BackgroundDexmedetomidine (Dex) can improve neuronal viability and protect the spinal cord from ischemia–reperfusion (I/R) injury, but the underlying mechanisms are not fully understood. This study investigated the effects of dexmedetomidine on the toll-like receptor 4 (TLR4)-mediated nuclear factor κB (NF-κB) inflammatory system and caspase-3 dependent apoptosis induced by spinal cord ischemia–reperfusion injury.MethodsTwenty-four rabbits were divided into three groups: I/R, Dex (10 µg/kg/h prior to ischemia until reperfusion), and Sham. Abdominal aortic occlusion was carried out for 30 min in the I/R and Dex groups. Hindlimb motor function was assessed using the Tarlov scoring system for gait evaluation. Motor neuron survival and apoptosis in the ventral grey matter were assessed by haematoxylin–eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labelling staining. The expression and localisation of ionised calcium-binding adaptor molecule 1, TLR4, NF-κB and caspase-3 were assessed by immunoreactivity analysis. The levels of interleukin 1β and tumour necrosis factor α were assessed using enzyme-linked immunosorbent assays.ResultsPerioperative treatment with dexmedetomidine was associated with a significant preservation of locomotor function following spinal cord ischemia–reperfusion injury with increased neuronal survival in the spinal cord compared to control. In addition, dexmedetomidine suppressed microglial activation, inhibited the TLR4-mediated NF-κB signalling pathway, and inhibited the caspase-3 dependent apoptosis.ConclusionsDexmedetomidine confers neuroprotection against spinal cord ischemia–reperfusion injury through suppression of spinal cord inflammation and neuronal apoptosis. A reduction in microglial activation and inhibition of both the TLR4-mediated NF-κB signalling pathway and caspase-3 dependent apoptosis are implicated.
Purpose: Microvascular decompression (MVD) surgery is considered as an effective method with which to treat trigeminal neuralgia (TN). However, sometimes MVD surgery fails due to incomplete decompression of the responsible vessels caused by a poor visual field. In this study, we evaluated the benefits of endoscopic visualization and the value of full endoscopic vascular decompression (EVD) by describing the surgical results of 20 patients with TN after EVD. Patients and Methods: This was a retrospective study in a single institution of 20 patients with TN who received EVD between April 2018 and October 2019. All patients underwent EVD via the suboccipital retrosigmoid approach without microscopy at any stage. Abnormal muscle response (AMR) and brainstem auditory evoked potentials (BAEPs) were routinely monitored throughout the procedure. Follow-up was conducted by outpatient and telephone interviews. The degree of facial pain was graded using the Barrow Neurological Institute (BNI) pain intensity score; a BNI of 1 was considered as the best result while a BNI of 2 or 3 was considered as a satisfactory result. Follow-up time ranged from 8 to 24 months, with a mean of 18±4.36 months. Results: All 20 patients with severe preoperative pain (BNI of 5) achieved immediate relief or complete control of pain after surgery (BNI of 1 to 2). Vascular conflicts were observed during surgery in all of the patients. None of the patients experienced hearing loss, facial paralysis, intracranial infection, cerebrospinal fluid leakage, cerebral hemorrhage, or death, following the operation. Conclusion: When carried out by surgeons with endoscopic experience, EVD can provide a clear surgical field of view and reduce the risk of surgical injury. Our findings indicate that EVD is a safe and effective surgical method for the treatment of TN.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.