Persistent Radiculopathy Subsequent to Selective Nerve Root Block.

Transforaminal selective nerve root blocks are commonly performed for low back pain but are not without risk. This case report describes a 55-year-old man who underwent transforaminal selective nerve root block at the left lumbar (L) 4, L5, and sacral (S) 1 levels for radiating low back pain in the setting of moderate narrowing of the left L4-L5 foramen with impingement on the exiting left L4 nerve roots seen on magnetic resonance imaging (MRI). He developed left foot drop immediately after the procedure and presented to the acupuncture clinic two weeks later with persistent pain, left foot drop, and paresthesia of the left lateral shin. A repeat MRI of the lumbar spine showed mild enhancement of the left cauda equina, including the L5 and possibly L4 nerve roots. The large volume of injection into an area with neuroforaminal narrowing as well as the cytotoxicity of the contrast and anesthetic agents may have contributed to axon damage and left foot drop.

CXCL12 defines lung endothelial heterogeneity and promotes distal vascular growth.

There is a growing amount of data uncovering the cellular diversity of the pulmonary circulation and mechanisms governing vascular repair after injury. However, the molecular and cellular mechanisms contributing to the morphogenesis and growth of the pulmonary vasculature during embryonic development are less clear. Importantly, deficits in vascular development lead to significant pediatric lung diseases, indicating a need to uncover fetal programs promoting vascular growth. To address this, we used a transgenic mouse reporter for expression of Cxcl12, an arterial endothelial hallmark gene, and performed single-cell RNA sequencing on isolated Cxcl12-DsRed+ endothelium to assess cellular heterogeneity within pulmonary endothelium. Combining cell annotation with gene ontology and histological analysis allowed us to segregate the developing artery endothelium into functionally and spatially distinct subpopulations. Expression of Cxcl12 is highest in the distal arterial endothelial subpopulation, a compartment enriched in genes for vascular development. Accordingly, disruption of CXCL12 signaling led to, not only abnormal branching, but also distal vascular hypoplasia. These data provide evidence for arterial endothelial functional heterogeneity and reveal conserved signaling mechanisms essential for pulmonary vascular development.