RESUMO
Background: Dry needling the lumbar multifidi is a technique used by physical therapists to effectively treat low back pain. While studies have examined the safety considerations in the upper lumbar spine related to the kidneys and lungs, none have investigated the possibility of entering the spinal canal in this region. Purpose: The purpose of this cadaveric ultrasound-guided dry needling exploration was to determine if a dry needle can penetrate the ligamentum flavum at the T12/L1 interspace and enter the spinal canal using a paramedian approach in a fresh-frozen, lightly fixed cadaver in the prone position. Study Design: Cadaveric study. Methods: The procedure was performed on a cadaver in the prone position. The needle was advanced under ultrasound guidance to determine if a 0.30 x 50 mm dry needle inserted 1.0 cm lateral to the spinous process of T12 and directed medially at a 22-degree angle could penetrate the ligamentum flavum and enter the spinal canal. Results: As determined via ultrasound, a dry needle can penetrate the ligamentum flavum and enter the spinal canal at the thoracolumbar junction using this technique. Conclusion: This interprofessional collaboration demonstrates that a dry needle can penetrate the ligamentum flavum to enter the spinal canal at T12/L1 using a documented technique for dry needling the multifidus. A thorough understanding of human anatomy along with the incorporation of available technology, such as ultrasound, may decrease the risk of adverse events when dry needling the multifidi at the thoracolumbar junction. Level of Evidence: Level IV.
RESUMO
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) comprise a spectrum of neurodegenerative diseases linked to TDP-43 proteinopathy, which at the cellular level, is characterized by loss of nuclear TDP-43 and accumulation of cytoplasmic TDP-43 inclusions that ultimately cause RNA processing defects including dysregulation of splicing, mRNA transport and translation. Complementing our previous work in motor neurons, here we report a novel model of TDP-43 proteinopathy based on overexpression of TDP-43 in a subset of Drosophila Kenyon cells of the mushroom body (MB), a circuit with structural characteristics reminiscent of vertebrate cortical networks. This model recapitulates several aspects of dementia-relevant pathological features including age-dependent neuronal loss, nuclear depletion and cytoplasmic accumulation of TDP-43, and behavioral deficits in working memory and sleep that occur prior to axonal degeneration. RNA immunoprecipitations identify several candidate mRNA targets of TDP-43 in MBs, some of which are unique to the MB circuit and others that are shared with motor neurons. Among the latter is the glypican Dally-like-protein (Dlp), which exhibits significant TDP-43 associated reduction in expression during aging. Using genetic interactions we show that overexpression of Dlp in MBs mitigates TDP-43 dependent working memory deficits, conistent with Dlp acting as a mediator of TDP-43 toxicity. Substantiating our findings in the fly model, we find that the expression of GPC6 mRNA, a human ortholog of dlp, is specifically altered in neurons exhibiting the molecular signature of TDP-43 pathology in FTD patient brains. These findings suggest that circuit-specific Drosophila models provide a platform for uncovering shared or disease-specific molecular mechanisms and vulnerabilities across the spectrum of TDP-43 proteinopathies.
