C6 nerve root palsy after double-door cervical laminoplasty

Background: This study correlated the relationship between postoperative C6 nerve root palsies and various patient-related clinical, radiographic, and surgical parameters. Methods: The medical records of 318 patients undergoing double-door cervical laminoplasty for myelopathy were reviewed. Twelve (3.8%) had postoperative C6 nerve root palsies. Their clinical, radiographic, and surgical procedures were analyzed looking for a correlation/explanation for these new C6 root deficits. Results: The following factors correlated with patients’ developing new postoperative C6 nerve root deficit following double-door cervical laminoplasty; a high correlation with additional C5 palsies, narrower C6 intervertebral foraminal widths, greater anterior protrusions of the C6 articular process, and larger posterior shifts of the spinal cord on magnetic resonance (MR) between the C4/C5-C6/C7 levels. Conclusion: Factors correlating with the new onset of C6 nerve root palsies following double-door cervical laminoplasty included; a high correlation with new C5 palsies, more severe foraminal stenosis, greater anterior protrusions of the C6 articular process, and more extensive dorsal spinal cord migration.

Syringomyelia after spinal anaesthesia: A case report

Lumbar spinal or epidural anaesthesia has a lower complication rate compared to general anaesthesia. An occasional patient may develop spinal cord injury during the procedure and develop neurological complications. We report an interesting case of paraparesis due to dorsal spinal cord involvement and syrinx formation following spinal anaesthesia for abdominal surgery.

Tlx3 Exerts Direct Control in Specifying Excitatory Over Inhibitory Neurons in the Dorsal Spinal Cord

The spinal cord dorsal horn is a major station for integration and relay of somatosensory information and comprises both excitatory and inhibitory neuronal populations. The homeobox gene Tlx3 acts as a selector gene to control the development of late-born excitatory (dILB) neurons by specifying glutamatergic transmitter fate in dorsal spinal cord. However, since Tlx3 direct transcriptional targets remain largely unknown, it remains to be uncovered how Tlx3 functions to promote excitatory cell fate. Here we combined a genomics approach based on chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq) and expression profiling, with validation experiments in Tlx3 null embryos, to characterize the transcriptional program of Tlx3 in mouse embryonic dorsal spinal cord. We found most dILB neuron specific genes previously identified to be directly activated by Tlx3. Surprisingly, we found Tlx3 also directly represses many genes associated with the alternative inhibitory dILA neuronal fate. In both cases, direct targets include transcription factors and terminal differentiation genes, showing that Tlx3 directly controls cell identity at distinct levels. Our findings provide a molecular frame for the master regulatory role of Tlx3 in developing glutamatergic dILB neurons. In addition, they suggest a novel function for Tlx3 as direct repressor of GABAergic dILA identity, pointing to how generation of the two alternative cell fates being tightly coupled.

Robo recruitment of the Wave Regulatory Complex plays an essential and conserved role in midline repulsion

The Roundabout (Robo) guidance receptor family induces axon repulsion in response to its ligand Slit by inducing local cytoskeletal changes; however, the link to the cytoskeleton and the nature of these cytoskeletal changes are poorly understood. Here, we show that the heteropentameric Scar/Wave Regulatory Complex (WRC) which drives Arp2/3-induced branched actin polymerization, is a direct effector of Robo signaling. Biochemical evidence shows that Slit triggers WRC recruitment to the Robo receptor's WIRS motif. In Drosophila embryos, mutants of the WRC enhance Robo1-dependent midline crossing defects. Additionally, mutating Robo1's WIRS motif significantly reduces receptor activity in rescue assays in vivo, and CRISPR-Cas9 mutagenesis shows that the WIRS motif is essential for endogenous Robo1 function. Finally, axon guidance assays in mouse dorsal spinal commissural axons and gain-of-function experiments in chick embryos demonstrate that the WIRS motif is also required for Robo1 repulsion in mammals. Together, our data support an essential conserved role for the WIRS-WRC interaction in Robo1-mediated axon repulsion.