High-cervical spinal cord compression at the C1–C2 level is uncommon and often associated with atlantoaxial instability, retro-odontoid soft-tissue formation, or hypertrophy of the posterior arch of the atlas. Although decompression combined with fusion is frequently considered, decompression alone may be an option in carefully selected patients without significant instability.
This case illustrates a staged, individualized approach using unilateral biportal endoscopic (UBE) decompression for severe C1–C2 stenosis.
Clinical Presentation
A man in his seventies presented with progressive numbness in all four extremities over the preceding two years. He also reported increasing gait instability and weakness of the lower extremities.
Neurological examination revealed hyperreflexia in both the upper and lower extremities and a positive Hoffmann sign. These findings were consistent with upper motor neuron dysfunction and suggested cervical spinal cord compression.
The patient did not report significant neck pain, and his cervical range of motion was relatively well preserved.
Imaging Findings
Plain radiographs demonstrated degenerative changes of the cervical spine. Dynamic flexion–extension radiographs showed only minimal variation in the atlantodental interval, measuring approximately 1.2 mm and remaining below 3 mm. No definite radiographic evidence of significant atlantoaxial instability was identified.
Cervical MRI revealed severe spinal canal stenosis and marked spinal cord compression at the C1–C2 level. A retro-odontoid pannus-like soft-tissue lesion was present posterior to the odontoid process.
The posterior arch of C1 was also markedly thickened, measuring approximately 8.7 mm, compared with the reported normal range of approximately 5.4–6.0 mm. The combination of retro-odontoid soft-tissue formation and posterior arch hypertrophy substantially reduced the space available for the spinal cord.
Surgical Indication
The patient had progressive cervical myelopathy with worsening quadrilateral numbness, lower-extremity weakness, gait disturbance, pathological reflexes, and severe radiographic spinal cord compression.
Posterior decompression combined with C1–C2 instrumentation and fusion was initially discussed because chronic atlantoaxial instability can contribute to retro-odontoid pannus formation. However, the patient had no meaningful neck pain, no definite instability on dynamic radiographs, and a strong preference to avoid instrumentation if possible.
After a detailed discussion of the potential benefits, limitations, and risk of future instability, a staged treatment strategy was selected. The first stage consisted of posterior neural decompression without fusion. Instrumented fusion would remain an option if postoperative instability, neck pain, recurrent compression, or neurological deterioration developed.
Operative Technique
Posterior C1–C2 decompression was performed using a unilateral biportal endoscopic (UBE) technique.
The endoscopic approach provided continuous irrigation and magnified visualization of the posterior osseous and neural structures. The hypertrophied posterior elements contributing to canal stenosis were carefully removed until adequate decompression of the spinal cord was achieved.
Particular attention was paid to limiting unnecessary disruption of the stabilizing structures of the atlantoaxial region. Because surgery at the upper cervical level may be associated with considerable epidural and venous bleeding, meticulous hemostasis and maintenance of a clear endoscopic field were essential throughout the procedure.
The operation was completed successfully without instrumentation or fusion.
Postoperative Outcome
The patient recovered well after surgery. Muscle strength and gait stability improved progressively and substantially during the first six postoperative months.
At the one-year follow-up, dynamic cervical radiographs showed no meaningful interval change or evidence of newly developed atlantoaxial instability. Follow-up MRI demonstrated satisfactory decompression of the spinal cord and substantial improvement in the previously severe C1–C2 canal stenosis.
The patient reported a favorable clinical recovery and did not require additional fusion surgery during the reported follow-up period.
What We Learn from This Case
Treatment decisions for C1–C2 stenosis should not be based solely on the anatomical level of compression or the presence of a retro-odontoid pannus-like lesion. The degree of instability, clinical symptoms, neurological progression, bony anatomy, and the patient’s preferences must all be considered.
Fusion remains an important treatment when definite atlantoaxial instability is present. However, decompression alone may be a reasonable first-stage option for carefully selected patients who have severe posterior compression but no significant neck pain or demonstrable dynamic instability.
UBE can provide magnified visualization and effective posterior decompression through a minimally invasive approach. Nevertheless, upper-cervical endoscopic surgery is technically demanding. A thorough understanding of the regional anatomy, careful preoperative planning, reliable hemostasis, preservation of stabilizing structures, and close postoperative surveillance are essential.
This case also demonstrates the value of shared decision-making. Spine surgery is not always a choice between two absolute options. A staged strategy can sometimes achieve neurological recovery while preserving future treatment options.
