Implications of the Precise Anatomical Location of Lumbar Stenosis for Minimally Invasive Decompressive Lumbar Surgery

Objective The purpose of this study was to characterize an observation that the most severe lumbar stenosis is often displaced from the disc. Methods A retrospective magnetic resonance (MRI) review of displacement and causes of lumbar canal stenosis, was undertaken. Lumbar MRIs (n=3000) were reviewed for stenosis defined as a canal diameter of ≤8 mm. Displacement of maximal stenosis from the disc was measured; measurements inferior to the disc were assigned negative values. Defined causes were; ligamentous hypertrophy, facet hypertrophy, lipomatosis, spondylolisthesis, synovial cyst, or adjacent segment disease. Results Lumbar stenosis levels (n=1,042) identified in 749 patients were; L1-2 (3.8%), L2-3(20.1%), L3-4 (35.3%), L4-5 (37.7%), and L5-S1 (3.2%). Of these levels 20.8% were attributed to facet hypertrophy, 29.8% ligamentous hypertrophy, 31.1% epidural lipomatosis, 11.2% spondylolisthesis, 5.6% adjacent segment disease, and 1.5% synovial cyst. Mean displacement stenosis (mm) was; synovial cyst (-0.3; range 7 to -5), epidural lipomatosis, (-1.1; 5 to -13), ligamentous hypertrophy (-3.5; 5 to -13); facet hypertrophy (-3.9; 7 to -11), adjacent segment disease (-4.7; 7 to -11), and spondylolisthesis (-4.9; 11 to -12). Sub-group analysis revealed a predominantly negative displacement for spondylolisthesis, adjacent segment disease, facet hypertrophy, and ligamentous hypertrophy. Conclusion The site of maximal lumbar stenosis is at or near the center of the disc with lipomatosis or synovial cyst, but significantly inferiorly displaced when ligamentous or facet hypertrophy, spondylolisthesis, or adjacent segment disease is the major cause. Lipomatosis as a cause of stenosis is more common than previously reported

Down-Regulation Of Sema4d On Follicular T Helper Cell Fine-Tunes Germinal Center B Cell Response

Follicular helper T (TFH) cells are a specialized subset of CD4+ T cells essential for the affinity-based selection of B cells in the germinal center (GC). However, it remains unclear how transient entanglement between TFH and GC B cells lead to selective B cell proliferation and differential somatic hypermutation, especially given the evidence that BCR signaling is closely guarded by phosphatases within the GC. Here we present a model involving the interaction between SEMA4D on TFH cells and CD72 on GC B cells. We found that as the GC response progressed during acute murine lymphocytic choriomeningitis virus infection, TFH cells temporally downregulated surface expression of SEMA4D, accompanied by increased CD40L expression and decreased IFNγ and IL-21 production. Different levels of SEMA4D expression on TFH cells correlated with significantly varied phosphorylation levels of B cell receptor signaling cascade molecules Syk, Btk, BLNK, and tyrosine kinases as a whole. Such variations in B cell receptor signaling in GC B cells affected their proliferation, localization, and somatic hypermutation. Therefore, TFH cells utilize SEMA4D and its temporal down-regulation to regulate affinity maturation and fine-tune selective pressure over GC B cells over the course of the GC response