An intraspinal extradural lipoma with spinal epidural lipomatosis: A case report and a review of literature.

BACKGROUND: Intraspinal extradural lipomas are very rare and should be differentiated from spinal epidural lipomatosis (SEL) and/or angiolipomas. CASE DESCRIPTION: A 76-year-old male presented with left lower extremity radiculopathy. The magnetic resonance imaging (MRI) revealed hyperplasia of epidural fat at the L2-3 and L3-4 levels accompanied by a lipomatous L4-5 mass. Following resection of this mass and hyperplastic epidural fat, the histological examination was consistent with an intraspinal extradural lipoma and SEL. CONCLUSION: This case indicates that asymmetrical compression of the dural sac may be attributed to an intraspinal extradural lipoma vs. just SEL and/or an angiolipoma.

Intradural Disk Herniation Mimicking a Spinal Tumor: Radiologic Imaging, Pathogenesis, and Operative Management.

Intradural disk herniation (IDH) is a rare condition, occurring more often at the L4-5 level. We examined a case of an IDH at the L1-2 level mimicking an intradural spinal tumor. A 71-year-old woman with a long history of backache and pain radiating down the left leg was admitted to our hospital with the worsening of these symptoms. Magnetic resonance imaging and computed tomographic myelography demonstrated an intradural mass at the L1-2 level. Given the radiologic findings and the location of the mass, the preoperative differential diagnosis centered on intradural spinal tumors. Dural incision was performed using a surgical microscope to resect the mass. Contrary to our expectation, the diagnosis made during the surgery was IDH. Despite advances in imaging techniques, IDH could not be definitively diagnosed preoperatively. The pathogenesis of IDH remains unclear. In our patient, the ventral dural defect was smooth and round, and the dural tissue around the defect was thickened. These intraoperative findings suggested that the patient's IDH resulted not from an acute new event but from a chronic process. We recommend dural incision using a surgical microscope for treating IDH because it provides a clear visual field.

Surgical outcomes of temporary short-segment instrumentation without augmentation for thoracolumbar burst fractures.

BACKGROUND: Short-segment posterior spinal instrumentation for thoracolumbar burst fracture provides superior correction of kyphosis by an indirect reduction technique, but it has a high failure rate. We investigated the clinical and radiological results of temporary short-segment pedicle screw fixation without augmentation performed for thoracolumbar burst fractures with the goal of avoiding treatment failure by waiting to see if anterior reconstruction was necessary. METHODS: We studied 27 consecutive patients with thoracolumbar burst fracture who underwent short-segment posterior instrumentation using ligamentotaxis with Schanz screws and without augmentation. Implants were removed approximately 1 year after surgery. Neurological function, kyphotic deformity, canal compromise, fracture severity, and back pain were evaluated prospectively. RESULTS: After surgery, all patients with neurological deficit had improvement equivalent to at least 1 grade on the American Spinal Injury Association impairment scale and had fracture union. Kyphotic deformity was reduced significantly, and maintenance of the reduced vertebra was successful even without vertebroplasty, regardless of load-sharing classification. Therefore, no patients required additional anterior reconstruction. Postoperative correction loss occurred because of disc degeneration, especially after implant removal. Ten patients had increasing back pain, and there are some correlations between the progression of kyphosis and back pain aggravation. CONCLUSION: Temporary short-segment fixation without augmentation yielded satisfactory results in reduction and maintenance of fractured vertebrae, and maintenance was independent of load-sharing classification. Kyphotic change was caused by loss of disc height mostly after implant removal. Such change might have been inevitable because adjacent endplates can be injured during the original spinal trauma. Kyphotic change after implant removal may thus be a limitation of this surgical procedure.

Neurological manifestations of thoracic myelopathy.

INTRODUCTION: Investigation of preoperative manifestations of thoracic myelopathy in a large population has not been reported. The aim of this study was to identify symptoms specific to anatomical pathology or compressed segments in thoracic myelopathy through investigation of preoperative manifestations. MATERIALS AND METHODS: Subjects were 205 patients [143 men, 62 women; mean age, 62.2 (range 21-87 years)] with thoracic myelopathy who underwent surgery at our affiliate institutions from 2000 to 2011. The disease distribution included ossification of the ligamentum flavum (OLF) in 106 patients, ossification of the posterior longitudinal ligament (OPLL) in 17, OLF with OPLL in 17, intervertebral disc herniation (IDH) in 23, OLF with IDH in 3, and spondylosis in 39. We assessed (1) initial and preoperative complaints, (2) neurological findings, (3) Japanese Orthopaedic Association scores (JOA, full score, 11 points), (4) the compressed segments, and (5) preoperative duration. Multivariate analyses were performed to examine potential relationships between preoperative manifestations and anatomical pathology or compressed segments. RESULTS: The multivariate analyses revealed relationships between lower limb muscle weakness and T10/11 anterior compression; lower limb pain and T11/12 anterior compression; low back pain and T11/12 compression; and hyporeflexia in the patellar tendon reflex/foot drop and T12/L1 anterior compression. CONCLUSION: This study elucidated symptoms specific to anatomical pathology or compressed segments in thoracic myelopathy. These relationships can be helpful in the initial investigation of thoracic diseases, although additional measures such as MRI or CT are necessary for definitive diagnosis.

Incidence of postoperative symptomatic epidural hematoma in spinal decompression surgery.

OBJECT: Neurological deterioration due to spinal epidural hematoma (SEH) is a rare but significant complication of spinal surgery. The frequency of hematoma evacuation after spinal surgery is reportedly 0.1%-3%. The objective of this study was to investigate the symptomatology of SEH and the frequency of evacuation for each surgical procedure after spinal decompression surgery. METHODS: This is a retrospective study of 26 patients who underwent SEH evacuation after spinal decompression surgery between 1986 and 2005. During this period, 6356 spinal decompression surgeries were performed. The factors studied were the frequency of SEH evacuation for each surgical procedure, symptoms, time to SEH evacuation, comorbidities, and neurological recovery. RESULTS: The frequency of SEH evacuation was 0.41% (26 of 6356) for all operations. The frequency for each surgical procedure was 0% (0 of 1568) in standard lumbar discectomy, 0.50% (8 of 1614) in lumbar laminectomy, 0.67% (8 of 1191) in posterior lumbar interbody fusion, 4.46% (5 of 112) in thoracic laminectomy, 0.44% (4 of 910) in cervical laminoplasty, and 0.21% (1 of 466) in cervical anterior spinal fusion. Nine patients had comorbidities involving hemorrhage. Spinal epidural hematoma evacuation was performed between 4 hours and 8 days after the initial operation. Whereas severe paralysis was observed within 24 hours in most patients undergoing cervical and/or thoracic surgery, half of the patients undergoing lumbar surgery had symptoms of SEH such as leg pain or bladder dysfunction after suction drain removal. The shorter the period to evacuation, the better were the results of neurological recovery. CONCLUSIONS: Postoperative SEH was most frequent after thoracic laminectomy. In cervical and thoracic surgeries, symptoms of SEH were noted within 24 hours, mostly severe paralysis, and almost half of the lumbar surgery patients had symptoms after suction drain removal.

Lamina horizontalization and facet tropism as the risk factors for adjacent segment degeneration after PLIF.

STUDY DESIGN: A retrospective case-control study. OBJECTIVE: To clarify associations between both lamina horizontalization and facet tropism and adjacent segment degeneration (ASD). SUMMARY OF BACKGROUND DATA: We have previously reported coexistence of lamina horizontalization and facet tropism adjacent to the cranial fusion segment as risk factors for ASD. METHODS: Subjects comprised 20 patients who underwent additional surgery for ASD after L4/5 posterior lumbar interbody fusion (PLIF) for L4 degenerative spondylolisthesis. Patients who underwent additional surgery for ASD (ASD group) were divided into 2 groups according to the duration until additional surgery: early group (n = 13), additional surgery < or =3 years after primary surgery; and late group (n = 7), additional surgery >3 years after primary surgery. As a control group, 20 age- and sex-matched patients who underwent L4/5 PLIF and could be followed for > or =5 years without ASD were selected. Lamina inclination angle at L3 and facet tropism at L3/4 in each group were measured 3 times by 3 individuals blinded to clinical results. Associations between clinical results and these risk factors and influences of these factors for periods up to the occurrence of ASD were investigated. RESULTS: All ASD was observed in the cranial adjacent segment and the most common condition at additional surgery was spondylolisthesis (n = 15, 75%). Lamina inclination angle was significantly higher in the ASD group than in the control group. ASD was observed in 86% of patients with lamina inclination >130 degrees . In addition, facet tropism was more significant in the early group than in the late and control groups. ASD was observed < or =3 years after primary surgery in all patients with both lamina inclination >130 degrees and facet tropism >10 degrees . CONCLUSION: Preexisting lamina horizontalization at the cranial fusion segment seems to affect ASD, and coexistence of lamina horizontalization and facet tropism seems to accelerate ASD after PLIF.

Monoclonal antibody to parathyroid hormone-related protein induces differentiation and apoptosis of chondrosarcoma cells.

We investigated the effects of treatment with anti-parathyroid hormone-related protein (1-34) monoclonal murine antibody (anti-PTHrP MoAb) on apoptosis and the differentiation of chondrosarcoma HTB-94 cells. Treatment with anti-PTHrP MoAb accelerated apoptosis of HTB-94 cells in a dose-dependent manner, and anti-PTHrP MoAb also promoted the chondrogenic differentiation of HTB-94 cells. The induction of apoptosis by anti-PTHrP MoAb via imbalance of Bcl-2/Bax ratio and activation of caspase-3 may provide a mechanistic explanation for its potential antitumor effects. Our results suggest the possibility that anti-PTHrP MoAb may be beneficial as a new treatment for chondrosarcoma.

Mechanical stress-induced apoptosis of endplate chondrocytes in organ-cultured mouse intervertebral discs: an ex vivo study.

STUDY DESIGN: Various amounts of static mechanical load were applied to mouse intervertebral discs in organ cultures. The apoptosis then was examined using nick end labeling. Two mitogen-activated protein kinase (MAPK) inhibitors were added to the medium. OBJECTIVES: To establish an experimental model for detecting factors regulating chondrocyte apoptosis induced by mechanical stress, and to determine the role of MAPK and p38 in the stress-induced apoptotic pathway of endplate chondrocytes. SUMMARY OF BACKGROUND DATA: The cause of degenerative change in the cartilaginous endplate (CEP) remains unclear. The authors' previous findings using a mouse model suggested that apoptosis in the cartilaginous endplate may play a role in intervertebral disc degeneration, and that mechanical stress may induce apoptosis. If apoptosis of endplate chondrocytes is involved in the cascade of intervertebral disc degeneration, then how apoptosis is induced by mechanical stress should be important in preventing disc degeneration. However, the mechanism of apoptosis induced by mechanical stress remains unclear. METHODS: Mouse coccygeal discs were harvested and organ cultured. Various static compression loads (0, 0.2, 0.4, 0.8, and 1.0 MPa) were applied on intervertebral discs placed in culture bottles for 24 hours. Paraffin-embedded sections of the harvested discs were stained using Safranin-O and the nick end labeling procedure. The apoptotic cells were counted in the cartilaginous endplate and junctional anulus fibrosus of each intervertebral disc. In addition, U0126 (MAPK inhibitor) and SB202190 (p38 inhibitor) were added to the culture medium to determine their regulatory roles in the apoptosis of endplate chondrocytes induced by mechanical load. RESULTS: Histologically, loaded discs became bulged, and the disc space became narrow. Apoptosis was absent in discs without load, but was particularly noticeable in loaded discs (load weight, 1.0 MPa). The number of apoptotic cells increased depending on the weight of the load. The two MAPK inhibitors significantly increased the number of apoptotic cells. CONCLUSIONS: Chondrocyte apoptosis was induced using a static mechanical load especially in the cartilaginous endplate in an organ culture. Apoptosis occurred similarly to previous findings using an in vivo model. This culture system thus reflected the apoptosis demonstrated in vivo. Because biologically active reagents such as MAPK inhibitors can be simply added to culture media, this system may be a useful method for detecting factors that influence apoptosis induced by mechanical stress. Both MAPK inhibitors increased the occurrence of apoptosis. This suggests that these two MAPKs can counteract the apoptotic pathway induced by mechanical stress.

Open treatment of syndactyly of the foot.

The aim of reconstruction of the webs for syndactyly of the foot is cosmetic improvement, so skin grafting should be avoided. We present our long-term results of 19 feet with simple cutaneous syndactyly in 15 patients who were treated by an open technique. The bottom of the web was covered with a dorsal rectangular flap and the remaining skin defect was left open to epithelialise spontaneously. This took about 4 weeks. After a mean follow-up of 5.7 years (range 3-9), no hypertrophic scar or pigmentation of the skin had developed. Creeping of the web was seen only during the first postoperative year. The final depth of the web satisfied the families of all patients. As the aim of web reconstruction for syndactyly of the foot is purely cosmetic, we conclude that this simple method is reasonable treatment.

Distribution of genes for parathyroid hormone (PTH)-related peptide, Indian hedgehog, PTH receptor and patched in the process of experimental spondylosis in mice.

OBJECT: Little is known about the molecular mechanisms underlying the process of spondylosis. The authors determined the extent of genetic localization of major regulators of chondrogenesis such as Indian hedgehog (Ihh) and parathyroid hormone (PTH)-related peptide (PTHrP) and their receptors during the development of spondylosis in their previously established experimental mouse model. METHODS: Experimental spondylosis was induced in 5-week-old ICR mice. The cervical spines were chronologically harvested, and histological sections were prepared. Messenger (m) RNA for PTHrP, Ihh, PTH receptor (PTHR; a receptor for PTHrP), patched (Ptc; a receptor for Ihh), bone morphogenetic protein (BMP)-6, and collagen type X (COL10; a marker for mature chondrocyte) was localized in the tissue sections by performing in situ hybridization. In the early stage, mRNA for COL10, Ihh, and BMP-6 was absent; however, mRNA for PTHrP, PTHR, and Ptc was detected in the anterior margin of the cervical discs. In the late stage, evidence of COL10 mRNA began to be detected, and transcripts for Ihh, PTHrP, and BMP-6 were localized in hypertrophic chondrocytes adjacent to the bone-forming area in osteophyte. Messenger RNA for Ptc and PTHR continued to localize at this stage. In control mice, expression of these genes was absent. CONCLUSIONS: The localization of PTHrP, Ihh, BMP-6, and the receptors PTHR and Ptc demonstrated in the present experimental model indicates the possible involvement of molecular signaling by PTHrP (through the PTHR), Ihh (through the Ptc), and BMP-6 in the regulation of chondrocyte maturation leading to endochondral ossification in spondylosis.