Predictive model for distal junctional kyphosis after cervical deformity surgery.

BACKGROUND CONTEXT: Distal junctional kyphosis (DJK) is a primary concern of surgeons correcting cervical deformity. Identifying patients and procedures at higher risk of developing this condition is paramount in improving patient selection and care. PURPOSE: The present study aimed to develop a risk index for DJK development in the first year after surgery. STUDY DESIGN/SETTING: This is a retrospective review of a prospective multicenter cervical deformity database. PATIENT SAMPLE: Patients over the age of 18 meeting one of the following deformities were included in the study: cervical kyphosis (C2-7 Cobb angle>10°), cervical scoliosis (coronal Cobb angle>10°), positive cervical sagittal imbalance (C2-C7 sagittal vertical axis (SVA)>4 cm or T1-C6>10°), or horizontal gaze impairment (chin-brow vertical angle>25°). OUTCOME MEASURES: Development of DJK at any time before 1 year. METHODS: Distal junctional kyphosis was defined by both clinical diagnosis (by enrolling surgeon) and post hoc identification of development of an angle<-10° from the end of fusion construct to the second distal vertebra, as well as a change in this angle by <-10° from baseline. Conditional Inference Decision Trees were used to identify factors predictive of DJK incidence and the cut-off points at which they have an effect. A conditional Variable-Importance table was constructed based on a non-replacement sampling set of 2,000 Conditional Inference Trees. Twelve influencing factors were found; binary logistic regression for each variable at significant cutoffs indicated their effect size. RESULTS: Statistical analysis included 101 surgical patients (average age: 60.1 years, 58.3% female, body mass index: 30.2) undergoing long cervical deformity correction (mean levels fused: 7.1, osteotomy used: 49.5%, approach: 46.5% posterior, 17.8% anterior, 35.7% combined). In 2 years after surgery, 6% of patients were diagnosed with clinical DJK; however, 23.8% of patients met radiographic definition for DJK. Patients with neurologic symptoms were at risk of DJK (odds ratio [OR]: 3.71, confidence interval [CI]: 0.11-0.63). However, no significant relationship was found between osteoporosis, age, and ambulatory status with DJK incidence. Baseline radiographic malalignments were the most numerous and strong predictors for DJK: (1) C2-T1 tilt>5.33 (OR: 6.94, CI: 2.99-16.14); (2) kyphosis<-50.6° (OR: 5.89, CI: 0.07-0.43); (3) C2-C7 lordosis<-12° (OR: 5.7, CI: 0.08-0.41); (4) T1 slope minus cervical lordosis>36.4 (OR: 5.6, CI: 2.28-13.57); (5) C2-C7 SVA>56.3° (OR: 5.4, CI: 2.20-13.23); and (6) C4_Tilt>56.7 (OR: 5.0, CI: 1.90-13.1). Clinically, combined approaches (OR: 2.67, CI: 1.21-5.89) and usage of Smith-Petersen osteotomy (OR: 2.55, CI: 1.02-6.34) were the most important predictors of DJK. CONCLUSIONS: In a surgical cohort of patients with cervical deformity, we found a 23.8% incidence of DJK. Different procedures and patient malalignment predicted incidence of DJK up to 1 year. Preoperative T1 slope-cervical lordosis, cervical kyphosis, SVA, and cervical lordosis all strongly predicted DJK at specific cut-off points. Knowledge of these factors will potentially help direct future study and strategy aimed at minimizing this potentially dramatic occurrence.

Design and Testing of 2 Novel Scores That Predict Global Sagittal Alignment Utilizing Cervical or Lumbar Plain Radiographs.

BACKGROUND: Global sagittal deformity is an established cause of disability. However, measurements of sagittal alignment are often ignored when patients present with symptoms localizing to the cervical or lumbar spine. OBJECTIVE: To develop scoring scales to predict the risk of sagittal malalignment in patients with only cervical or lumbar spine radiographs. METHODS: A retrospective review of a prospectively maintained multicenter adult spinal deformity database was performed. Primary outcome (sagittal malalignment) was defined as a C7 plumbline ≥ 50 mm. Two multivariate logistic regressions were performed using patient characteristics and measurements derived from cervical or lumbar radiographs as covariates. Point scores were assigned to age, body mass index (BMI), and lumbar lordosis or T1 slope by rounding their ß coefficients to the nearest integer. RESULTS: Nine hundred seventy-nine patients were included, with 652 randomly assigned to the derivation cohort (used to build the score) and 327 comprising the validation set. Final cervical score for the primary outcome included BMI ≥ 25 (1 point), age ≥ 55 yr (2 points), and T1 slope ≥ 27o (2 points). Final lumbar score for the primary outcome included BMI ≥ 25 (1 point), age ≥ 55 yr (1 point), and lumbar lordosis ≥ 45o (-1 points). High scores for both the cervical and lumbar spine presented with high specificity and positive likelihood ratios of sagittal malalignment. CONCLUSION: We developed scoring scales to predict global sagittal malalignment utilizing clinical covariates and cervical or lumbar radiographs. Patients with high scores may prompt imaging with long-cassette plain films to evaluate for global sagittal imbalance.

Anterior Column Realignment has Similar Results to Pedicle Subtraction Osteotomy in Treating Adults with Sagittal Plane Deformity.

OBJECTIVE: Anterior column realignment (ACR) is a minimally invasive surgical technique used for the correction of adult sagittal plane deformity. ACR is performed via a minimally invasive lateral transpsoas approach with anterior longitudinal ligament release and hyperlordotic cage placement. The objective of this study was to compare radiographic outcomes and complications in patients treated by ACR or Pedicle subtraction osteotomy (PSO). METHODS: Patients who underwent ACR were matched with patients from a retrospective PSO dataset, by pelvic incidence, lumbar lordosis, and thoracic kyphosis. Inclusion criteria included pelvic incidence and lumbar lordosis mismatch > 10°, pelvic tilt > 25°, and/or C7 sagittal vertical axis >5 cm, and minimum 1-year follow-up. RESULTS: All (n = 17) patients who underwent ACR underwent second-stage open posterior instrumented fusion. There were no differences in baseline demographic or radiographic parameters. Both groups were found to have significant improvement from preoperative to final follow-up for lumbar lordosis, T1 spinopelvic inclination, and T1 pelvic angle. Pelvic tilt did not improve with PSO (31° to 28°) at final follow-up but did improve in ACR group (34° to 25°). No differences were identified at 3-month or final follow-up for lumbar lordosis (51° vs. 47°), pelvic tilt (25° vs. 28°), and T1 pelvic angle (23° vs. 24°). The group undergoing PSO achieved greater T1 spinopelvic inclination correction (8° vs. 1.9°). Patients who underwent ACR had significantly less estimated blood loss than patients who underwent PSO (1.6 vs. 3.6 L, respectively), but no difference in the overall major complication rates was found (35.3% vs. 41.2%, respectively). CONCLUSIONS: ACR achieved similar radiographic results as PSO in a matched cohort with significantly less estimated blood loss and similar overall complication rate.

Brain-specific knock-out of hypoxia-inducible factor-1alpha reduces rather than increases hypoxic-ischemic damage.

Hypoxia-inducible factor-1alpha (HIF-1alpha) plays an essential role in cellular and systemic O(2) homeostasis by regulating the expression of genes important in glycolysis, erythropoiesis, angiogenesis, and catecholamine metabolism. It is also believed to be a key component of the cellular response to hypoxia and ischemia under pathophysiological conditions, such as stroke. To clarify the function of HIF-1alpha in the brain, we exposed adult mice with late-stage brain deletion of HIF-1alpha to hypoxic injuries. Contrary to expectations, the brains from the HIF-1alpha-deficient mice were protected from hypoxia-induced cell death. These surprising findings suggest that decreasing the level of HIF-1alpha can be neuroprotective. Gene chip expression analysis revealed that, contrary to expectations, the majority of hypoxia-dependent gene-expression changes were unaltered, whereas a specific downregulation of apoptotic genes was observed in the HIF-1alpha-deficient mice. Although the role of HIF-1alpha has been extensively characterized in vitro, in cancer models, and in chronic preconditioning paradigms, this is the first study to evaluate the role of HIF-1alpha in vivo in the brain in response to acute hypoxia/ischemia. Our data suggest, that in acute hypoxia, the neuroprotection found in the HIF-1alpha-deficient mice is mechanistically consistent with a predominant role of HIF-1alpha as proapoptotic and loss of function leads to neuroprotection. Furthermore, our data suggest that functional redundancy develops after excluding HIF-1alpha, leading to the preservation of gene expression regulating the majority of other previously characterized HIF-dependent genes.