The Lumbar Ligamentum Flavum Does Not Have Two Layers and Is Confluent with the Interspinous Ligament: Anatomical Study with Application to Surgical and Interventional Pain Procedures.

Numerous authors over the years have reported that the lumbar ligamentum flavum has two layers. Our routine cadaveric dissections raised the question whether this understanding is correct, as we always have observed only one layer. Thus, the goal of this cadaveric study was to reevaluate the layers of the ligamentum flavum. Twenty lumbar levels from five fresh-frozen cadaveric specimens were used in this study. After dissection of the lumbar spine, the ligamentum flavum and interspinous ligament were exposed. Each lumbar level was transected through the zygapophyseal joint, and hematoxylin and eosin staining, Masson's trichrome staining and Verhoeff-van Gieson staining were performed. Continuation of the interspinous ligament and ligamentum flavum were observed invariably. There was no evidence of the existence of a two-layered ligamentum flavum. The lumbar ligamentum flavum does not consist of two layers, but is confluent instead with the interspinous ligament that attaches to the zygapophyseal joints. To convey this anatomy better, we suggest describing the lumbar ligamentum flavum as a structure that consists of interlaminar and interspinous parts. Precise knowledge of the ligamentum flavum's anatomy can be of clinical value, particularly when epidural anesthesia or lumbar puncture are performed. Clin. Anat. 32:34-40, 2019. © 2019 Wiley Periodicals, Inc.

Prognostic value of needle electromyography in traumatic brachial plexus injury.

INTRODUCTION: In this study we aimed to determine whether needle electromyographic assessment of voluntary motor unit recruitment in traumatic brachial plexus injuries could predict spontaneous motor recovery. METHODS: A retrospective study was performed on patients with brachial plexus injury affecting deltoid, supraspinatus/infraspinatus, and biceps brachii. The outcome measure was strength on manual muscle testing at least 1 year after injury. Good outcome was considered strength >3/5 on the Medical Research Council (MRC) scale. RESULTS: No muscles with no recruitment (n = 27) at 1-9 months improved to MRC 4/5 strength at a mean of 2.0 years postinjury. Twenty-five percent of muscles with discrete or severely reduced recruitment (n = 8) regained strength to >3/5 at a mean of 1.4 years postinjury (P = .047). DISCUSSION: Absent voluntary motor unit potential recruitment at 1-9 months predicted poor prognosis for spontaneous recovery. A high percentage of patients with discrete recruitment did not improve to >3/5 strength. These patients should be considered for early nerve transfer surgery.

Fenofibrate-induced nuclear translocation of FoxO3A triggers Bim-mediated apoptosis in glioblastoma cells in vitro.

Anti-neoplastic potential of calorie restriction or ligand-induced activation of peroxisome proliferator activated receptors (PPARs) has been demonstrated in multiple studies; however, mechanism(s) by which tumor cells respond to these stimuli remain to be elucidated. One of the potent agonists of PPARα, fenofibrate, is a commonly used lipid-lowering drug with low systemic toxicity. Fenofibrate-induced PPARα transcriptional activity is expected to shift energy metabolism from glycolysis to fatty acid ß-oxidation, which in the long-term, could target weak metabolic points of glycolysis-dependent glioblastoma cells. The results of this study demonstrate that 25 µM fenofibrate can effectively repress malignant growth of primary glial tumor cells and glioblastoma cell lines. This cytostatic action involves G(1) arrest accompanied by only a marginal level of apoptotic cell death. Although the cells treated with 25 µM fenofibrate remain arrested, the cells treated with 50 µM fenofibrate undergo massive apoptosis, which starts after 72 h of the treatment. This delayed apoptotic event was preceded by FoxO3A nuclear accumulation, FoxO3A phosphorylation on serine residue 413, its elevated transcriptional activity and expression of FoxO-dependent apoptotic protein, Bim. siRNA-mediated inhibition of FoxO3A attenuated fenofibrate-induced apoptosis, indicating a direct involvement of this transcription factor in the fenofibrate action against glioblastoma. These properties of fenofibrate, coupled with its low systemic toxicity, make it a good candidate in support of conventional therapies against glial tumors.