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Background: Radiofrequency ablation (RFA) of the medial branches of the dorsal rami has been reported to relieve facet joint–related back pain for 6 months to 1 year in 60% of patients. Although providing benefit in a significant proportion of patients, there remains a group of patients who do not experience any pain relief from RFA or experience only benefit from the ablation for a short period. Failure of RFA has been attributed to technical failure of coagulating the nerve or coagulation of a minimal section of the nerve, allowing for early reinnervation. Increasing the success rate and duration of relief may require techniques that increase the likelihood of successful nerve ablation over a relevant distance by maximizing lesion size. Objectives: The aim of this technical note is to detail a modification to the current commonly used lumbar medial branch radiofrequency (RF) denervation approach to increase lesion size. Study Design: This is a technical report describing a novel two-needle approach to lumbar RF medial branch denervation. Setting: Large private interventional pain management institute. Methods: A dual needle placement of two 10-mm active tip RF cannulas separated by 6 mm is used to optimally contact the superior articular process (SAP) from its ventral to dorsal borders, which encompasses the anticipated course of the medial branch nerves. Results: The described technique creates a lesion that we estimate to be 11.0-mm wide and 11.6-mm long along the course of the medial branch adjacent to the SAP ensuring adequate coverage and treatment. Limitations: This report does not encompass a systematic evaluation of the clinical safety and efficacy of the two-needle RFA approach. Future studies will have to assess the longterm efficacy and safety of the approach. Conclusions: The detailed two-needle approach to lumbar RF medial branch denervation appears to be promising in terms of projected treatment success by coagulating a large volume of tissue, in a cost- and time-efficient manner. Key words: Radiofrequency ablation, RFA, lumbar, medial branch, facet joint, pain, rhizotomy

Item does not contain fulltext BACKGROUND: Dorsal root ganglion stimulation (DRG-S) has emerged as a treatment for complex regional pain syndrome (CRPS) of the lower extremities, and recent small studies are demonstrating its potential efficacy in pain syndromes that are traditionally considered nociceptive in nature, such as axial low back pain. While improvements in neuromodulation technology have been substantial over the past decade, with DRG-S systems patients occasionally require additional interventional pain treatments for treatment of pain from other sources. Radiofrequency ablation (RFA) of medial branch nerves innervating the facet joints is an accepted therapy for pain arising from the facet joints. METHODS: We describe 2 cases from the same practice where we observed similar phenomena while performing a 2-needle monopolar lumbar RFA in patients with a DRG-S system implanted with leads positioned bilaterally at the S1 DRGs. RESULTS: Initiation of RFA resulted in motor activation and discomfort in an S1 distribution in the legs in both individual cases. CONCLUSIONS: RFA can interfere with implanted DRG-S systems, resulting in overstimulation with motor recruitment. Specific anatomical considerations and device settings that may prevent interference are discussed.

Autism is a neurodevelopmental disorder characterized by impairments in social interaction, verbal communication and repetitive behaviors. To date the etiology of this disorder is poorly understood. Studies suggest that astrocytes play critical roles in neural plasticity by detecting neuronal activity and modulating neuronal networks. Recently, a number of studies suggested that an abnormal function of glia/astrocytes may be involved in the development of autism. However, there is yet no direct evidence showing how astrocytes develop in the brain of autistic individuals. Study subjects include brain tissue from autistic subjects, BTBR T + tfJ (BTBR) and Neuroligin (NL)-3 knock-down mice. Western blot analysis, Immunohistochemistry and confocal microscopy studies have be used to examine the density and morphology of astrocytes, as well as Wnt and β-catenin protein expression. In this study, we demonstrate that the astrocytes in autisitcsubjects exhibit significantly reduced branching processes, total branching length and cell body sizes. We also detected an astrocytosis in the frontal cortex of autistic subjects. In addition, we found that the astrocytes in the brain of an NL3 knockdown mouse exhibited similar alterations to what we found in the autistic brain. Furthermore, we detected that both Wnt and β-catenin proteins are decreased in the frontal cortex of autistic subjects. Wnt/β-catenin pathway has been suggested to be involved in the regulation of astrocyte development. Our findings imply that defects in astrocytes could impair neuronal plasticity and partially contribute to the development of autistic-like behaviors in both humans and mice. The alteration of Wnt/β-catenin pathway in the brain of autistic subjects may contribute to the changes of astrocytes.

BackgroundAutism is a neurodevelopmental disorder characterized by impairments in social interaction, verbal communication and repetitive behaviors. To date the etiology of this disorder is poorly understood. Studies suggest that astrocytes play critical roles in neural plasticity by detecting neuronal activity and modulating neuronal networks. Recently, a number of studies suggested that an abnormal function of glia/astrocytes may be involved in the development of autism. However, there is yet no direct evidence showing how astrocytes develop in the brain of autistic individuals.MethodsStudy subjects include brain tissue from autistic subjects, BTBR T + tfJ (BTBR) and Neuroligin (NL)-3 knock-down mice. Western blot analysis, Immunohistochemistry and confocal microscopy studies have be used to examine the density and morphology of astrocytes, as well as Wnt and β-catenin protein expression.ResultsIn this study, we demonstrate that the astrocytes in autisitcsubjects exhibit significantly reduced branching processes, total branching length and cell body sizes. We also detected an astrocytosis in the frontal cortex of autistic subjects. In addition, we found that the astrocytes in the brain of anNL3knockdown mouse exhibited similar alterations to what we found in the autistic brain. Furthermore, we detected that both Wnt and β-catenin proteins are decreased in the frontal cortex of autistic subjects. Wnt/β-catenin pathway has been suggested to be involved in the regulation of astrocyte development.ConclusionsOur findings imply that defects in astrocytes could impair neuronal plasticity and partially contribute to the development of autistic-like behaviors in both humans and mice. The alteration of Wnt/β-catenin pathway in the brain of autistic subjects may contribute to the changes of astrocytes.