[Show abstract][Hide abstract] ABSTRACT: Hemorrhage caused by spinal cord hemangioblastoma is rare, usually presenting as a subarachnoid hemorrhage. Intramedullary hemorrhage is an extremely rare manifestation of spinal cord hemangioblastoma.
Forty-year-old Japanese male patient presented with acute paraplegia. Magnetic resonance (MR) imaging of the spinal cord revealed intramedullary hemorrhage. An intramedullary mass lesion was detected at the 8th thoracic vertebral level (T8) in a gadolinium enhanced-MR image. Spinal angiography revealed an intramedullary tumor stain at the level of T8. Therefore we diagnosed the problem as intramedullary hemorrhage caused by the hemangioblastoma. One month after the onset, extirpation of the intramedullary hemangioblastoma was performed. The tumor was completely removed. Pathological findings revealed a typical hemangioblastoma. At his final follow-up visit, the patient showed no apparent neurological recovery.
Hemangioblastoma can be a cause of intramedullary hemorrhage should be considered in such cases.
[Show abstract][Hide abstract] ABSTRACT: Context We present a rare and interesting case of hemorrhagic lumbar facet cysts accompanying a spinal subdural hematoma at the same level suggesting a possible mechanism by which spinal subdural hematomas can arise. Findings A 71-year-old man presented with persistent sciatic pain and intermittent claudication. Magnetic resonance imaging demonstrated a multilocular mass lesion that showed high signal intensity in both T1- and T2-weighted images, and was located both inside and outside of the spinal canal. Computed tomographic myelography showed a cap-shaped block of the dural tube at L5 and computed tomography with L5-S facet arthrography demonstrated cystic masses. The patient was diagnosed with lumbar radiculopathy caused by hemorrhagic facet cysts, and then progressed to surgical treatment. Surgery revealed that the cysts contained blood clots, and intraoperative findings that the inside of the dural tube appeared blackish and that the dural tube was tensely ballooned after removal of the cysts led us to explorative durotomy. The durotomy demonstrated concentrated old blood pooling both in the dorsal and ventral subdural space, and these spaces were subsequently drained. After surgery, his sciatic pain and intermittent claudication resolved. There was no evidence of cyst mass recurrence at 2 years of follow-up. Conclusion We propose a newly described mechanism for the formation of spinal subdural hematomas. We recommend surgeons be alert to epidural lesions causing repeated acute compression of the dural tube, which can cause spinal subdural hematoma, and consider the possible coexistence of these lesions in diagnosis and strategic surgical decisions.
The journal of spinal cord medicine 06/2014; · 1.88 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Study Design. An open-labeled multicenter prospective non-randomized controlled clinical trialObjective. To confirm the feasibility of using granulocyte colony-stimulating factor (G-CSF) for treatment of acute spinal cord injury (SCI)Summary of Background Data. We previously reported that G-CSF promotes functional recovery after compression-induced spinal cord injury (SCI) in mice. Based on these findings, we conducted a multicenter prospective controlled clinical trial to assess the feasibility of G-CSF therapy for patients with acute SCI.Methods. The trial ran from August 2009 to March 2011, and included 41 SCI patients treated within 48 hours of onset. Informed consent was obtained from all patients. After providing consent, patients were divided into two groups. In the G-CSF group (17 patients), G-CSF (10 μg/kg/day) was intravenously administered for five consecutive days, and in the control group (24 patients), patients were similarly treated except for the G-CSF administration. We evaluated motor and sensory functions using the American Spinal Cord Injury Association (ASIA) score and ASIA impairment scale (AIS) at one week, three months, six months, and one year after onset.Results. Only two patients did not experience AIS improvement in the G-CSF group. In contrast, fifteen patients in the control group did not experience AIS improvement. In the analysis of increased ASIA motor score, a significant increase in G-CSF group was detected from one week after the administration compared to the control group. After that, some spontaneous increase of motor score was detected in control group, but the significant increase in G-CSF group was maintained until one year follow-up. Conclusion: Despite the limitation that patient selection was not randomized, the present results suggest the possibility that G-CSF administration has beneficial effects on neurological recovery in patients with acute SCI.
[Show abstract][Hide abstract] ABSTRACT: PURPOSE: Adjacent segment degeneration (ASD) is one of the major complications of lumbar fusion. Several previous retrospective studies reported ASD after PLIF. However, few reports evaluated whether decompression surgery combined with fusion surgery increases the rate of complications in adjacent segments. The purpose of the current study was to investigate the degeneration in decompressed adjacent segments after PLIF. METHODS: A total of 23 patients (12 men, 11 women; average age, 58.6) who underwent PLIF surgery [1 level (n = 9), 2 levels (n = 8), 3 levels (n = 4), 4 levels (n = 2)] were included. Additional adjacent decompression above or below the level of interbody fusion was performed at 25 levels and no adjacent decompression was performed at 15 levels. We retrospectively investigated ASD by X-ray films of all 40 adjacent segments (above and below fusion level) and clinical outcomes of all 23 cases. RESULTS: Of the 40 adjacent segments, 19 (47.5 %) showed ASD and 9 (22.5 %) showed symptomatic ASD. In the 19 segments with ASD, ASD occurred in 16 of 25 (64.0 %) segments at decompressed sites compared with 3 of 15 (20.0 %) non-decompressed sites. The ratio of ASD in adjacent segments was significantly higher at decompressed sites than at non-decompressed sites (p < 0.01). CONCLUSION: ASD occurs frequently in association with additional decompression above or below the level of PLIF. In cases in which the adjacent segments require decompression, a surgical strategy that preserves as much of the posterior complex as possible should be selected.
European Spine Journal 02/2013; · 2.47 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: An open-labeled multicenter prospective controlled clinical trial.
To confirm the feasibility of granulocyte colony-stimulating factor (G-CSF) administration for patients with thoracic myelopathy.
Although G-CSF is best known as an important cytokine commonly used to treat neutropenia, it also has nonhematopoietic functions. Previous experimental studies have shown that G-CSF can enhance tissue regeneration of several organs, such as the heart and the brain. We previously reported that G-CSF promotes functional recovery after spinal cord injury in rodents. On the basis of those findings, we started a clinical trial of neuroprotective therapy, using G-CSF for patients with worsening symptoms of thoracic myelopathy.
Patients whose Japanese Orthopaedic Association (JOA) score for thoracic myelopathy had decreased 2 points or more during a recent 1-month period were eligible for entry. After giving informed consent, patients were assigned to G-CSF and control groups. The G-CSF group (n = 10) received G-CSF 10 μg/kg per day intravenously for 5 consecutive days. The control group (n = 14) received similar treatments as the G-CSF group except for G-CSF administration. The primary outcome was JOA recovery rate at 1 month after G-CSF administration or initial treatment.
There was greater improvement in neurological functioning between baseline and 1-month follow-up in the G-CSF group (JOA recovery rate: 29.1 ± 20.5%) than in the control group (JOA recovery rate: 1.1 ± 4.2%) (P < 0.01). No serious adverse events occurred during or after the G-CSF administration.
The results provide evidence that G-CSF administration caused neurological recovery in patients with worsening symptoms of thoracic compression myelopathy.
[Show abstract][Hide abstract] ABSTRACT: Radial glial cells are neural stem cells (NSC) that are transiently found in the developing CNS. To study radial glia, we isolated clones following immortalization of E13.5 GFP rat neurospheres with v-myc. Clone RG3.6 exhibits polarized morphology and expresses the radial glial markers nestin and brain lipid binding protein. Both NSC and RG3.6 cells migrated extensively in the adult spinal cord. However, RG3.6 cells differentiated into astroglia slower than NSC, suggesting that immortalization can delay differentiation of radial glia. Following spinal cord contusion, implanted RG3.6 cells migrated widely in the contusion site and into spared white matter where they exhibited a highly polarized morphology. When injected immediately after injury, RG3.6 cells formed cellular bridges surrounding spinal cord lesion sites and extending into spared white matter regions in contrast to GFP fibroblasts that remained in the lesion site. Behavioral analysis indicated higher BBB scores in rats injected with RG3.6 cells than rats injected with fibroblasts or medium as early as 1 week after injury. Spinal cords transplanted with RG3.6 cells or dermal fibroblasts exhibited little accumulation of chondroitin sulfate proteoglycans (CSPG) including NG2 proteoglycans that are known to inhibit axonal growth. Reduced levels of CSPG were accompanied by little accumulation in the injury site of activated macrophages, which are a major source of CSPG. However, increased staining and organization of neurofilaments were found in injured rats transplanted with RG3.6 cells suggesting neuroprotection or regrowth. The combined results indicate that acutely transplanted radial glia can migrate to form bridges across spinal cord lesions in vivo and promote functional recovery following spinal cord injury by protecting against macrophages and secondary damage.
[Show abstract][Hide abstract] ABSTRACT: Neurotrophins have been shown to promote axonal regeneration, but the techniques available for delivering neurotrophins have limited effectiveness. The aim of this study was to evaluate the effect of adenovirus vector mediated gene transfer of brain-derived neurotrophic factor (BDNF) on axonal regeneration after spinal cord injury. We prepared adenovirus vectors encoding either beta-galactosidase (AxCALacZ) or BDNF (AxCABDNF). AxCALacZ was used to assess infection levels of the adenovirus BDNF produced by AxCABDNF was detected by Western blotting and its bioactivity was confirmed by bioassay. As a model of spinal cord injury, the rat spinal cord was completely transected at the T8 level. Immediately after transection, the vectors were injected into both stumps of the spinal cord. Axonal regeneration after transection was assessed by retrograde and anterograde tracing. In AxCALacZ-injected rats, adenovirus-infected cells were observed not only at the injected site but also in brainstem nuclei, as shown by LacZ expression. After the injection of the retrograde tracer fluorogold (FG) distal portion to the transection, AxCABDNF-injected rats showed FG-labeled neurons in the red nucleus. The anterograde tracer biotinylated dextran amine (BDA) injected into the red nucleus was also found in regenerating rubrospinal fibers distal to the transection. These tracing experiments demonstrated the regeneration of descending axons. In addition, rats of the AxCABDNF group showed significant locomotor recovery of hindlimb function, which was completely abolished by re-transection. These results indicate that the recovery was caused by regeneration of rubrospinal axons, not by simple enhancement of the central pattern generator.
Journal of Neurotrauma 04/2004; 21(3):329-37. · 3.97 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We evaluated the effect of brain-derived neurotrophic factor (BDNF) on cell death after spinal cord injury. A rat spinal cord injury model was produced by static load, and continuous intrathecal BDNF or vehicle infusion was carried out either immediately or 3 days after the injury. Cell death was examined by nuclear staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). After injury, typical apoptotic cells were observed. Double staining with TUNEL and specific cell markers revealed that, soon after the injury, the apoptotic or necrotic cells at the injury site were neurons and microglia. One week after the injury, apoptotic oligodendrocytes, but not apoptotic astrocytes, were observed in the white matter rostral and caudal to the injury site, whereas few apoptotic cells were found in the gray matter. The immediate BDNF treatment significantly reduced the number of TUNEL-positive cells in the adjacent rostral site 1 and 2 weeks after the injury, and in the adjacent caudal site 3 days and 1 week after the injury, even though there was no significant difference between BDNF-treated and control rats at the injury site itself. In addition, similar antiapoptotic effects were observed in these regions 1 week after injury in rats that received BDNF treatment from the third day after injury. These findings suggest that BDNF suppresses delayed apoptosis of oligodendrocytes after spinal cord injury, for which even delayed injections are effective. BDNF administration may therefore be useful for the clinical treatment of spinal cord injury through the suppression of secondary events.
Journal of Neurotrauma 07/2002; 19(6):777-85. · 3.97 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Neurotrophins enhance the survival of cells in the nervous system under both physiological and pathological conditions, such as those caused by disease or trauma. We recently demonstrated that expression of brain-derived neurotrophic factor (BDNF) was up-regulated in neurons and glia after compression-induced spinal cord injury (SCI). We show here the effects of BDNF on the oligodendrocyte survival and functional recovery after SCI. The effects of intrathecally administered BDNF on both Cu/Zn superoxide dismutase (CuZnSOD) and myelin basic protein (MBP) expression were examined using rats that had received compression-induced spinal cord injury. CuZnSOD expression in the spinal cord was down-regulated within 24 h of compression-induced injury and then recovered. Continuous infusion of BDNF inhibited the acute down-regulation of CuZnSOD expression. In situ hybridization showed that CuZnSOD was expressed in both neurons and glia. Although MBP expression was greatly reduced after injury, BDNF administration promoted the recovery of MBP expression nearly to a control level after 2 wk. Furthermore, BDNF administration also prompted behavioral recovery. These results suggest BDNF's usefulness in human clinical applications. The attenuation of CuZnSOD down-regulation may be related to a protective effect of BDNF and the promotion of MBP up-regulation may be related to a long-lasting restorative effect.
Journal of Neuropathology and Experimental Neurology 03/2002; 61(2):142-53. · 4.37 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Brain-derived neurotrophic factor (BDNF), a member of the nerve growth factor family of trophic factors, has multiple functions including a role in the promotion of neuronal survival and nerve fiber elongation in both the central and the peripheral nervous systems. We assessed the expression of endogenous BDNF following an experimentally induced compression injury to the spinal cord. Expression of BDNF mRNA was increased following the spinal cord injury; reaching maximum levels 24 h after the injury. Expression of BDNF mRNA returned to the levels observed in sham-operated control animals within 3 days of the injury. Using the in situ hybridization technique, we observed a wide distribution of BDNF expression among the different cell types in the spinal cord, including motor and sensory neurons, and in glia cells, including astrocytes. We also observed expression of BDNF in putative macrophages and/or microglia; however, this effect was not observed until day 7 following spinal cord injury. These results suggest that BDNF is synthesized in both neurons and astrocytes during the acute response to injury to the spinal cord, functioning in a mainly neuroprotective role. This is followed by a later phase of expression in which BDNF is produced by macrophages and/or microglia, apparently functioning in a restorative capacity.