Recent studies suggested a predominant role of spinopelvic parameters to explain lumbosacral spondylolisthesis pathogeny. We compare the pelvic incidence and other parameters of sagittal spinopelvic balance in adolescents and young adults with developmental spondylolisthesis to those parameters in a control group of healthy volunteers. We compared the angular parameters of the sagittal balance of the spine in a cohort of 244 patients with a developmental L5-S1 spondylolisthesis with those of a control cohort of 300 healthy volunteers. A descriptive and correlation study was performed. The L5 anterior slipping and lumbosacral kyphosis in spondylolisthesis patients was described using multiple regression analysis study. Our study demonstrates that the related measures of sagittal spinopelvic alignment are disturbed in adolescents and young adults with developmental spondylolisthesis. These subjects stand with an increased sacral slope, pelvic tilt and lumbar lordosis but with a decreased thoracic kyphosis. Pelvic incidence was significantly higher in spondylolisthesis patients as compared with controls but was not clearly correlated with the grade of slipping. We showed the same ''sagittal balance strategy'' in spondylolisthesis patients as in the control group regarding correlations between pelvic incidence, sacral slope, pelvic tilt and lumbar lordosis. We believe that the lumbosacral kyphosis is a stronger factor than pelvic incidence which need to be taken into account as a predominant factor in theories of pathogenesis of lumbosacral spondylolithesis. We thus believe that increased lumbar lordosis associated with L5-S1 spondylolisthesis is secondary to the high pelvic incidence and is an important factor causing high shear stresses at the L5-S1 pars interarticularis. However, the ''local'' sagittal imbalance of the lumbosacral junction is compensated by adjacent mobile segments in the upper lumbar spine, the pelvis orientation and the thoracic spine. The result is not optimal but a satisfactory global sagittal balance of the trunk, even in the most severe grade of slipping.

Level V.

Introduction Restitution of sagittal balance is important after lumbar fusion, because it improves fusion rate and may reduce the rate of adjacent segment disease. The purpose of the present study was to describe the impact of transforaminal lumbar interbody fusion (TLIF) procedures on pelvic and spinal parameters and sagittal balance. Materials and methods Forty-five patients who had single-level TLIF were included in this study. Pelvic and spinal radiological parameters of sagittal balance were measured preoperatively, postoperatively and at latest follow-up. Results Age at surgery averaged 58.4 (±9.6) years. Mean follow-up was 35.1 months (±4.1). Twenty-nine percent of the patients exhibited anterior imbalance preoperatively, with high pelvic tilt (17.6°± 7.9°). Of the 32 (71%) patients well balanced before the procedure, 22 (70%) had a large pelvic tilt ([20°), due to retroversion of the pelvis as an adaptive response to the loss of lordosis. Three dural tears (7%) were reported intraoperatively. Interbody cages were more posterior than intended in 27% of the cases. Disc height and lumbar lordosis at fusion level significantly increased postoperatively (p \ 0.05 and p \ 0.001). Pelvic tilt was significantly reduced (p \ 0.01) postoperatively, whereas the global sagittal balance was not significantly modified (p = 0.07). ConclusionSingle-level circumferential fusion helps patients reducing their pelvic compensation, but the amount of correction does not allow for complete correction of sagittal imbalance.

Camptocormia, also referred to as bent spine syndrome (BSS) is defined as an abnormal flexion of the trunk, appearing in standing position, increasing during walking and abating in supine position. BSS was initially considered, especially in wartime, as a psychogenic disorder. It is now recognized that in addition to psychiatric syndromes, many cases of reducible BSS have a somatic origin related to a number of musculo-skeletal or neurological disorders. The majority of BSS of muscular origin is related to a primary idiopathic axial myopathy of late onset, appearing progressively in elderly patients. Diagnosis of axial myopathy first described by Laroche et al. is based upon CT/MRI examination demonstrating massive fatty infiltration of paravertebral muscles. The non-specific histological aspect includes an extensive endomysial fibrosis and fat tissue with irregular degenerated fibers. Weakness of the paravertebral muscles can be secondary to a wide variety of diseases generating diffuse pathologic changes in the muscular tissue. BSS can be the predominant and sometimes revealing symptom of a more generalized muscular disorder. Causes of secondary BSS are numerous. They must be carefully assessed and ruled out before considering the diagnosis of primary axial myopathy. The principal etiologies include on the one hand inflammatory myopathies, muscular dystrophies of late onset, myotonic myopathies, endocrine and metabolic myopathies, and on the other hand neurological disorders, principally Parkinson's disease. Camptocormia in Parkinsonism is caused by axial dystonia, which is the hallmark of Parkinson's disease. There is no specific pharmacologic treatment for primary axial myopathy. General activity, walking with a cane, physiotherapy, and exercises should be encouraged. Treatment of secondary forms of BSS is dependent upon the variety of the disorder generating the muscular pathology. Pharmacologic and general management of camptocormia in Parkinson's disease merge with that of Parkinsonism. Levodopa treatment, usually active on tumor rigidity and akinesia, has poor or negative effect on BSS.

In this homogenous cohort of 50 patients with EOSII, treatment consisting of debridement surgery with implant retention followed by combination antibiotic therapy for 3 months appeared safe and effective.