowing the spinal canal (arrow), and significant segmental kyphosis overlying the pseudoarthrosis. Magnetic resonance imaging [] reveals spinal cord compression ventrally with tension over the posterior osteophyte and the remainder of the C2 body. Further, significant subaxial spinal spondylotic disease is evident. At surgery, following awake preoperative halo traction revealing the deformity to be mobile, permitting kyphosis reduction [], the patient was in the supine position without further attempt to reduce the ventral translation. A two-stage procedure was planned including first a transoral decompression of the odontoid fragment with resection of posterior vertebral body osteophyte to achieve anterior spinal cord decompression. Second, C1 laminectomy was performed along with subaxial decompression to address the remaining spondylotic disease performed with an occipitothoracic fusion. The patient was discharged home in a halo orthosis. At 4 months follow-up, she neurologically improved to functional independence (mJOA 17), with no evidence of pseudoarthrosis or implant failure on CT scan []. She was weaned from the halo and remains neurologically and structurally stable at 6 months postoperatively.