Kummell's disease is a rare, delayed posttraumatic collapse of a vertebral body that can occur several months or even years after an osteoporotic compression fracture. However, there are few reports of posterior element fractures associated with Kummell's disease. A 72-year-old man who had sustained an L1 osteoporotic compression fracture 14 months prior was admitted to our institution with incapacitating back pain. Plain radiographs showed progressive collapse of the L1 vertebral body and severe kyphosis at the thoracolumbar junction. Magnetic resonance imaging revealed a posterior element fracture as well as osteonecrosis of the L1 vertebral body. An L1 percutaneous vertebroplasty was performed, followed by bone cement-augmented screw fixation to maintain stability and correct the kyphotic deformity. After surgery, pain relief was immediate, and the patient was able to walk unassisted. This case illustrates that continuous axial distraction stress caused by aggravated kyphosis secondary to Kummell's disease may result in posterior element fractures. Our discussion concludes with a literature review.

Background Studies over the past 20 years have shown that fibromyalgia (FM) is a pain amplification disorder with clear evidence for a pathogenesis within the central nervous system. Brain-derived neurotrophic factor (BDNF) signaling pathway participates in plasticity mechanisms and serves as a neurotransmitter modulator. The pathway includes cyclic adenosine monophosphate response element-binding protein 1 (CREB1), BDNF, and its receptor (neurotrophic tyrosine kinase receptor, type 2 [NTRK2]). The variations of the genes were known to be associated with human neuropsychiatric disorders. Objectives We proposed to determine whether these BDNF-NTRK2-CREB1 pathway gene single nucleotide polymorphisms (SNPs) were associated with FM and/or any of its clinical variables. Methods Patients with FM (N = 422) and age-sex matched healthy normal controls (HNC, N = 410) were studied. Patients were carefully diagnosed by well trained rheumatologists at 13 tertiary hospitals. The SNPs were determined using Taq-Man analysis. In this study, three SNPs of BDNF (rs6265), NTRK2 (rs1187323), and CREB1 (rs2253206) genes were selected for the analysis. The patients and control groups were compared using case-control association analysis. The χ2 test was used to estimate the Hardy-Weinberg equilibrium (HWE). Allele frequency was defined as the percentage of the individuals carrying the allele among the total number of the individuals. Logistic regression analyses were used to calculate odds ratios (95% confidence interval). A P-value of less than 0.05 was considered to indicate statistical significance. Results Of the SNPs, CREB1 gene SNP (rs2253206) is statistically associated with the susceptibility of FM. The CREB1 SNP distribution was 150 (36%) GG, 204 (48%) GA, and 68 (16%) AA for HNC and 173 (42%) GG, 187(46%) GA, and 50 (12%) AA for HNC, respectively (Table 1). Conclusions This is the first study to associate the BDNF-NTRK2-CREB1 pathway gene polymorphisms with FM and its subgroup phenotype. References Castren E, Voikar V, Rantamaki T (2006): Role of neurotrophic factors in depression. Curr Opin Pharmacol 7:18 –21. Duman RS, Monteggia LM (2006): A neurotrophic model for stressrelated mood disorders. Biol Psychiatry 59:1116 –1127. Carlson PJ, Singh JB, Zarate CA Jr, Drevets WC, Manji HK (2006): Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets. NeuroRx 3:22– 41. Disclosure of Interest None Declared

No abstract