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Can preoperative spino-cranial angle predict cervical sagittal imbalance after laminoplasty?

ObjectiveThis study aimed to determine whether the preoperative spino-cranial angle (SCA) predicts cervical sagittal imbalance (CSI) after laminoplasty (LP).MethodsWe retrospectively screened 298 consecutive patients with degenerative cervical myelopathy (DCM) who underwent LP at our hospital from January 2018 to June 2021. Of these, 116 met the inclusion criteria and were analyzed. Radiographic and clinical parameters were collected preoperatively and at the last follow-up. Patients were stratified based on the change in cervical sagittal vertical axis (cSVA), calculated as ΔcSVA = postoperative−preoperative, into three categories: improvement (ΔcSVA≤ − 10 mm), stability (−10 mm < ΔcSVA≤10 mm), and deterioration (ΔcSVA>10 mm). Group comparisons were conducted using the χ2 test, t-test, analysis of variance, or non-parametric equivalents, as appropriate. Multivariable logistic regression was used to identify factors associated with postoperative CSI (ΔcSVA>10 mm). Receiver operating characteristic (ROC) analysis was performed to determine the SCA cutoff.ResultsPatients in the deterioration group exhibited the lowest preoperative SCA, along with poorer JOA recovery and worse postoperative neck pain compared to the improvement group. In the adjusted model, a lower SCA independently predicted postoperative cSVA deterioration (OR = 0.575, 95%CI: 0.372–0.808, p = 0.012), while other preoperative variables were not significant. The ROC analysis showed fair discrimination (AUC = 0.662), and an SCA threshold of 81.8° yielded 62.6% sensitivity and 96.0% specificity.ConclusionThe preoperative SCA influences postoperative cervical alignment after LP. Patients with a low SCA are at increased risk for CSI and may benefit from enhanced preoperative counseling and strategies that preserve alignment during LP.

The ferroptosis-mediated domino effect: metabolic crosstalk from intervertebral disc degeneration to spinal deformity and cord injury: a mini review

Spinal degeneration, spinal deformity, and spinal cord injury (SCI) are classically managed as discrete biomechanical or neurological entities. However, emerging evidence reveals them as an interconnected pathological continuum. This mini-review introduces the “ferroptosis-mediated domino effect” as the core metabolic driver linking these conditions. The cascade initiates within the avascular intervertebral disc, where aberrant mechanotransduction (e.g., via Piezo1) provokes severe oxidative stress and subsequent ferroptosis, leading to extracellular matrix degradation and structural collapse. The ensuing spinal deformity chronically compresses the spinal microvasculature, disrupting the blood-spinal cord barrier (BSCB) and facilitating localized iron deposition. This chronic ischemic insult generates a metabolically “primed” spinal cord characterized by extreme vulnerability. Upon secondary acute trauma, the sudden influx of heme and labile iron ignites an uncontrollable “ferroptotic storm,” synergizing with neuroinflammation to drive irreversible neural loss. Finally, we evaluate cutting-edge translational interventions—including reactive oxygen species (ROS)-responsive nanoparticles and nanozyme-loaded hydrogels—that offer spatiotemporal precision to halt this pathological crosstalk. By dismantling disciplinary silos, this framework advocates for next-generation, dual-action therapeutic strategies that simultaneously restore biomechanical stability and mitigate metabolic collapse.
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