UNASSIGNED: Patients undergoing cardiothoracic surgery frequently encounter perioperative neurocognitive disorders (PND), which can include postoperative delirium (POD) and postoperative cognitive decline (POCD). Currently, there is not enough evidence to support the use of electroencephalograms (EEGs) in preventing POD and POCD among cardiothoracic surgery patients. This meta-analysis examined the importance of EEG monitoring in POD and POCD.
UNASSIGNED: Cochrane Library, PubMed, and EMBASE databases were searched to obtain the relevant literature. This analysis identified trials based on the inclusion and exclusion criteria. The Cochrane tool was used to evaluate the methodological quality of the included studies. Review Manager software (version 5.3) was applied to analyze the data.
UNASSIGNED: Four randomized controlled trials (RCTs) were included in this meta-analysis, with 1096 participants. Our results found no correlation between EEG monitoring and lower POD risk (relative risk (RR): 0.81; 95% CI: 0.55-1.18; p = 0.270). There was also no statistically significant difference between the EEG group and the control group in the red cell transfusions (RR: 0.86; 95% CI: 0.51-1.46; p = 0.590), intensive care unit (ICU) stay (mean deviation (MD): -0.46; 95% CI: -1.53-0.62; p = 0.410), hospital stay (MD: -0.27; 95% CI: -2.00-1.47; p = 0.760), and mortality (RR: 0.33; 95% CI: 0.03-3.59; p = 0.360). Only one trial reported an incidence of POCD, meaning we did not conduct data analysis on POCD risk.
UNASSIGNED: This meta-analysis did not find evidence supporting EEG monitoring as a potential method to reduce POD incidence in cardiothoracic surgery patients. In the future, more high-quality RCTs with larger sample sizes are needed to validate the relationship between EEG monitoring and POD/POCD further.

Damage to the peripheral and central nervous systems is frequently irreversible. Surgically induced neurological damage and anesthesia may result in catastrophic situations for patients and their families. The incidence of significant neurological complications during the perioperative period is examined in this article. In contrast to other organs like the kidney, heart, liver, lungs, and skeletal system, native neurological function cannot be replaced with artificial parts or devices soon. Ignoring brain function during the perioperative period has been a systemic problem in anesthesiology, even though the central and peripheral nervous systems are crucial. This bold claim is intended to draw attention to the fact that, unlike the circulatory and respiratory systems, which have been routinely monitored for decades, the brain and other neural structures do not have a standard monitoring during surgery and anesthesia. Given that the brain and spinal cord are the principal therapeutic targets of analgesics and anesthetics, this deficiency in clinical care is even more alarming. Organs that are notoriously hard to repair or replace after damage have, up until now, received comparatively little attention. In this article, a succinct overview of five neurological complications associated with surgery and anesthesia is presented. After critically reviewing the literature on the subject, the article is focused to common (delirium), controversial (postoperative cognitive decline), and potentially catastrophic (stroke, spinal cord ischemia, or postoperative visual loss) adverse events in the neurological surgery setting. The findings will increase awareness of major neurological complications to the involved surgical and anesthesia team and enhance preventive and treatment strategies during the perioperative period.

OBJECTIVE: Postoperative cognitive decline (POCD) is characterised by deficits in attention, memory, executive function, and information processing that persist beyond the early postoperative period. Its incidence ranges from 10%-25% after noncardiac surgery. Limited literature exists on POCD after gynecologic oncology surgery. Our primary objective was to identify the incidence of POCD among patients 55 years or older undergoing major gynecologic oncology surgery.
METHODS: This mixed-methods, prospective, observational cohort study followed patients 55 years or older who underwent surgery for gynecologic malignancies between February and July 2022. Semi-structured interviews and the Mini-Mental State Exam (MMSE) were administered before surgery as well as 1 and 3 months after. Assessments were delivered virtually and in-person in the context of the COVID-19 pandemic. POCD was defined as ≥2-point decline from baseline MMSE score.
RESULTS: Twenty-four patients participated; 19 completed the 1-month follow-up, and 15 completed the 3-month follow-up. The average age was 64 (range: 56-90). The mean preoperative MMSE score was 16.6 out of 17 (virtual) and 12.9 out of 13 (in-person). Two patients had a 1-point decline in their 1-month MMSE score; both recovered by 3 months. One patient had a 1-point decline in their 3-month MMSE score. Semi-structured interviews revealed common themes of \"brain fog\" at the 1-month follow-up and mild, persistent attention and word-finding deficits at 3 months postoperatively.
CONCLUSIONS: This study\'s qualitative component captured subtle subjective findings suggestive of potential POCD. Larger studies are required, and a more extensive neuropsychological test battery may be required to elicit subtle findings not clearly reflected by MMSE scores.

Postoperative cognitive dysfunction (POCD) is characterized by impaired learning and memory. 6 h duration isoflurane anesthesia is an important factor to induce POCD, and the dysfunction of ryanodine receptor (RyR) in the hippocampus may be involved in this process. We investigated the expression of RyR3 in the hippocampus of mice after 6-h duration isoflurane anesthesia, as well as the improvement of RyR receptor agonist caffeine on POCD mice, while attempting to identify the underlying molecular mechanism.
We constructed a POCD model using 8-week-old male C57BL/6J mice that were exposed to 6-h duration isoflurane. Prior to the three-day cognitive behavioral experiment, RyR agonist caffeine were injected. Fear conditioning and location memory tests were used in behavioral studies. We also exposed the mouse neuroblastoma cell line Neuro-2a (N2A) to 6-h duration isoflurane exposure to simulate the conditions of in vivo cognitive dysfunction. We administered ryanodine receptor agonist (caffeine) and inhibitor (ryanodine) to N2a cells. Following that, we performed a series of bioinformatics analysis to discover proteins that are involved in the development of cognitive dysfunction. Rt-PCR and Western blot were used to assess mRNA level and protein expression.
6-h duration isoflurane anesthesia induced cognitive dysfunction and increased RyR3 mRNA levels in hippocampus. The mRNA levels of RyR3 in cultured N2a cells after anesthesia were comparable to those in vivo, and the RyR agonist caffeine corrected the expression of some cognitive-related phenotypic proteins that were disturbed after anesthesia. Intraperitoneal injection of RyR agonist caffeine can improve cognitive function after isoflurane anesthesia in mice, and bioinformatics analyses suggest that CaMKⅣ may be involved in the molecular mechanism.
Ryanodine receptor agonist caffeine may improve cognitive dysfunction in mice after isoflurane anesthesia.

BACKGROUND: Some patients show persistent cognitive decline for weeks, months or even years after surgery, which seriously affects their long-term prognosis and quality of life. However, most previous basic studies have focused mainly on the mechanisms of early postoperative cognitive decline, whereas cognitive decline in the longer term after surgery is less well-understood. The subgranular zone of the dentate gyrus exhibits life-long neurogenesis, supporting hippocampus-dependent learning and memory.
METHODS: The aim of this study was to investigate whether adult hippocampal neurogenesis (AHN) involves in cognitive decline later following surgery and to further explore the roles of CD8 + T lymphocytes infiltrating the hippocampal parenchyma after surgery in this pathological process. Cognitive function was examined in adult mice that underwent laparotomy combined with partial hepatectomy, and the results showed that cognitive decline persisted in mice who underwent surgery during the first postoperative month, even though there was a trend toward continuous improvement over time. Significantly decreased numbers of DCX + cells, BrdU + cells, and BrdU + /DCX + cells were observed on day 8 after surgery, and a significantly decreased number of NeuN + /BrdU + cells was observed on day 28 after surgery, which indicated inhibition of AHN. After surgery, T lymphocytes, the majority of which were CD8 + T cells, infiltrated the hippocampus and secreted Interferon-γ (IFN-γ). Depletion of CD8 + T cells could inhibit the increase of IFN-γ synthesis, improve hippocampal neurogenesis, and improve postoperative cognitive function. Hippocampal microinjection of IFN-γ neutralizing antibody or adeno-associated virus to knock down IFN-γ receptor 1 (IFNGR1) could also partially attenuate the inhibition of AHN and improve postoperative cognitive function.
CONCLUSIONS: These results demonstrate that postoperative infiltration of CD8 + T cells into the hippocampus and subsequent secretion of IFN-γ contribute to the inhibition of AHN and cognitive decline later following surgery.

UNASSIGNED: This study aimed to explore the effects of different injection rates of propofol on postoperative cognition in elderly patients undergoing laparoscopic inguinal hernia repair.
UNASSIGNED: A total of 180 elderly patients who planned to undergo laparoscopic inguinal hernia repair were randomly divided into three groups: slow injection of propofol (VS-Group, 30 mg kg-1 h-1); medium injection of propofol (VM-Group, 100 mg kg-1 h-1) or fast injection of propofol (VF-Group, 300 mg kg-1 h-1). Propofol was induced by microinfusion pump, and the depth of anesthesia was monitored by bispectral index (BIS). Propofol and remifentanil were continuously infused during anesthesia maintenance and adjusted according to BIS. The primary outcome was the use of the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) to measure the incidence of postoperative cognitive decline (POCD) in elderly patients on the first and seventh postoperative day. Secondary outcomes included induced dose of propofol, incidence of burst suppression and maximum electroencephalographic (EEG) effect of propofol (BIS-min) during induction.
UNASSIGNED: The incidence of POCD on the first and seventh day postoperatively was similar among the three groups (P > 0.05). However, with the increase of propofol injection rate, induced dose of propofol, incidence of burst suppression and BIS-min during induction, the number of patients requiring vasoactive agents were significantly increased (P < 0.001). Multivariate regression analysis showed that the brief duration of burst suppression during induction did not affect the occurrence of POCD, while age and duration of hospitalization were risk factors for POCD.
UNASSIGNED: For elderly patients undergoing laparoscopic inguinal hernia repair, lowering the injection rate of propofol (such as 30 mg kg-1 h-1) cannot decrease the incidence of early POCD, but reduces induction dose of propofol and use of vasoactive drugs, making the patient\'s hemodynamics more stable.

Background Durable memory decline may occur in older adults after surgical (coronary artery bypass grafting [CABG]) or nonsurgical (percutaneous coronary intervention) coronary revascularization. However, it is unknown whether individual memory risk can be predicted. We reanalyzed an epidemiological cohort of older adults to predict memory decline at ≈1 year after revascularization. Methods and Results We studied Health and Retirement Study participants who underwent CABG or percutaneous coronary intervention at age ≥65 years between 1998 and 2015 and participated in ≥1 biennial postprocedure assessment. Using a memory score based on direct and proxy cognitive tests, we identified participants whose actual postprocedure memory score was 1-2 (\"mild\") or >2 (\"major\") SDs below expected postprocedure performance. We modeled probability of memory decline using logistic regression on preoperatively known factors and evaluated model discrimination and calibration. A total of 1390 participants (551 CABG, 839 percutaneous coronary intervention) underwent CABG/percutaneous coronary intervention at 75±6 years old; 40% were women. The cohort was 83% non-Hispanic White, 8.4% non-Hispanic Black, 6.4% Hispanic ethnicity, and 1.7% from other groups masked by the HRS (Health and Retirement Study) to preserve participant confidentiality. At a median of 1.1 (interquartile range, 0.6-1.6) years after procedure, 267 (19%) had mild memory decline and 88 (6.3%) had major memory decline. Factors predicting memory decline included older age, frailty, and off-pump CABG; obesity was protective. The optimism-corrected area under the receiver operator characteristic curve was 0.73 (95% CI, 0.71-0.77). A cutoff of 50% probability of memory decline identified 14% of the cohort as high risk, and was 94% specific and 30% sensitive for late memory decline. Conclusions Preoperative factors can be used to predict late memory decline after coronary revascularization in an epidemiological cohort with high specificity.

UNASSIGNED: Postoperative delirium (POD) and postoperative cognitive decline (POCD) can be observed after cardiosurgical interventions. Taken together, these postoperative neurocognitive disorders (PNCDs) contribute to increased morbidity and mortality. Preoperative risk factors of PNCD, such as decreased neuropsychometric performance or decreased cognitive daily activities, can be interpreted as reduced cognitive reserve. This study aims to build up cognitive reserves to protect against the development of PNCD through preoperative, home-based, cognitive training.
UNASSIGNED: The planned research project is a monocentric, two-arm randomized controlled intervention study involving 100 patients undergoing elective cardiac surgery with extracorporeal circulation. Patients will be assigned to a training group or control group. The intervention involves a standardized, paper-and-pencil-based cognitive training that will be performed by the patients at home for ~40 min per day over a preoperative period of 2-3 weeks. The control group will receive neither cognitive training nor a placebo intervention. A detailed assessment of psychological functions will be performed ~2-3 weeks before the start of training, at the end of the training, during hospitalization, at discharge from the acute clinic, and 3 months after surgery. The primary objective of this study is to investigate the interventional effect of preoperative cognitive training on the incidence of POD during the stay in the acute clinic, the incidence of POCD at the time of discharge from the acute clinic, and 3 months after surgery. Secondary objectives are to determine the training effect on objective cognitive functions before the surgery and subjective cognitive functions, as well as health-related quality of life 3 months after surgery.
UNASSIGNED: Should it become evident that the use of our cognitive training can both reduce the incidence of POCD and POD and improve health-related quality of life, this intervention may be integrated into a standardized prehabilitation program.

BACKGROUND: Patients who undergo cardiac surgery are at increased risk of stroke, postoperative cognitive decline, and delirium. These neurocognitive complications have led to increased costs, intensive care unit stays, morbidity, and mortality. As a result, there is a significant push to mitigate any neurological complications in cardiac surgery patients. Near-infrared spectroscopy to measure regional cerebral oxygen saturations has gained consideration due to its noninvasive and user-friendly nature. Cerebral oximetry desaturations during cardiac surgery have been linked to an array of adverse clinical outcomes. However, the most effective intraoperative interventions to protect this vulnerable patient population have yet to be ascertained.
OBJECTIVE: To provide a comprehensive summary of the intraoperative management for cerebral oximetry desaturations during cardiac surgery. The review highlights clinical outcomes from cerebral oximetry use to quantify the importance of identifying cerebral desaturations during cardiac surgery. The review then interrogates possible interventions for cerebral oximetry desaturations in an effort to determine which interventions are most efficacious and to enlighten possible areas for further research.
METHODS: A narrative review of randomized controlled trials, observational studies, and systematic reviews with metanalyses was performed through August 2021.
RESULTS: There is significant heterogeneity among patient populations for which cerebral oximetry monitoring has been studied in cardiac surgery. Further, the definition of a clinically significant cerebral desaturation and the assessment of neurocognitive outcomes varied substantially across studies. As a result, metanalysis is challenging and few conclusions can be drawn. Cerebral oximetry use during cardiac surgery has not been associated with improvements in neurocognitive outcomes, morbidity, or mortality to date. The evidence to support a particular intervention for an acute desaturation is equivocal.
CONCLUSIONS: Future research is needed to quantify a clinically significant cerebral desaturation and to determine which interventions for an acute desaturation effectively improve clinical outcomes.

Postoperative cognitive decline (POCD) is a common complication after surgery and anesthesia among the elderly. Yet the potential mechanism of POCD remains ambiguous, with limited therapeutic measures currently available. Ketamine has been reported to attenuate POCD after cardiac surgery. Herein, we tried to determine the effect of esketamine (the S-enantiomer of ketamine) on POCD and the possible molecular mechanisms.
We investigated the effects of esketamine (10 mg/kg) on POCD using an exploratory laparotomy model in aged SD rats (24 months). Open field, novel object recognition, and morris water maze tests were performed on day 30 post-surgery. 24 h or 30 d post-surgery, brain tissue from the hippocampus and ventromedial prefrontal cortex (vmPFC) was harvested and subjected to histopathology and molecular biology analysis. During the in vitro experiment, primary astrocytes from the hippocampus and vmPFC were exposed to lipopolysaccharide (LPS) to investigate the pathological changes in astrocytes during the process of POCD.
Our results indicated that exploratory laparotomy could induce significant cognitive and memory decline, accompanied by A2-type astrocytes phenotype loss and increased expression of neuron Aβ-42, astrocytes GABA, stimulator of interferon genes (STING) and TANK-binding kinase 1 (TBK1). In addition, LPS exposure significantly decreased the mitochondrial membrane potential and upregulated the level of pyroptosis-associated proteins, including cleaved caspase-1 and IL-18. Notably, treatment with esketamine reversed these abnormalities in vivo and vitro. However, ADU-S100, a special STING activator, suppressed the protective effects of esketamine to a certain extent. Finally, C-176, an antagonist of STING, further enhanced the protective effects of esketamine against POCD.
Findings of our study suggest that esketamine can alleviate surgery-induced POCD in rats via inhibition of the STING/TBK1 signaling pathway.