Objective: A thoracolumbar burst fracture (TLBF) is defined as the failure of the anterior and middle columns of the vertebra due to high-energy trauma, such as motor vehicle collisions and falls from heights. Debate has continued for decades regarding the standard treatment, especially for TLBFs without neurological deficits (TLBF-WONDs). The aim of this study was to understand the role of expandable intravertebral titanium implants (EITIs) in treating TLBF-WONDs. Methods: We included patients aged 18–65 years who presented at our hospital Emergency Department with severe back pain (visual analogue scale [VAS] score ≥ 8), were neurologically intact, were diagnosed with TLBF-WOND by either computed tomography or magnetic resonance imaging, underwent percutaneous bilateral transpedicular EITI implantation, and were followed-up for ≥12 months. Radiological and clinical outcomes were analyzed. Results: Thirty patients satisfied the study inclusion criteria, including 9 men and 21 women, with an average age of 48.2 years. Thirteen A3 and 17 A4 burst fractures were included. The mean duration of hospitalization was 3.3 days. The mean follow-up period was 4.4 years. All patients exhibited significant improvements in radiographical (anterior, middle, and posterior vertebral heights); vertebral kyphotic angle (p<0.001); and functional outcomes (VAS and Oswestry Disability Index scores, p<0.001). One case of cement leakage into the paraspinal muscle was observed; however, no major complications occurred. Conclusion Percutaneous bilateral transpedicular EITI placement with cement augmentation under local anesthesia may be an effective strategy for the treatment of high-energy traumatic TLBFs with neurological integrity.

PURPOSE: The urinary bladder (UB) is innervated by both sensory and autonomic nerves. Recent studies have shown that sensory neuropeptides induced contractions in the detrusor muscle. Therefore, in a mouse model, we investigated the presence of interactions between the submucosal sensory nerves and the autonomic nerves that regulate the motor function of the detrusor muscle. METHODS: UB samples from male C57BL/6 mice were isolated, cut into strips, and mounted in an organ bath. Dose-response curves to norepinephrine and phenylephrine were studied in UB strips with and without mucosa, and the effects of preincubation with a receptor antagonist and various drugs on relaxation were also studied using tissue bath myography. RESULTS: Phenylephrine-induced relaxation of the UB strips showed concentration-related effects. This relaxation appeared in both mucosa-intact and mucosa-denuded UB strips, and was significantly inhibited by lidocaine, silodosin, and guanethidine (an adrenergic neuronal blocker). Meanwhile, phenylephrine-induced relaxation was inhibited by pretreatment with propranolol and calcitonin gene-related peptide (CGRP)–depletory capsaicin in UB strips with and without mucosa. CONCLUSIONS: The present study suggests that phenylephrine activates the α-1A adrenergic receptor (AR) of the sensory nerve, and then activates capsaicin-sensitive sensory nerves to release an unknown substance that facilitates the release of norepinephrine from adrenergic nerves. Subsequently, norepinephrine stimulates β-ARs in the detrusor muscle in mice, leading to neurogenic relaxation of the UB. Further animal and human studies are required to prove this concept and to validate its clinical usefulness.
Adrenergic Neurons ; Animals ; Autonomic Pathways ; Baths ; Calcitonin Gene-Related Peptide ; Capsaicin ; Guanethidine ; Humans ; Lidocaine ; Male ; Mice ; Mucous Membrane ; Myography ; Neuropeptides ; Norepinephrine ; Phenylephrine ; Propranolol ; Receptors, Adrenergic ; Receptors, Adrenergic, alpha-1 ; Relaxation ; Urinary Bladder*