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We investigated the relationship between trunk muscle mass and spinal pathologies by gender. This multicenter cross-sectional study included patients aged ≥ 30 years who visited a spinal outpatient clinic. Trunk and appendicular muscle mass were measured using bioelectrical impedance analysis. The Oswestry Disability Index (ODI), visual analog scale (VAS) score for low back pain, sagittal vertical axis (SVA), and EuroQol 5 Dimension (EQ5D) score were investigated to evaluate spinal pathology. The association between trunk muscle mass and these parameters was analyzed by gender using a non-linear regression model adjusted for patients’ demographics. We investigated the association between age and trunk muscle mass. We included 781 men and 957 women. Trunk muscle mass differed significantly between men and women, although it decreased with age after age 70 in both genders. Lower trunk muscle mass was significantly associated with ODI, SVA, and EQ5D score deterioration in both genders; its association with VAS was significant only in men. Most parameters deteriorated when trunk muscle mass was

Sacral insufficiency fractures (SIFs) are common in the elderly. In patients with SIF, objective neurological abnormalities such as sphincter dysfunction or leg paresthesia are uncommon. We present a case of SIF accompanied by spinopelvic dissociation with late neurological compromise treated by spinopelvic fixation. A 61-year-old woman presented to our hospital with low back pain without obvious trauma history. She had a past history of eosinophilic granulomatosis with polyangiitis and treatment with steroids. Her low back pain became worse, and she started to have radiating left posterior thigh pain and motor weakness in the left ankle and both great toes with symptoms of stress urinary incontinence, constipation, and loss of anal sensation. Magnetic resonance imaging revealed an H-shaped sacrum fracture. We attributed the neurological symptoms to unstable SIF and performed lumbopelvic fixation. After the surgery, her leg pain and symptoms of stress urinary incontinence improved markedly, as did anal sensation. At a 6-month follow-up, the patient reported no low back pain and she was walking independently without pelvic complaints. CT showed bone union was achieved. Even minimally displaced SIF in patients with osteoporosis can be a cause of bowel and bladder disturbance. Lumbopelvic fixation is a treatment option for SIF with spinopelvic dissociation presenting neurological deficit.

An occipital condyle fracture (OCF) is a relatively rare trauma that is now increasingly diagnosed because of the wide availability of computed tomography. For nondisplaced OCFs, conservative treatment is generally recommended, and there is no previous report of a nondisplaced OCF requiring surgery. We report a patient who had a nondisplaced OCF with craniocervical misalignment (a condyle-C1 interval > 2.0 mm) and C1-C2 translation treated with a halo vest and occipitocervical fusion surgery. An 87-year-old Asian woman fell from a 4-meter height and hit her head. She was transferred to our emergency room. Computed tomography revealed a nondisplaced impaction OCF with a 2.5 mm occipital condyle-C1 interval and a 5 mm C1-C2 translation. The fracture pattern was considered stable. However, since craniocervical misalignment and C1-C2 translation were present, the patient was placed in a halo device, and we reduced the occipitoatlantoaxial joint, adjusting the halo ring position preoperatively. Confirming reduction of the atlantooccipital facet joint and the atlantoaxial joint by computed tomography, we performed an occipitocervical fusion. This is the first report of a nondisplaced OCF with craniocervical misalignment and C1-C2 translation that required surgical treatment. Clinicians should be aware of craniocervical misalignment and atlantoaxial instability even in Tuli type 1 OCFs.

Study design Case report. Objective To describe the usefulness of simulated surgery for evaluation of a patient with neurofibromatosis type-1 (NF-1) who had severe cervicothoracic kyphoscoliosis and an anomalous vertebral artery (VA). Summary of background data Several surgical procedures have been used in the treatment of cervicothoracic kyphoscoliosis associated with myelopathy in patients with NF-1. However, to our knowledge, there has been no report that describes a surgical procedure for NF-1 patients with anomalous VA at the cervical spine. Methods A 45-year-old man with NF-1 developed cervical myelopathy. Preoperative examinations revealed severe cervicothoracic kyphoscoliosis, dystrophic changes of the cervical vertebrae, and the anomalous course of a VA and VA aneurysms. To assist in the preoperative planning and intraoperative navigation, we created 3-dimensional (3D) full-scale models of the patient's spine. Using a model, we performed a simulation of the planned surgery for spinal cord decompression with spinal fusion through both anterior and posterior approaches. Results Through the simulation, we could evaluate the risk of VA injury at the process of corpectomy, and altered the surgical procedure for the spinal cord decompression with spinal fusion from a posterior approach and a bone graft alone from an anterior approach. We accomplished the surgery successfully without any neurovascular complications. After surgery, the patient experienced relief from myelopathy. Conclusion Preoperative surgical simulation using a 3D full-scale model was useful for improving the accuracy and safety of the surgery for cervicothoracic kyphoscoliosis with NF-1.

Granulocyte colony-stimulating factor (G-CSF) is a cytokine that is clinically used to treat neutropenia. G-CSF also has non-hematopoietic functions and could potentially be used to treat neuronal injury. To confirm the safety and feasibility of G-CSF administration for acute spinal cord injury (SCI), we have initiated a phase I/IIa clinical trial of neuroprotective therapy using G-CSF.The trial included a total of 16 SCI patients within 48 h of onset. In the first step, G-CSF (5 μg/kg/day) was intravenously administered for 5 consecutive days to 5 patients. In the second step, G-CSF (10 μg/kg/day) was similarly administered to 11 patients. We evaluated motor and sensory functions of patients using the American Spinal Cord Injury Association (ASIA) score and ASIA impairment scale (AIS) grade.In all 16 patients, neurological improvement was obtained after G-CSF administration. AIS grade increased by one step in 9 of 16 patients. A significant increase in ASIA motor scores was detected 1 day after injection (P0.01), and both light touch and pin prick scores improved 2 days after injection (P0.05) in the 10 μg group. No severe adverse effects were observed after G-CSF injection.These results indicate that intravenous administration of G-CSF (10 μg/kg/day) for 5 days is essentially safe, and suggest that some neurological recovery may occur in most patients. We suggest that G-CSF administration could be therapeutic for patients with acute SCI.

In peripheral nerve injury, Schwann cells (SCs) must survive to exert a continuing and essential role in successful nerve regeneration. Herein, we show that peripheral nerve injury is associated with activation of endoplasmic reticulum (ER) stress and the adaptive unfolded protein response (UPR). The UPR culminates in expression of C/EBP homology protein (CHOP), a proapoptotic transcription factor in SCs, unless counteracted by LDL receptor-related protein-1 (LRP1), which serves as a major activator of phosphatidylinositol 3-kinase (PI3K). Sciatic nerve crush injury in rats induced expression of the ER chaperone GRP78/BIP, reflecting an early, corrective phase of the UPR. However, when LRP1 signaling was inhibited with receptor-associated protein, PI3K activity was decreased and CHOP protein expression increased, particularly in myelinating SCs. In cultured SCs, the PKR-like ER kinase target eIF2α was phosphorylated and CHOP was induced by (1) inhibiting PI3K, (2) treating the cells with tumor necrosis factor-α (TNF-α), or (3) genetic silencing of LRP1. CHOP gene deletion in SCs decreased cell death in response to TNF-α. Furthermore, the effects of TNF-α on phosphorylated eIF2α, CHOP, and SC death were blocked by adding LRP1 ligands that augment LRP1-dependent cell signaling to PI3K. Collectively, our results support a model in which UPR-activated signaling pathways represent a major challenge to SC survival in nerve injury. LRP1 functions as a potent activator of PI3K in SCs and, by this mechanism, limits SC apoptosis resulting from increased CHOP expression in nerve injury.

Schwann cells play an important role in injury to the peripheral nervous system (PNS). These cells de-differentiate, migrate, and secrete cytokines and chemokines involved in recruitment of inflammatory cells (Jessen and Mirsky, 1999; Campana, 2007). Recruited macrophages are essential to clear irreversibly damaged debris so that Schwann cells may establish extracellular scaffolds and direct regenerating axons (Stoll and Muller, 1999). Although the molecular mediators that promote macrophage recruitment remain incompletely understood, monocyte chemattractant protein-1 (MCP-1/CCL-2) is known to play a central role (Martini et al., 2008). Shortly after PNS injury, the type-1 transmembrane protein LDL receptor-related protein-1 (LRP1) is substantially up-regulated in Schwann cells (Campana et al., 2006). LRP1 functions as a broad-spectrum endocytic receptor for diverse ligands and as a phagocytic receptor for apoptotic cells and degenerated myelin debris (Strickland et al., 2002; Kinchen and Ravichandran, 2007; Gaultier et al., 2009). In Schwann cells, LRP1 also functions as a robust cell-signaling receptor. Ligand binding to LRP1 activates ERK/MAP kinase and Akt, promoting Schwann cell survival and migration (Campana et al., 2006; Mantuano et al., 2008a,b). Tissue-type plasminogen activator (tPA) and matrix metalloprotease-9 (MMP-9) are examples of proteases implicated in the response to PNS injury (La Fleur et al., 1996; Akassoglou et al., 2000; Kobayashi et al., 2008), which bind directly to LRP1 and activate LRP1-dependent cell signaling (Hu et al., 2006; Mantuano et al., 2008b; Shi et al., 2009). Other proteases may bind to the protease inhibitor α2-macroglobulin (α2M) and trigger α2M conformational change so that the complex becomes a high-affinity ligand for LRP1 (Barrett and Starkey, 1973; Barrett et al., 1979; Imber and Pizzo, 1981; Sottrup-Jensen, 1989; Strickland et al., 2002). By this pathway, diverse proteases, including those that do not bind directly to LRP1, may trigger LRP1-dependent Schwann cell signaling. The goal of this study was to determine whether the cell-signaling pathways activated by ligand binding to LRP1, which are known to promote cell survival and migration, also regulate expression of chemokines and cytokines by Schwann cells. We performed these studies with primary cultures of rat Schwann cells. Our results demonstrate that binding of activated α2M to LRP1 substantially increases expression of MCP-1. This response is selective, because α2M does not induce expression of the potent proinflammatory cytokine tumor necrosis factor-α (TNF-α), which is expressed by Schwann cells in response to other mediators in vivo and in vitro (Campana, 2007). The increase in MCP-1 expression was dependent on ERK/MAP kinase activation downstream of LRP1 (Mantuano et al., 2008a). These results support a model in which LRP1-dependent cell signaling contributes to a wide spectrum of activities demonstrated by Schwann cells in PNS injury.