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Owing to failure to achieve positive long-term effects, the currently performed treatment methods for lumbar facet joint syndrome (LFJS) are still under debate. Interspinous distraction devices unload the facet joints. Thus, these devices might be an alternative surgical treatment method for LFJS. The aim of this study was to evaluate the clinical and radiological outcome of an interspinous distraction device for the treatment of LFJS. Subjects had verified single level LFJS at level L4-5. They received percutaneous facet joint denervation (PFJD). If pain persisted, they were offered implantation of an interspinous device (Coflex) and/or repeat PFJD. Clinical and radiological outcome was determined before and after PFJD or surgery up to 2 years afterwards in all cases. Forty-one patients with LFJS at L4-5 underwent PFJD. Twenty patients with persisting pain underwent a subsequent surgery for implantation of an interspinous device. Five patients with recurrent pain at 6-12 months opted for an additional PFJD. Three obese patients (body weight > 100 kg) had persistent pain at 3 months after surgery and received additionally dorsal semi-dynamic stabilization. The clinical outcome improved significantly in the surgically treated patients; however, it did not differ compared with patients receiving PFJD only after 24 months.Radiological evaluation revealed a restricted range of motion (ROM) of the operated and an elevated ROM of the adjacent segment. Surgical or device-related complications were not observed. In conclusions, the implantation of an interspinous Coflex device in case of recurrent facet joint pain succeeds to improve facet joint pain in clinical shortand mid-term settings. However, it does not exceed the outcome of denervated patients. [ABSTRACT FROM AUTHOR]

In posterior lumbar interbody fusion, cage migrations and lower fusion rates compared to autologous bone graft used in the anterior lumbar interbody fusion procedure are documented. Anatomical and biomechanical data have shown that the cage positioning and cage type seem to play an important role. Therefore, the aim of the present study was to evaluate the impact of cage positioning and cage type on cage migration and fusion. We created a grid system for the endplates to analyze different cage positions. To analyze the influence of the cage type, we compared "closed" box titanium cages with "open" box titanium cages. This study included 40 patients with 80 implanted cages. After pedicle screw fixation, 23 patients were treated with a "closed box" cage and 17 patients with an "open box" cage. The follow-up period averaged 25 months. Twenty cages (25%) showed a migration into one vertebral endplate of <3 mm and four cages (5%) showed a migration of > or =3 mm. Cage migration was highest in the medio-medial position (84.6%), followed by the postero-lateral (42.9%), and the postero-medial (16%) cage position. Closed box cages had a significantly higher migration rate than open box cages, but fusion rates did not differ. In conclusion, cage positioning and cage type influence cage migration. The medio-medial cage position showed the highest migration rate. Regarding the cage type, open box cages seem to be associated with lower migration rates compared to closed box cages. However, the cage type did not influence bone fusion. [ABSTRACT FROM AUTHOR]

Degeneration of the intervertebral disc is the most common cause of lower back pain. Interestingly, all available treatments are limited to treat the symptoms and not the underlying biologic alterations of the disc. Freeze-dried resorbable non-woven polyglycolic acid (PGA) - hyaluronan implants were used in a degenerated disc disease (DDD) model in New Zealand white rabbits. The constructs were immersed in allogenic serum and implanted into the disc defect. Animals with discectomy only served as controls. The T2-weighted/fat suppression sequence signal intensity of the operated discs as assessed by magnet resonance imaging decreased in both groups one week after the operation compared to a healthy disc. After 12 months the implanted group showed an increase of 51% in the signal intensity compared to the 1-week results whereas the signal intensity in the sham group remained on the same level from one week to 12 months. Histological and quantitative immunohistochemical examination after 12 months indicated cell migration into the defect and showed formation of disc repair tissue. In controls, repair tissue containing type II collagen was not evident. In conclusion, the implantation of polymer-based constructs after discectomy induces tissue regeneration resulting in improvement of the disc water content., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Object: A variety of anterior, posterior, and combined approaches exist to decompress the spinal cord, restore sagittal alignment, and avoid kyphosis, but the optimal surgical strategy remains controversial. The authors compared the anterior and posterior approach used to treat multilevel cervical spondylotic myelopathy (CSM), focusing on sagittal alignment and clinical outcome., Methods: The authors studied 48 patients with CSM who underwent multilevel decompressive surgery using an anterior or posterior approach with instrumentation (24 patients in each group), depending on preoperative sagittal alignment and direction of spinal cord compression. In the anterior group, a 1-2-level corpectomy was followed by placement of an expandable titanium cage. In the posterior group, a multilevel laminectomy and posterior instrumentation using lateral mass screws was performed. Postoperative radiography and clinical examinations were performed after 1 week, 12 months, and at last follow-up (range 15-112 months, mean 33 months). The radiological outcome was evaluated using measurement of the cervical and segmental lordosis., Results: Both the posterior multilevel laminectomy (with instrumentation) and the anterior cervical corpectomy (with instrumentation) improved clinical outcome. The anterior group had a significantly lower preoperative cervical and segmental lordosis than the posterior group. The cervical and segmental lordosis improved in the anterior group by 8.8 and 6.2 degrees, respectively, and declined in the posterior group by 6.5 and 3.8 degrees, respectively. The loss of correction was higher in the anterior than in the posterior group (-2.0 vs -0.7 degrees, respectively) at last follow-up., Conclusions: These results demonstrate that both anterior and posterior decompression (with instrumentation) are effective procedures to improve the neurological outcome of patients with CSM. However, sagittal alignment may be better restored using the anterior approach, but harbors a higher rate of loss of correction. In cases involving a preexisting cervical kyphosis, an anterior or combined approach might be necessary to restore the lordotic cervical alignment.

Recent data suggest that ubiquitin has anti-inflammatory properties and therapeutic potential after severe trauma and brain injuries. However, direct evidence for its neuroprotective effects has not yet been provided. We hypothesized that ubiquitin treatment is neuroprotective, and thus reduces brain edema formation and cortical contusion volume after closed traumatic brain injuries. To test this hypothesis, a focal cortical contusion was induced using a controlled cortical impact (CCI) model in Sprague-Dawley rats. Animals (n = 27) were randomized to either 1.5 mg/kg ubiquitin or vehicle (placebo) intravenously within 5 min after CCI. Blood pressure, arterial blood gases (ABG) and intracranial pressure (ICP) were monitored. Ubiquitin serum and cerebrospinal fluid levels were measured by ELISA. Brain water content was quantified gravimetrically after 24 h and cerebral contusion volume was determined in triphenyltetrazolium-chloride stained brains after 7 days. All animals recovered to normal activity. ICP and cerebral perfusion pressures were normal at the end of the observation period. Ubiquitin serum and CSF levels at 24 h and 7 days after CCI were similar in both groups. With ubiquitin brain water content of the injured hemisphere was slightly lower (n = 6/group; 79.97 +/- 0.29% vs. 81.11 +/- 0.52%; p = 0.08). Cortical contusion volume was significantly lower with ubiquitin (n = 7-8/group; 32.88 +/- 2.1 mm(3) vs. 43.96 +/- 4.56 mm(3); p = 0.025). This study shows that ubiquitin treatment after brain injury has direct neuroprotective effects, as demonstrated by improved brain morphology 7 days after brain injury. In connection with its beneficial effects in our previous studies, these data suggest ubiquitin as a promising candidate protein therapeutic for the treatment of brain injuries.

Objective: Intra-operative movements due to mechanical ventilation or manipulations are a limiting factor for accurate spinal navigation or robotic-assisted spinal surgery. The purpose of this study was to assess the accuracy of an intra-operative spinal fixation device in an experimental setup., Materials and Methods: We developed a fixation device, attached to the operating table, that combines soft tissue retraction with spinal process fixation. Using a lumbar spine cadaver, tightness of fixation was evaluated using two measurement systems. Accuracy measurements using changes in spatial co-ordinates of implanted reference markers were performed in three segments, following different manipulations of the spine. In addition, for intra-operative movements of the spine during mechanical ventilation, the range of motion was determined in 10 patients during lumbar interbody fusion., Results: The spine frame was easy to use and did not restrict screw insertion. Mean deviations of the markers' in all segments were measured at between 0.35 and 0.8 mm, following pedicle screw insertion and lateral traction. Intra-operative range of motion of the spine was measured with a mean value of 8.7 +/- 3.3 mm., Conclusion: Using our spine frame, a rigid fixation following manipulation of the spine was demonstrated. By overcoming the intra-operative movement-dependent inaccuracy, safety in navigated spine surgery and robotic-assisted procedures might be improved.

Background: Degenerative spondylolisthesis of the cervical spine is rare. Patients show signs of progredient myelopathy, radiculopathy and pain. Treatment strategies include ventral, dorsal and combined fusion techniques with or without repositioning and decompression., Methods: In this study, we present 16 patients with degenerative cervical spondylolisthesis. The leading symptom was severe myelopathy in 8 patients, radiculomyelopathy in 5 patients and neck pain in 3 patients. However, neck pain was the initial symptom in all the patients and decreased when neurological symptoms became more evident. Radiographic examinations included plain radiography, MRI, CT, myelography and lateral tomography., Results: Spondylolisthesis was located five times at level C3/4, C4/5 and C5/6. In three cases spondylolisthesis was located at level C7/T1. There were two patients with spondylolisthesis on two levels. Instability could be demonstrated by flexion/extension radiography in five cases. Patients were divided into three groups according to a newly introduced classification system. The surgical approach corresponded to this classification. In ten patients the spondylolisthesis could be corrected by extension and positioning, so discectomy and fusion on one or two levels with cage, plate and screws was sufficient. In five cases a corpectomy was necessary due to severe spondylosis. In one case a combined approach with dorsal decompression and release followed by ventral fusion was applied due to additional dorsal spinal cord compression. The follow-up period was 6-52 months. After surgery, none of the patients showed any signs of neurological deterioration. In all cases, a stable fusion was achieved with no signs of instability on flexion/extension radiographs. Neurological improvement was seen in 6 of 8 patients with myelopathy and 4 of 5 patients with radiculomyelopathy. The others showed stable disease. Pain relief was seen in all patients who complained of pain preoperatively., Conclusion: The aims of treatment for cervical spondylolisthesis are spinal cord decompression (ventral, dorsal or both), correction and fusion. The used procedure should depend on the severity of the cervical deformity, degree and side of the spinal cord compression, and the possibility of correction by extension and positioning.

Background: Gliosis is a characteristic pathology in many central nervous system (CNS) diseases. Cytokines are considered to be effectors of gliosis. It has been shown that pro-inflammatory cytokines such as interleukin (IL)-1 and IL-6 boost glia scar formation. On the other hand, anti-inflammatory cytokines, such as IL-10 and IL-1 receptor antagonist (ra), can act neuroprotectively. Furthermore, various immune mediators and neurotransmitters can modulate the onset of gliosis., Material/methods: We used 100 male Sprague-Dawley rats to investigate the mechanisms of brain-cytokine-induced astrogliosis using an in vivo model of convection-enhanced delivery of cytokines (IL-beta, IL-6, tumor necrosis factor (TNF)-alpha) into the cerebro-ventricular system. The protective effects of the anti-inflammatory cytokine IL-10 and the neurotransmitter propranolol were also investigated., Results: With this paradigm, we could clearly demonstrate that IL-6 is a key cytokine mediating astrogliosis, noticeable in the increased expression of glial fibrillary acidic protein (GFAP). Thus intra-cerebroventricular infusion of IL-6 increased GFAP expression in a dose-dependent manner. Furthermore, GFAP expression was also increased by IL-beta, which correspondingly triggered an IL-6 release into the CSF. Accordingly, TNF-alpha, which did not induce IL-6 release, also did not induce gliosis. On the other hand, substances which decrease IL-beta-induced IL-6 production, such as propranolol and IL-10, also dramatically decreased IL-beta triggered gliosis., Conclusions: IL-6 infusion, as well as IL-beta-induced IL-6 release into the CSF, increase GFAP expression in the cerebral cortex and hippocampus. Accordingly, blockade of the IL-beta-induced IL-6 release by IL-10 and propranolol decreases GFAP expression.

Although intracranial hemorrhage has frequently been found responsible for mortality in adult patients with Alagille syndrome (AGS), no specific underlying cause has been identified. We describe the case of severe subarachnoid hemorrhage in a 30-year-old woman harboring five intracranial aneurysms and multiple peripheral vascular anomalies. To evaluate a possible higher incidence of intracranial aneurysms, a study of the cerebral vasculature in all AGS patients by using noninvasive imaging techniques should be considered.

Background: Significantly increased plasma and CSF IL-6 levels reflect underlying tissue damage following clinical and experimental traumatic brain injury (TBI). Catecholamines, used under clinical conditions to maintain adequate cerebral perfusion pressure, induce a sustained IL-6 release. Thus an additional elevation in IL-6 could aggravate brain edema in the acute posttraumatic phase. We studied the changes in plasma and cerebrospinal fluid (CSF) IL-6 levels 4 and 24 hours after experimental TBI and assessed possible time-dependent effects of norepinephrine infusion on IL-6 and brain edema., Material/methods: Paired plasma and CSF IL-6 measured at 4 and 24 hours following TBI (n=10) were compared to levels in non-traumatized rats (n=5). In a placebo-controlled trial, 20 brain-injured male Sprague-Dawley rats were randomized to receive norepinephrine or NaCl for 90 minutes at 4 or 24 hours after TBI. Plasma IL-6 was measured before, during, and after the infusion period. One hour after stopping the infusion, CSF IL-6 and hemispheric swelling were determined., Results: During the first posttraumatic day, plasma and CSF IL-6 levels were significantly increased compared to non-traumatized rats, reaching the highest values at 24 hours (p<0.05). Norepinephrine infusion significantly increased plasma IL-6 at 7 and 27 hours after TBI; IL-6 was significantly elevated in CSF only at 7 hours (p<0.05). Brain edema was not aggravated., Conclusions: The norepinephrine-induced increase in plasma and CSF IL-6 suggests that concomitant norepinephrine administration needs to be considered when interpreting systemic and local changes in IL-6 levels in TBI patients.

Overwhelming inflammatory immune response can result in systemic inflammation and septic shock. To prevent excessive and deleterious action of proinflammatory cytokines after they have produced their initial beneficial effects, the immune system can release several anti-inflammatory mediators, including interleukin-10, interleukin-1 receptor antagonist, and soluble tumor necrosis factor receptors, thus initiating a compensatory anti-inflammatory response syndrome. However, in vivo the delicate balance between pro- and anti-inflammatory responses is additionally controlled by the central nervous system. Therefore, proinflammatory cytokines stimulate the hypothalamic-pituitary-adrenal axis and enhance sympathetic nerve system activity. The mediators of these neuroimmune pathways can again suppress immune cell functions to control systemic inflammation. The question is, however, what happens if the immunoinhibitory CNS pathways are activated without systemic inflammation? This can result from production of cytokines in the brain following infection, injury, or ischemia or in response to various stressors (e.g., life events, depression, anxiety) or directly from brainstem irritation. The answer is that this may generate a brain-mediated immunodepression. Many animal and clinical studies have demonstrated a stress and brain cytokine mediated decrease in the cellular immune response at the lymphocyte level. More recently, the importance of monocytes in systemic immunocapacity has been shown. Monocytic inactivation with decreased capability of antigen presentation and depressed secretion of proinflammatory cytokines increases the risk of infectious complications. Interestingly, cytokines in the brain and other stressors can also generate systemic immunodepression at the monocyte level. In this scenario the catecholamine-induced release of the potent anti-inflammatory cytokine interleukin-10 is a newly discovered mechanism of the brain-mediated monocyte deactivation in addition to the "well known" immunosuppressive action of glucocorticoids. Furthermore, other neuropeptides such as alpha-melanocyte-stimulating hormone and beta-endorphin which can be released in stressful situations have also inhibitory effects on immune cells. Thus mediators of the CNS are implicated in the regulation of immune functions and may play a role in both conditioning the host's response to endogenous or exogenous stimuli and generating a "brain-mediated" immunodepression.

The mechanism of immunodepression after brain injury is not yet clear. Here we demonstrate rapid systemic release of the immunoinhibitory cytokine interleukin-10, monocytic deactivation and a high incidence of infection in patients with 'sympathetic storm' due to acute accidental or iatrogenic brain trauma. In vitro studies showed that within minutes catecholamines trigger the secretion of interleukin-10 from unstimulated monocytes through a beta-adrenoreceptor-mediated, cAMP/protein kinase A-dependent pathway. We found that in a rat model of acute brain injury, the beta-receptor antagonist propranolol prevented the increase of interleukin-10 plasma levels. Rapid monocytic interleukin-10 release after sympathetic activation may represent a common pathway for immunodepression induced by stress and injury.