T12-L3 Nerve Transfer-Induced Locomotor Recovery in Rats with Thoracolumbar Contusion: Essential Roles of Sensory Input Rerouting and Central Neuroplasticity.

Locomotor recovery after spinal cord injury (SCI) remains an unmet challenge. Nerve transfer (NT), the connection of a functional/expendable peripheral nerve to a paralyzed nerve root, has long been clinically applied, aiming to restore motor control. However, outcomes have been inconsistent, suggesting that NT-induced neurological reinstatement may require activation of mechanisms beyond motor axon reinnervation (our hypothesis). We previously reported that to enhance rat locomotion following T13-L1 hemisection, T12-L3 NT must be performed within timeframes optimal for sensory nerve regrowth. Here, T12-L3 NT was performed for adult female rats with subacute (7-9 days) or chronic (8 weeks) mild (SCImi: 10 g × 12.5 mm) or moderate (SCImo: 10 g × 25 mm) T13-L1 thoracolumbar contusion. For chronic injuries, T11-12 implantation of adult hMSCs (1-week before NT), post-NT intramuscular delivery of FGF2, and environmentally enriched/enlarged (EEE) housing were provided. NT, not control procedures, qualitatively improved locomotion in both SCImi groups and animals with subacute SCImo. However, delayed NT did not produce neurological scale upgrading conversion for SCImo rats. Ablation of the T12 ventral/motor or dorsal/sensory root determined that the T12-L3 sensory input played a key role in hindlimb reanimation. Pharmacological, electrophysiological, and trans-synaptic tracing assays revealed that NT strengthened integrity of the propriospinal network, serotonergic neuromodulation, and the neuromuscular junction. Besides key outcomes of thoracolumbar contusion modeling, the data provides the first evidence that mixed NT-induced locomotor efficacy may rely pivotally on sensory rerouting and pro-repair neuroplasticity to reactivate neurocircuits/central pattern generators. The finding describes a novel neurobiology mechanism underlying NT, which can be targeted for development of innovative neurotization therapies.

Hospital volume of thoracoabdominal aneurysm repair does not affect mortality in California.

OBJECTIVES: Open thoracoabdominal aneurysm repair (TAAR) is a rarely performed but a complicated and morbid procedure. This study compares the morbidity and mortality of open TAAR at high- versus low-volume hospitals. METHODS: Included patients from California Office of Statewide Health Policy and Development patient discharge database who underwent an open TAAR between 1995 and 2010. High volume was ≥ 9 cases per year. Outcomes included mortality and postoperative complications. Multivariate analyses compared patients at high- versus low-volume hospitals. RESULTS: A total of 122 hospitals were included, with 5 designated as high volume. Adjusted analysis found no difference in the odds ratio (OR) of mortality or morbidity at high-volume hospitals compared to low-volume hospitals (OR 0.37, P = .077; OR 0.94, P = .834, respectively). However, there was a decreased OR of mortality in high- versus low-volume hospitals when a high-volume hospital was defined as each year after meeting the initial threshold of 9 cases (OR 0.40, P = .040). CONCLUSION: We found no difference in mortality between low- and high-volume institutions in California, until high-volume hospitals were defined as each year after meeting initial threshold case volume. This may suggest that the benefits of high-volume hospitals on outcomes are maintained after reaching the requisite case volume.