A Retrospective Case Series of a Novel Spinal Cord Stimulator Trial Technique with Less Displacement and Migration of the Trial Leads.

Background: Spinal cord stimulation is an established treatment option for certain chronic pain conditions which have been previously unresponsive to conservative therapies or potentially for a subset of patients who have not improved following spine surgery. Prior to permanent lead implantation, stimulator lead trials are performed to ensure adequate patient benefit. During these trials, one of the most common complications and reasons for failure is the displacement and migration of the trial leads, resulting in lost therapeutic coverage. Other complications include infection and dislodged bulky dressings. There is a paucity of literature describing an adequate procedural method to prevent these common complications. Objective: This study utilizes a series of 19 patients to evaluate a new technique for securing percutaneous spinal cord simulator trial leads, which may minimize dislodgement and migration complications and improve the rate of trial success. Study Design: Retrospective case series. Setting: New Jersey Medical School, Department of Anesthesiology, Pain Management Division. Methods: A retrospective chart review was conducted on 19 consecutive patients undergoing placement of the percutaneous thoracic spinal cord stimulator trial leads for pain associated with lumbar spine pathology over a two-year period (2010-2012). Results: Of the 19 patients in our cohort, there was one trial lead displacement, no lead migrations, and no site infections. Thirteen patients went on to permanent lead implantation. This improved trial lead placement technique had a high success rate with a low number of complications. Limitations: Small sample size, retrospective case series, and no control group for comparison. Conclusion: This case series was able to demonstrate that our described novel spinal cord stimulator trial lead placement and dressing technique can decrease the incidence of lead displacement and migration, thus improving trial success.

Neural HO-1/sterol interactions in vivo: implications for Alzheimer's disease.

BACKGROUND: Up-regulation of heme oxygenase-1 (HO-1) and altered cholesterol (CH) metabolism are characteristic of Alzheimer-diseased (AD) neural tissues. We previously provided evidence of significant HO-1/sterol interactions in vitro (cultured rat astroglia) and in post-mortem human AD brain (Religious Orders Study). METHODS: The current experiments were designed to further delineate these interactions in vivo by comparing the behavior of HO-1/sterol interactions in two mouse models; (1) a novel HO-1 transgenic mouse (GFAP.HMOX1) engineered to selectively express human HO-1 in the astrocytic compartment and (2) the previously described triple transgenic AD mouse (3xTg-AD). In samples of frontal cortex, total CH, CH precursors and relevant oxysterols were quantified by gas chromatography-mass spectrometry (GC-MS) and HO-1 protein expression was assessed by ELISA. The relationships of HO-1 expression to total CH, CH precursors and total oxysterols were determined for both mouse models using linear regression analysis. RESULTS: HO-1 expression is increased in GFAP.HMOX1 mice relative to wild type and in 11-12-month-old 3xTg-AD mice (with AD-like phenotype) relative to control mice and 5-6-month-old 3xTg-AD mice (no AD-like phenotype). Total oxysterols significantly decreased as HO-1 expression increased in GFAP.HMOX1 mice expressing high levels of HO-1, whereas total oxysterols increased as HO-1 expression increased in aged 3xTg-AD mice. Total CH and total CH precursors increased as HO-1 protein expression increased in 11-12-month-old 3xTg-AD mice relative to 5-6-month old 3xTg-AD mice. CONCLUSIONS: Our findings indicate a differential impact of HO-1 on patterns of brain sterol and redox homeostasis that is contingent on the presence or absence of AD-like neuropathology. These data provide fresh insight concerning the regulation of sterol homeostasis within the aging and degenerating CNS which may inform the development of novel therapeutic and preventive strategies for the management of AD and related conditions.