Endoleaks following endovascular repair of abdominal aortic aneurysm: the predictive value of preoperative anatomic factors--a review of 100 cases.
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OBJECTIVE: The failure to maintain a secure exclusion of aortic aneurysms with intraluminally placed grafts has been termed endoleak. We performed a retrospective review of our first 100 transluminally repaired abdominal aortic aneurysms (AAAs) in an effort to identify preoperative factors that could predict which patients would have endoleaks. METHODS: Between February 1993 and September 1998, 100 infrarenal aneurysms were treated with tube (39), bifurcated (45), and aortoiliac grafts (16). Endoleaks (early and late) developed in 34 patients. Preoperative computed tomography scans and angiograms for all patients were individually inspected by a single reviewer. Aortic characteristics analyzed included number of patent lumbar arteries, presence of a patent inferior mesenteric artery (IMA), calcification and thrombus at proximal and distal attachment sites, proximal aortic angulation, and graft-vessel size discrepancy at proximal and distal attachment sites. The prevalence of the preoperative factors was compared among patients with and without endoleaks. RESULTS: Endoleaks developed in 44% of tube, 33% of bifurcated, and 47% of aortoiliac grafts (P =.51). Correlation between total number of patent lumbar arteries, presence of a patent IMA, and endoleaks was not significant (P =.44,.95). Calcification at either proximal or distal attachment site did not increase the risk of endoleaks (P =.50,.62). The presence of thrombus at the attachment site (proximally or distally) also failed to increase endoleak rates (P =.12,.78). Degree of proximal aortic angulation did not differ between groups (P =.39). Size discrepancies between graft and aorta or iliac vessels at proximal or distal sites did not significantly differ (P >.54, >.13). Subgroup analysis of endoleaks with different tube types also failed to demonstrate significant differences among the three graft types (P >.05). CONCLUSION: Endoleaks develop in a significant number of endovascularly repaired AAAs. We were unable to demonstrate a statistically significant association with anatomic characteristics thought to predispose to the development of endoleaks. We find no predictive value associated with these anatomic factors. (+info)
Intrathecal HIV-1 envelope glycoprotein gp120 induces enhanced pain states mediated by spinal cord proinflammatory cytokines.
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Perispinal (intrathecal) injection of the human immunodeficiency virus-1 (HIV-1) envelope glycoprotein gp120 creates exaggerated pain states. Decreases in response thresholds to both heat stimuli (thermal hyperalgesia) and light tactile stimuli (mechanical allodynia) are rapidly induced after gp120 administration. gp120 is the portion of HIV-1 that binds to and activates microglia and astrocytes. These glial cells have been proposed to be key mediators of gp120-induced hyperalgesia and allodynia because these pain changes are blocked by drugs thought to affect glial function preferentially. The aim of the present series of studies was to determine whether gp120-induced pain changes involve proinflammatory cytokines [interleukin-1beta (IL-1) and tumor necrosis factor-alpha (TNF-alpha)], substances released from activated glia. IL-1 and TNF antagonists each prevented gp120-induced pain changes. Intrathecal gp120 produced time-dependent, site-specific increases in TNF and IL-1 protein release into lumbosacral CSF; parallel cytokine increases in lumbar dorsal spinal cord were also observed. Intrathecal administration of fluorocitrate (a glial metabolic inhibitor), TNF antagonist, and IL-1 antagonist each blocked gp120-induced increases in spinal IL-1 protein. These results support the concept that activated glia in dorsal spinal cord can create exaggerated pain states via the release of proinflammatory cytokines. (+info)
Effects of three different training modalities on the cross sectional area of the lumbar multifidus muscle in patients with chronic low back pain.
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OBJECTIVES: To determine the effect of different training schedules on the cross sectional area (CSA) of the lumbar multifidus muscle in patients with chronic low back pain. METHODS: Each of 59 nine patients was randomly assigned to one of three programmes: 10 weeks of stabilisation training (group 1; n = 19); 10 weeks of stabilisation training combined with dynamic resistance training (group 2; n = 20); 10 weeks of stabilisation training combined with dynamic-static resistance training (group 3; n = 20). Before and after 10 weeks of training, multifidus CSAs were measured from standard computed tomography images at three different levels (upper end plate of L3 and L4, and lower end plate of L4). RESULTS: The CSA of the multifidus muscle was significantly increased at all levels after training in group 3. In contrast, no significant differences were found in groups 1 and 2. CONCLUSIONS: General stabilisation exercises and dynamic intensive lumbar resistance training have no significant effect on the CSA of the lumbar multifidus muscle in patients with chronic low back pain. The static holding component between the concentric and eccentric phase was found to be critical in inducing muscle hypertrophy during the first 10 weeks. Treatment consisting of stabilisation training combined with an intensive lumbar dynamic-static strengthening programme seems to be the most appropriate method of restoring the size of the multifidus muscle. (+info)
Sacral meningeal cyst associated with valve-like mechanism--case report.
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A 58-year-old woman presented with low back pain radiating to the lower extremities. Magnetic resonance imaging revealed a cystic lesion in the sacrum compressing the nerve roots. At operation, a valve-like communication was found between the subarachnoid space and the cyst cavity in the vicinity of the sacral nerve root. The communication was obliterated with a purse-string suture and reinforced with a free muscle graft. Postoperatively, she reported improvement of the pain. Valve-like communication between the cyst cavity and subarachnoid space can cause enlargement of spinal meningeal cyst, and could also explain enlargement of sacral meningeal cyst. Surgical obliteration of the communication rather than the cyst resection is more important for sacral meningeal cyst. (+info)
Blockade of endogenous neurotrophic factors prevents the androgenic rescue of rat spinal motoneurons.
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Target-derived neurotrophic factors are assumed to regulate motoneuron cell death during development but remain unspecified. Motoneuron cell death in the spinal nucleus of the bulbocavernosus (SNB) of rats extends postnatally and is controlled by androgens. We exploited these features of the SNB system to identify endogenously produced trophic factors regulating motoneuron survival. Newborn female rat pups were treated with the androgen, testosterone propionate, or the oil vehicle alone. In addition, females received trophic factor antagonists delivered either into the perineum (the site of SNB target muscles) or systemically. Fusion molecules that bind and sequester the neurotrophins (trkA-IgG, trkB-IgG, and trkC-IgG) were used to block activation of neurotrophin receptors, and AADH-CNTF was used to antagonize signaling through the ciliary neurotrophic factor receptor-alpha (CNTFRalpha). An acute blockade of trkB, trkC, or CNTFRalpha prevented the androgenic sparing of SNB motoneurons when antagonists were delivered to the perineum. Trophic factor antagonists did not significantly reduce SNB motoneuron number when higher doses were injected systemically. These findings demonstrate a requirement for specific, endogenously produced trophic factors in the androgenic rescue of SNB motoneurons and further suggest that trophic factor interactions at the perineum play a crucial role in masculinization of this neural system. (+info)
Brain-derived neurotrophic factor increases in the uninjured dorsal root ganglion neurons in selective spinal nerve ligation model.
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Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are two major members of the neurotrophin family. Using immunohistochemistry and in situ hybridization histochemistry, we examined the effect of L5 spinal nerve ligation (SPNL), a neuropathic pain model, on the expression of BDNF in the uninjured L4 dorsal root ganglion (DRG). After L5 SPNL, both immunoreactivity for BDNF and the hybridization intensity for BDNF mRNA increased mainly in the small- and medium-sized neurons. The percentage of BDNF mRNA-expressing neurons increased in the ipsilateral L4 DRG compared with the contralateral DRG from the third to 28th day after ligation. A significantly greater number of BDNF-immunoreactive neurons were observed in the ipsilateral L4 DRG than contralateral side 14 d after ligation. To test the contribution of BDNF to the thermal hyperalgesia produced in this model, we intrathecally injected anti-BDNF antibody at third day after ligation. This treatment clearly attenuated thermal hyperalgesia for a few hours. Almost all BDNF mRNA-expressing neurons coexpressed trkA, a high-affinity NGF receptor, mRNA. The percentage of BDNF mRNA-expressing cells of trkA cells significantly increased in the ipsilateral L4 DRG 14 d after ligation. Furthermore, we examined the contribution of NGF on this phenotypic change using ELISA, Northern blot analysis, and anti-NGF antibody. NGF content in the ipsilateral L4 DRG linearly increased and reached a statistical significant level 14 d after L5 SPNL. Moreover, at this time point, the increase in NGF mRNA was observed in the ipsilateral L5 DRG and sciatic nerve, but not in the ipsilateral L4 DRG or L4 spinal nerve. Local application of anti-NGF antibody to the L4 spinal nerve beside the L5 spinal nerve-ligation site prevented the development of thermal hyperalgesia for 5 d after ligation. Our data suggest that BDNF, which increased in the uninjured L4 DRG neurons, acts as a sensory neuromodulator in the dorsal horn and contributes to thermal hyperalgesia in this neuropathic pain model. The contribution of locally synthesized NGF to thermal hyperalgesia was also demonstrated. These dynamic alterations in the expression and content of BDNF and NGF in the uninjured DRG neurons might be involved in the pathomechanisms of neuropathic pain. (+info)
Developmental changes in galanin in lumbosacral sympathetic ganglionic neurons innervating the avian uterine oviduct and galanin induction by sex steroids.
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We recently found lumbosacral sympathetic ganglionic galanin neurons innervating the quail uterine oviduct. Galaninergic innervation of the uterine muscle may be essential for avian oviposition, as galanin evoked oviposition through a mechanism of induction of vigorous uterine contraction. The questions arising from these findings are: what changes occur in galanin expression in the sympathetic ganglionic galanin neuron during development, and what is the hormonal factor(s) that induces galanin expression in this neuron? Therefore, the present study examined the developmental changes in galanin of the quail sympathetic ganglionic neuron and uterus, and the effect of administration of ovarian sex steroids on galanin induction. Immature birds reared under long-day photoperiods from 4 weeks of age demonstrated progressive increases in galanin levels both per unit ganglionic protein (concentration) and per ganglia (content) concurrent with ganglionic development during weeks 4--13. The uterine galanin content and uterine weight also increased progressively during the same period, but the galanin concentration in the uterus at 4 weeks was high due to the much smaller tissue mass. Immunocytochemical analysis with anti-galanin serum showed that immunoreactive ganglionic cells were few and small at 4 weeks and increased progressively thereafter. Administration of oestradiol-17 beta to immature birds at 3 weeks of age for 1 week increased both the galanin concentration and content in the ganglia without ganglionic growth. A marked increase in galanin-immunoreactive ganglionic cells was detected following oestradiol treatment. In contrast, progesterone increased ganglionic galanin levels, but the effects were low. Expression of the mRNAs encoding oestrogen receptor-alpha and -beta (ER alpha and ER beta) in the ganglionic tissue was verified by RT-PCR/Southern blot analysis. Immunocytochemical staining with anti-ER serum further revealed an intense immunoreaction restricted to the nucleus of ganglionic neurons. These results suggest that ovarian sex steroids, in particular oestradiol-17 beta, contribute as hormonal factors to galanin induction, which takes place in the lumbosacral sympathetic ganglionic neurons innervating avian uterine oviduct during development. Oestradiol may act directly on this ganglionic neuron through intra-nuclear receptor-mediated mechanisms to induce galanin. (+info)
Hoxd10 induction and regionalization in the developing lumbosacral spinal cord.
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We have used Hoxd10 expression as a primary marker of the lumbosacral region to examine the early programming of regional characteristics within the posterior spinal cord of the chick embryo. Hoxd10 is uniquely expressed at a high level in the lumbosacral cord, from the earliest stages of motor column formation through stages of motoneuron axon outgrowth. To define the time period when this gene pattern is determined, we assessed Hoxd10 expression after transposition of lumbosacral and thoracic segments at early neural tube stages. We present evidence that there is an early prepattern for Hoxd10 expression in the lumbosacral neural tube; a prepattern that is established at or before stages of neural tube closure. Cells within more posterior lumbosacral segments have a greater ability to develop high level Hoxd10 expression than the most anterior lumbosacral segments or thoracic segments. During subsequent neural tube stages, this prepattern is amplified and stabilized by environmental signals such that all lumbosacral segments acquire the ability to develop high levels of Hoxd10, independent of their axial environment. Results from experiments in which posterior neural segments and/or paraxial mesoderm segments were placed at different axial levels suggest that signals setting Hoxd10 expression form a decreasing posterior-to-anterior gradient. Our experiments do not, however, implicate adjacent paraxial mesoderm as the only source of graded signals. We suggest, instead, that signals from more posterior embryonic regions influence Hoxd10 expression after the early establishment of a regional prepattern. Concurrent analyses of patterns of LIM proteins and motor column organization after experimental surgeries suggest that the programming of these characteristics follows similar rules. (+info)