Spinal cord injury

Inflammation resolution failure is a pathological hallmark of spinal cord injury. Here, the authors show in rodents that chondroitin sulfate proteoglycans contribute to failed resolution by preventing immune cells at the injury core from converting to a pro-resolution phenotype, and this is mediated by TLR4.

Bertels et al. identify that spinal neurons switch neurotransmitter phenotype from excitation to inhibition after spinal cord injury. Manipulation of neurotransmitter phenotype reveals that maintaining excitatory phenotype is essential for locomotor recovery.

By combining experimental models with prospective clinical studies, the authors show that spinal cord injury causes a rapid reduction in cardiac function that precedes structural changes, and that the loss of descending sympathetic control is the major cause of reduced cardiac function following spinal cord injury.

Implantation of a multielectrode paddle that allows personalized electrical stimulation to all regions of the spinal cord involved in leg and trunk movements rapidly restores motor function in patients with spinal cord injury with complete paralysis.