PurposeThis study aims to investigate the effect of transcutaneous electrical acupoint stimulation (TEAS) on postoperative delirium (POD) in elderly patients with silent lacunar infarct and preliminarily to determine the relationship among TEAS, blood–brain barrier (BBB), neuroinflammation, and POD.Patients and methodsSixty-four-old patients with silent lacunar infarct were randomly divided into two groups: group TEAS and control group (group C). Patients in the group TEAS received TEAS (disperse-dense waves; frequency, 2/100 Hz) on acupoints Hegu and Neiguan of both sides starting from 30 minutes before induction of anesthesia until the end of surgery, and the intensity was the maximum current that could be tolerated. In group C, electrodes were placed on the same acupoints before anesthesia induction, but no current was given. At 0 minute before the treatment of TEAS, 30 minutes after skin incision, and after completion of surgery (T1–3), blood samples were extracted to detect the concentration of serum tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), matrix metalloproteinase-9 (MMP-9), and S100β. We assessed patients for delirium and coma twice daily in the first 3 postoperative days using the Confusion Assessment Method for the intensive care unit and the Richmond Agitation-Sedation Scale.ResultsThis study preliminarily suggests that TEAS can reduce the development of POD in elderly patients with silent lacunar infarction (6.3% vs 25.0%; P=0.039). Compared with the baseline value at T1, the serum concentrations of IL-6, TNF-α, MMP-9, and S100β were significantly increased at T2–3 in both the groups (P<0.05). Compared with group TEAS, serum levels of TNF-α and IL-6 were higher at T2–3 and serum levels of MMP-9 and S100β were higher at T3 in group C (P<0.05). The intraoperative anesthetic consumptions were less in group TEAS than group C.ConclusionTEAS can alleviate POD in older patients with silent lacunar infarction and may be related to reduce the neuroinflammation by lowering the permeability of BBB.

Background. Postoperative cognitive dysfunction (POCD) is an impairment of cognition that affects postsurgery patients. Sevoflurane anesthesia is linked to cognitive dysfunction correlated to the expression of miRNA levels.Objectives. In the current study, we investigated if miR-124 can offer protection against cognitive deficits induced by sevoflurane in a spatial learning paradigm, and examined the molecular mechanisms through cell cultures.Materials and methods. Escape latency, platform crossings in probe trials and swimming speed in the Morris water maze in sevoflurane-treated mice were utilized as a measure of cognitive function. The relative miR-124 expression, and mRNA expressions of Bax, caspase-3 and Bcl-2 in sevoflurane-treated hippocampal cultures were measured using real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the changes in interleukin (IL)-1β, tumor necrosis factor alpha (TNF-α) and IL-6 were determined using enzyme-linked immunosorbent assay (ELISA). The binding between miR-124 and calpain small subunit 1 (Capn4) was verified with site-directed mutagenesis. The involvement of the nuclear factor kappa B (NF-κB) signaling pathway was examined using western blot analysis. Results.Our findings indicated that the miR-124 expression was inhibited by sevoflurane treatment in live rats and mouse hippocampal neurons to prevent apoptosis and inflammatory responses. We confirmed Capn4 as a target of miR-124. Treatment with sevoflurane enhanced the expression of Capn4, while overexpression of miR124 suppressed the enhanced expression of Capn4. Also, miR-124 inhibited apoptosis in murine hippocampal neurons induced by sevoflurane via the NF-κB signaling pathway. Conclusions.Our findings demonstrated that miR-124 exerted its neuroprotective role against sevoflurane via targeting Capn4 and NF-κB signaling pathways. Our work may provide a novel and efficacious treatment for sevoflurane anesthesia-related cognitive dysfunction.

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Introduction Single nerve block provides excellent analgesia, but rebound pain after the nerve block disappears has gradually attracted people’s attention. Perineural dexamethasone has been shown to extend the duration of a single nerve block and reduce rebound pain. However, no studies have compared the effect of reducing rebound pain between the two. The hypothesis was tested that perineural or intravenous would have an equivalent effect on prevent the rebound pain after nerve block. Methods We recruited 135 patients with ankle fractures scheduled for open reduction and internal fixation (ORIF), each of whom received a single sciatic-popliteal nerve block in combination with a single nerve block. Patients were randomized into three group: 40ml ropivacaine 0.375% (C); 40ml ropivacaine 0.375% with perineural dexamethasone 10mg(PN); 40ml ropivacaine 0.375% with intravenous dexamethasone (IV). The primary outcome was the incidence of rebound pain. Results The incidence of rebound pain was significantly lower in group PN (11%)and group IV(17.8%), compared with group C(42.2%). Both Groups PN and IV had reduced pain score, reduced postoperative consumption of analgesics and improved the quality of sleep on the night of surgery compared with Group C.Conclusions Dexamethasone 10mg can prevent the rebound pain after combined femoral nerve and sciatic nerve blocks nerve block, which has nothing to do with the way of dexamethasone. Trial registration number www.chictr.org.cn/index.aspx ChiCTR2100049075