Chapter Clinical Summary
Academic synthesis, diagnostic methodology, and surgical recommendationsCervical spondylotic myelopathy (CSM) and multi-level ossification of the posterior longitudinal ligament (OPLL) represent major causes of progressive spinal cord dysfunction in adults. While anterior multi-level decompression and fusion (ACDF/ACCF) or posterior laminectomy with instrumented fusion are effective, they permanently eliminate cervical mobility and carry risks of pseudarthrosis, dysphagia, and adjacent segment degeneration. Cervical laminoplasty was developed as a non-fusion, motion-preserving posterior decompressive technique that expands the dimensions of the spinal canal while maintaining the protective posterior arch and preserving baseline cervical alignment. By hinging the lamina open on one side (open-door / Hirabayashi) or splitting the spinous processes down the midline (double-door / French-door / Kurokawa) and securing the lamina with miniplates or spacers, laminoplasty achieves direct canal expansion and allows the spinal cord to drift posteriorly away from ventral compressive ridges. Successful outcomes depend on strict patient selection, preserved baseline cervical lordosis, and precise surgical technique.
Detail the biomechanical principles, clinical indications, surgical techniques (open-door and double-door), fixation methods (miniplates, spacers), and clinical evidence for cervical laminoplasty. The reader will learn to calculate canal expansion, select ideal candidates based on sagittal alignment, perform unhinged opening, and prevent complications such as C5 nerve root palsy, hinge closure, axial neck pain, and post-laminoplasty kyphosis.
Laminoplasty widens the sagittal diameter of the cervical spinal canal, relieving direct dorsal compression and enabling the spinal cord to migrate posteriorly ('drift back') away from ventral osteophytes and OPLL bars. This posterior drift relies entirely on preserved cervical lordosis; in a kyphotic spine, the spinal cord remains draped over anterior compressive ridges despite posterior canal expansion.
Ideal indications include multi-level (≥3 levels) cervical spondylotic myelopathy, continuous or mixed-type OPLL, posterior canal stenosis, and congenital narrow canal with preserved cervical lordosis (C2-C7 Cobb angle >10°). Absolute contraindications include fixed cervical kyphosis (>5°–10°), severe anterior single-level focal compression, gross translational instability, and severe axial neck pain (which may worsen after laminoplasty).
A unilateral open trough (complete bicortical osteotomy) is created at the laminofacet junction on the more symptomatic side, while a contralateral greenstick hinge trough (outer cortical thinning, inner cortex preserved) is drilled. The lamina is gently elevated 4–5 mm and secured open with titanium miniplates or bone struts (Figure 77.1).
The spinous processes are split down the exact midline, and bilateral partial-thickness greenstick troughs are drilled at the bilateral laminofacet junctions. Both hemi-laminae are opened outward like a French door and secured with ceramic/allograft spacers or titanium miniplates.
Randomized trials and meta-analyses show neurological recovery (JOA score gains) comparable to laminectomy with fusion and ACDF, with lower blood loss, shorter hospital stay, preserved cervical range of motion (50–70% maintained), and lower adjacent segment disease rates. Recognized complications include postoperative C5 nerve root palsy (3–10%), hinge spring-back closure, axial neck pain, and progressive loss of lordosis.
In clinical practice, laminoplasty is the procedure of choice for multi-level (C3-C7) cervical myelopathy in patients with preserved cervical lordosis (>10° C2-C7 Cobb angle) and minimal neck pain. Preoperative sagittal radiographs in standing position must be measured for cervical lordosis and modified K-line (especially in OPLL). If the spine is kyphotic, laminoplasty is contraindicated and anterior reconstruction or posterior instrumented fusion is required. Intraoperatively, hinge troughs must be created with high-speed diamond burrs with cold irrigation, thinning the dorsal cortex while keeping the ventral cortex pliable without complete fracture. Opening the lamina must be gradual and smooth to avoid sudden cord traction or hinge fracture. Postoperatively, C5 nerve root palsy (deltoid/biceps weakness) must be recognized as a traction phenomenon resulting from rapid posterior cord drift, typically managed conservatively with high-dose steroids and physical therapy.