ObjectivesEvidence comparing the effectiveness of surgical and conservative treatment of symptomatic lumbar disc herniation is controversial. We sought to compare short-term and long-term effectiveness of surgical and conservative treatment in sciatica symptom severity and quality of life in patients with lumbar disc herniation in a routine clinical setting.MethodsA prospective cohort study of a routine clinical practice registry consisting of 370 patients. Outcome measures were the North American Spine Society questionnaire and the 36-Item Short-Form Health Survey to assess patient-reported back pain, physical function, neurogenic symptoms and quality of life. Primary outcomes were back pain at 6 and 12 weeks. Standard open discectomy was assessed versus conservative interventions at 6, 12, 52 and 104 weeks. We filled in missing outcome variable values with multiple imputation, accounted for repeated measures within patients with mixed-effects models and adjusted baseline group differences in relevant prognostic indicators by inverse probability of treatment weighting.ResultsSurgical treatment patients reported less back pain at 6 weeks than those receiving conservative therapy (−0.97; 95% CI −1.89 to −0.09), were more likely to report ≥50% decrease in back pain symptoms from baseline to 6 weeks (48% vs 17%, risk difference: 0.34; 95% CI 0.16 to 0.47) and reported less physical function disability at 52 weeks (−3.7; 95% CI −7.4 to −0.1). The other assessments showed minimal between-group differences with CIs, including the null effect.ConclusionsCompared with conservative therapy, surgical treatment provided faster relief from back pain symptoms in patients with lumbar disc herniation, but did not show a benefit over conservative treatment in midterm and long-term follow-up.

Repetitive mass tissue depolarizations accompanied a negative course of hemorrhagic lesion progression in the presence of ischemic conditions after traumatic brain injury. Whether as cause or effect, CSD may represent an inherent component of progressive metabolic failure leading to tissue death, and temperature appears to be an important factor influencing their occurrence. Continuous ECoG is a valuable tool for monitoring subclinical events such as CSD and seizures and for translational research in acute brain injury mechanisms and therapeutics.

Multipotent neural stem/progenitor cells (NS/NPCs) that are capable of generating neurons and glia offer enormous potential for treating neurological diseases. Adult NS/NPCs that reside in the mature mammalian brain can be isolated and expanded in vitro, and could be a potential source for autologous transplantation to replace cells lost to brain injury or disease. When these cells are transplanted into the normal brain, they can survive and become region-specific cells. However, it has not been reported whether these cells can survive for an extended period and become functional cells in an injured heterotypic environment. In this study, we tested survival, maturation fate, and electrophysiological properties of adult NS/NPCs after transplantation into the injured rat brain. NS/NPCs were isolated from the subventricular zone of adult Fisher 344 rats and cultured as a monolayer. Recipient adult Fisher 344 rats were first subjected to a moderate fluid percussive injury. Two days later, cultured NS/NPCs were injected into the injured brain in an area between the white matter tracts and peri-cortical region directly underneath the injury impact. The animals were sacrificed 2 or 4 weeks after transplantation for immunohistochemical staining or patch-clamp recording. We found that transplanted cells survived well at 2 and 4 weeks. Many cells migrated out of the injection site into surrounding areas expressing astrocyte or oligodendrocyte markers. Whole cell patch-clamp recording at 4 weeks showed that transplanted cells possessed typical mature glial cell properties. These data demonstrate that adult NS/NPCs can survive in an injured heterotypic environment for an extended period and become functional cells.

Following severe traumatic brain injury (TBI), increasing oxygen delivery to the brain has been advocated as a useful strategy to reverse mitochondrial dysfunction and improve neurological outcome. However, this might also promote overproduction of free radicals, responsible for lipid peroxidation and hence brain cell damage. Therefore, a method for monitoring this potential adverse effect in humans is desirable. Glycerol, an end product of phospholipid breakdown, easily detectable in the human brain by means of microdialysis, might represent a reliable indicator of free radical-induced cell membrane damage. Brain microdialysates were collected from 24 adult male Sprague-Dawley rats over a 3-hour period following sham operation (n=6), chemical brain injury via administration of Fenton's reagent (n=6), a powerful hydroxyl radical generator, and lateral fluid percussion injury (FPI; n=12). In the FPI animals, post-traumatic i.v. administration of either normal saline or the free radical scavenger Tempol (10 mg/kg, followed by an infusion of 30 mg/kg/h over 3 h) was carried out to evaluate the effect of blockade of free radical generation. Samples were analyzed for the presence of glycerol and the marker of hydroxyl radical (OH.) by generation of 2,3-DHBA (dihydroxybenzoic acid). Brain tissue staining with TTC (2,3,5-triphenyltetrazoium chloride) was performed for lesion size assessment. Rats subjected to either Fenton's reagent administration or FPI exhibited significantly higher levels of glycerol as compared with shams (p=0.05). However, when the FPI was followed by Tempol administration, concentration of both glycerol and 2,3-DHBA decreased significantly (p=0.05). Furthermore, TCC staining revealed a significant reduction of secondary brain tissue damage in Tempol-treated animals (p=0.05). Our data suggest that injury-induced increases in microdialysate glycerol levels are a valid indicator of free radical activity, and their amelioration following Tempol treatment accords with less histological damage in response to FPI.

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