Alterations of the gut microbiota in patients with schizophrenia.

Introduction: Schizophrenia is a complex psychiatric disorder, of which molecular pathogenesis remains largely unknown. Accumulating evidence suggest that gut microbiota may affect brain function via the complex gut-brain axis, which may be a potential contributor to schizophrenia. However, the alteration of gut microbiota showed high heterogeneity across different studies. Therefore, this study aims to identify the consistently altered gut microbial taxa associated with schizophrenia. Methods: We conducted a systematic search and synthesis of the up-to-date human gut microbiome studies on schizophrenia, and performed vote counting analyses to identify consistently changed microbiota. Further, we investigated the effects of potential confounders on the alteration of gut microbiota. Results: We obtained 30 available clinical studies, and found that there was no strong evidence to support significant differences in α-diversity and ß-diversity between schizophrenic patients and healthy controls. Among 428 differential gut microbial taxa collected from original studies, we found that 8 gut microbial taxa were consistently up-regulated in schizophrenic patients, including Proteobacteria, Gammaproteobacteria, Lactobacillaceae, Enterobacteriaceae, Lactobacillus, Succinivibrio, Prevotella and Acidaminococcus. While 5 taxa were consistently down-regulated in schizophrenia, including Fusicatenibacter, Faecalibacterium, Roseburia, Coprococcus and Anaerostipes. Discussion: These findings suggested that gut microbial changes in patients with schizophrenia were characterized by the depletion of anti-inflammatory butyrate-producing genera, and the enrichment of certain opportunistic bacteria genera and probiotics. This study contributes to further understanding the role of gut microbiota in schizophrenia, and developing microbiota-based diagnosis and therapy for schizophrenia.

Norepinephrine versus phenylephrine on cerebral tissue oxygen saturation during prophylactic infusion to prevent spinal hypotension for Caesarean birth.

BACKGROUND: Phenylephrine may cause a reduction in maternal cerebral tissue oxygen saturation (SctO2) during Caesarean birth to prevent spinal hypotension; however, the effect of norepinephrine has not been assessed. We hypothesized that norepinephrine was more effective than phenylephrine in maintaining SctO2 when preventing spinal hypotension during Caesarean birth. METHODS: We conducted a randomized, double-blind, controlled study. Sixty patients were randomly assigned to prophylactic norepinephrine or phenylephrine to maintain blood pressure during spinal anesthesia for Caesarean birth. SctO2, systolic blood pressure, and heart rate were recorded. The primary outcome was the incidence of a 10% reduction of intraoperative SctO2 from baseline or more during Caesarean birth. RESULTS: The norepinephrine group had a lower incidence of more than 10% reduction of intraoperative SctO2 from baseline than that of the phenylephrine group (13.3% vs 40.0%, P = .02). The change in SctO2 after 5 minutes of norepinephrine infusion was higher than that after phenylephrine infusion (-3.4 ±â€…4.7 vs -6.2 ±â€…5.6, P = .04). The change in SctO2 after 10 minutes of norepinephrine infusion was higher than that after phenylephrine infusion (-2.5 ±â€…4.4 vs -5.4 ±â€…4.6, P = .006). The norepinephrine group showed greater left- and right-SctO2 values than the phenylephrine group at 5 to 10 minutes. However, the change in systolic blood pressure was comparable between the 2 groups. CONCLUSION: Norepinephrine was more effective than phenylephrine in maintaining SctO2 when preventing spinal hypotension during Caesarean birth. However, the changes in clinical outcomes caused by differences in SctO2 between the 2 medications warrant further studies.

A novel subcritical water synergistic co-treatment of brominated epoxy resin and copper-based spent catalysts: debromination, phenol production, and copper recovery.

In this study, a high-efficiency co-treatment strategy for brominated epoxy resin (BER) and copper-based spent catalyst (CBSC) was developed by using subcritical water (SubCW) process. Multivalent species of copper released from CBSC could accelerate the electron transfer of the SubCW system and efficiently catalyze radical reactions to promote the debromination and decomposition of BER, and had an effect on the capture and binding of bromine species. Meanwhile, the formation of HBr by the BER debromination resulted in a decrease in the system pH and markedly enhanced the leaching/recovery of Cu from CBSC. The optimal conditions of the SubCW co-treatment process were as follows: reaction temperature of 350 °C, solid-to-liquid ratio of 1:30 g/mL, BER-to-CBSC mass ratio of 10:1 g/g, and reaction time of 60 min. Under the optimal conditions, 97.12 % of the Br could be removed from BER by the SubCW co-treatment process and a high-purity phenol (64.09 %) could be obtained in the oil phase product, and 86.44 % of Cu in the CBSC could be leached and recovered. The introduction of CBSC significantly changed the decomposition path of BER. Compared to the SubCW process without CBSC, bromine-free oils products could be obtained by the co-treatment process of BER and CBSC at low-temperature. This study provided a novel understanding of resource conversion mechanism of BER and CBSC in subcritical water medium via the synergistic effect between the two different waste streams to improve treatment efficiency and synchronously recover high-value products.

Effect of phenylephrine rescue injection on hypotension after spinal anaesthesia for caesarean delivery when guided by both heart rate and SBP during an early warning window: A randomised controlled trial.

BACKGROUND: Spinal anaesthesia is now the most common technique for caesarean delivery. However, because of the intermittent nature of noninvasive blood pressure (NIBP) measurements, maternal blood pressure may become hypotensive between the measurements. There is thus an inbuilt delay before the anaesthesiologist can intervene to counteract the hypotension. Based on the principle that changes in blood pressure can induce compensatory changes in the heart rate (HR), combining the NIBP with real-time HR, we designed two warning windows to predict hypotension and hypertension. OBJECTIVE: To evaluate whether phenylephrine administration guided by these warning windows would help maintain haemodynamic stability. SETTING: A teaching hospital. DESIGN: A randomised controlled trial. PATIENTS: One hundred and ten pregnant women scheduled for elective caesarean delivery were enrolled, from which, after exclusions, 86 were eligible for the study. INTERVENTIONS: All eligible patients received a continuous intravenous infusion of phenylephrine as soon as spinal anaesthesia was initiated. Thereafter, patients were randomly assigned to two groups. In the test group (Win-Group): rescue phenylephrine administration was triggered by an early warning window of HR above 100 beats per minute (bpm) and SBP 90 to 110 mmHg; pausing the infusion phenylephrine was triggered by a HR lower than 60 bpm and SBP greater than 90 mmHg. In the control group, phenylephrine was guided by BP only when it appeared on the monitor: SBP less than 90 mmHg was the trigger for administering rescue phenylephrine; SBP greater than 110 mmHg was the trigger for pausing the phenylephrine infusion. MAIN OUTCOME MEASURES: The primary outcome was incidence of hypotension. Secondary outcomes were the incidence of hypertension and other adverse haemodynamic events. RESULTS: The incidence of hypotension was significantly lower in the Win-Group than in the BP-Group (27.8 vs. 66.7%, P = 0.001). The minimum SBP was significantly higher in Win-Group than in BP-Group (93.9 ±â€Š9.49 vs. 86.7 ±â€Š11.16 mmHg, P  = 0.004). There was no significant difference in the incidence of hypertension between groups. CONCLUSION: After spinal anaesthesia for caesarean delivery, when phenylephrine infusion is guided by HR along with BP from a warning window it effectively reduces the incidence of hypotension without any significant effect on incidence of hypertension. TRIAL REGISTRATION: Chictr.org.cn; Identifier: ChiCTR 2100041812.

Effect of Process Parameters on Joint Performance in Hot Pressure Welding of 6061 Aluminum Alloy to CF/PA66.

Polymer-metal hybrid structures combine the merits of polymer and metal materials, making them widely applicable in fields such as aerospace and automotive industries. However, the main challenge lies in achieving efficient and strong connections between the metal and polymer components. This paper uses the jet electrochemical machining (Jet-ECM) method to customize the surface morphologies on 6061 aluminum alloy (AA6061) sheets. The connection between AA6061 and carbon fiber-reinforced PA66 (CF/PA66) is then achieved through hot pressure welding (HPW). The effects of aluminum alloy surface morphology, welding force, and welding time on the mechanical properties and microstructure of the joint are investigated. The optimal process parameters are determined by the design of the experiment. The results show that the aluminum alloy surface morphology has the greatest impact on the mechanical property of the welded joint. The optimal process parameters are surface morphology with wider, shallower, and sparsely distributed grooves on the aluminum alloy surface, the welding force is 720 N, the welding time is 12 s, the welding temperature is 360 °C, the cooling time is 16 s, and the optimal peak load of the joint is 6690 N. Under the optimal parameters, the fracture morphology in the AA6061 side is almost entirely covered with CF/PA66. The joint experiences cohesive failure in most areas and fiber-matrix debonding in a small area.

The Effects of Appropriate Perioperative Exercise on Perioperative Neurocognitive Disorders: a Narrative Review.

Perioperative neurocognitive disorders (PNDs) are now considered the most common neurological complication in older adult patients undergoing surgical procedures. A significant increase exists in the incidence of post-operative disability and mortality in patients with PNDs. However, no specific treatment is still available for PNDs. Recent studies have shown that exercise may improve cognitive dysfunction-related disorders, including PNDs. Neuroinflammation is a key mechanism underlying exercise-induced neuroprotection in PNDs; others include the regulation of gut microbiota and mitochondrial and synaptic function. Maintaining optimal skeletal muscle mass through preoperative exercise is important to prevent the occurrence of PNDs. This review summarizes current clinical and preclinical evidence and proposes potential molecular mechanisms by which perioperative exercise improves PNDs, providing a new direction for exploring exercise-mediated neuroprotective effects on PNDs. In addition, it intends to provide new strategies for the prevention and treatment of PNDs.

An alkali-enhanced subcritical water treatment strategy of short-chain chlorinated paraffins: Dechlorination and hydrocarbons recovery.

As persistent organic pollutants, short-chain chlorinated paraffins (SCCPs) have attracted wide attention in the field of environmental health risk and hazardous waste management. Efficient dechlorination of high content of SCCPs in plastic waste is the committed step for its detoxification and safety treatment. In this study, a high-efficiency and low-temperature process for dechlorination and hydrocarbons recovery from typical SCCPs (52#SCCPs) by subcritical water (SubCW) with alkali enhancer was developed. The introduction of alkali enhancer in the SubCW process had significantly enhanced effect on the dechlorination of 52#SCCPs, and the order of the enhanced effect of alkali enhancer for the dechlorination was NaOH > Na2CO3 > NaHCO3 > NH3·H2O > KOH. The dechlorination behaviors of 52#SCCPs in the NaOH-enhanced SubCW process were studied systematically under different conditions including temperature, residence time, alkali concentration, and volume ratio. The results showed that high-efficiency dechlorination (100 %) of 52#SCCPs could be achieved by the NaOH-enhanced SubCW process at low temperature for a short time (250 °C, 5 min). All of the chlorine released from the molecular chain of 52#SCCPs was transferred to the aqueous phase in the form of inorganic chlorine. The continuous HCl elimination reaction was the primary dechlorination mechanism for 52#SCCPs in the NaOH-enhanced SubCW process. After the dechlorination of 52#SCCPs, high value-added hydrocarbons such as 2,4-hexadiyne (31.74 %) could be obtained. The alkali-enhanced SubCW process proposed in this study is believed to be an environmentally friendly and high-efficiency method for dechlorination/detoxification and resource recovery of SCCPs.

Integrated pathway and network analyses of metabolomic alterations in peripheral blood of patients with depression.

Depression is a serious mental illness, but the molecular mechanisms of depression remain unclear. Previous research has reported metabolomic changes in the blood of patients with depression, while integrated analysis based on these altered metabolites was still lacking. The objective of this study was to integrate metabolomic changes to reveal the underlying molecular alternations of depression. We retrieved altered metabolites in the blood of patients with depression from the MENDA database. Pathway analysis was conducted to explore enriched pathways based on candidate metabolites. Pathway crosstalk analysis was performed to explore potential correlations of these enriched pathways, based on their shared candidate metabolites. Moreover, potential interactions of candidate metabolites with other biomolecules such as proteins were assessed by network analysis. A total of 854 differential metabolite entries were retrieved in peripheral blood of patients with depression, including 555 unique candidate metabolites. Pathway analysis identified 215 significantly enriched pathways, then pathway crosstalk analysis revealed that these pathways were clustered into four modules, including amino acid metabolism, nucleotide metabolism, energy metabolism and others. Additionally, eight molecular networks were identified in the molecular network analysis. The main functions of these networks involved amino acid metabolism, molecular transport, inflammatory responses and others. Based on integrated analysis, our study revealed pathway-based modules and molecular networks associated with depression. These results will contribute to the underlying knowledge of the molecular mechanisms in depression.

Preventing Spinal Hypotension During Cesarean Birth With Two Initial Boluses of Norepinephrine in Chinese Parturients: A Randomized, Double-Blind, Controlled Trial.

BACKGROUND: Norepinephrine is effective in preventing spinal hypotension during cesarean birth; however, an optimal regimen has not been determined. We hypothesized that an initial bolus of norepinephrine improves efficacy of spinal hypotension prophylaxis beyond continuous norepinephrine alone. METHODS: In this double-blind, controlled study, 120 patients scheduled for cesarean birth under spinal anesthesia were randomly allocated to receive a norepinephrine bolus at 0.05 or 0.10 µg/kg, followed by norepinephrine infusion at a rate of 0.05 µg·kg -1 ·min -1 . The primary outcome was the frequency of spinal hypotension during cesarean birth. The doses of the rescue drug (phenylephrine), frequency of nausea or vomiting, duration of hypotension, frequency of intraoperative hypertension, frequency of bradycardia, and fetal outcomes were also compared. RESULTS: One-hundred-fifteen patients were included in the analysis. Compared with the 0.05 µg/kg group, the frequency of spinal hypotension was lower in the 0.10 µg/kg group (20.7% vs 45.6%; odds ratio [OR], 0.31; 95% confidence interval (CI), 0.14-0.71; P = .004). Fewer rescue doses of phenylephrine (0 [0,0] vs 0 [0,80]; 95% CI for the difference, 0 (0-0); P = .006) were required, and the frequency of nausea or vomiting was lower (5.2% vs 17.5%; OR, 0.26; 95% CI, 0.07-0.99; P = .04) in the 0.10 µg/kg group. The duration of hypotension was shorter in the 0.10 µg/kg group than that in the 0.05 µg/kg group (0 [0,0] vs 0 [0,2]; 95% CI for the difference, 0 [0-0]; P = .006). The incidence of intraoperative hypertension, frequency of bradycardia, and fetal outcomes were comparable between the 2 groups. CONCLUSIONS: With a fixed-rate norepinephrine infusion of 0.05 µg·kg -1 ·min -1 , the 0.10 µg/kg initial bolus was more effective in reducing the incidence of spinal hypotension compared with the 0.05 µg/kg initial bolus.

α7 Nicotinic Acetylcholine Receptor May Be a Pharmacological Target for Perioperative Neurocognitive Disorders.

Background: The α7 nicotinic acetylcholine receptor (α7nAChR) is a promising therapeutic target in neurodegenerative diseases. This study examined the effects of surgery and anesthesia on α7nAChR expression in the central nervous system and determined the mechanisms by which α7nAChR mediates neuroprotection in perioperative neurocognitive disorders (PNDs) in aged mice. Methods: Eighteen-month-old male C57BL/6J mice underwent aseptic laparotomy under isoflurane anesthesia, maintaining spontaneous ventilation to establish the PNDs model. Agonists and antagonists of the α7nAChR and tropomyosin receptor kinase B (TrkB) receptors were administered before anesthesia. The α7nAChR expression, peripheral as well as hippocampal interleukin-1ß (IL-1ß), and the brain-derived neurotrophic factor (BDNF) levels were assessed. Separate cohorts of aged mice were tested for cognitive decline using the Morris water maze (MWM). Results: Surgery and anesthesia significantly suppressed α7nAChR expression in the hippocampus and cortex. Surgery-induced IL-1ß upregulation in the serum as well as hippocampus and hippocampal microglial activation were reversed by the α7nAChR agonist. A significant reduction in the hippocampal BDNF levels were also observed. The α7nAChR stimulation reversed, and α7nAChR suppression promoted BDNF reduction in the hippocampus. Blocking the BDNF/TrkB signaling pathway abolished α7nAChR-induced neuroprotection in PNDs, as evidenced by poor cognitive performance in the MWM test. Conclusions: These data reveal that α7nAChR plays a key role in PNDs. The mechanisms of the anti-inflammatory pathway and BDNF/TrkB signaling pathways are involved in α7nAChR-meidiated neuroprotection in PNDs.

Transplanted Human Oligodendrocyte Progenitor Cells Restore Neurobehavioral Deficits in a Rat Model of Preterm White Matter Injury.

Background: Preterm white matter injury (PWMI) is a common brain injury and a leading cause of life-long neurological deficits in premature infants; however, no effective treatment is available yet. This study aimed to investigate the fate and effectiveness of transplanted human oligodendrocyte progenitor cells (hOPCs) in a rat model of PWMI. Methods: Hypoxia-ischemia was induced in rats at postnatal day 3, and hOPCs (6 × 105 cells/5 µL) were intracerebroventricularly transplanted at postnatal day 7. Neurobehavior was assessed 12 weeks post-transplant using the CatWalk test and Morris water maze test. Histological analyses, as well as immunohistochemical and transmission electron microscopy, were performed after transcardial perfusion. Results: Transplanted hOPCs survived for 13 weeks in PWMI brains. They were widely distributed in the injured white matter, and migrated along the corpus callosum to the contralateral hemisphere. Notably, 82.77 ± 3.27% of transplanted cells differentiated into mature oligodendrocytes, which produced myelin around the axons. Transplantation of hOPCs increased the fluorescence intensity of myelin basic protein and the thickness of myelin sheaths as observed in immunostaining and transmission electron microscopy, while it reduced white matter atrophy at the level of gross morphology. With regard to neurobehavior, the CatWalk test revealed improved locomotor function and inter-paw coordination after transplantation, and the cognitive functions of hOPC-transplanted rats were restored as revealed by the Morris water maze test. Conclusions: Myelin restoration through the transplantation of hOPCs led to neurobehavioral improvements in PWMI rats, suggesting that transplanting hOPCs may provide an effective and promising therapeutic strategy in children with PWMI.

Case Report: Pink Urine Syndrome Following Exposure to Propofol: A Rare, Impressive but Benign Complication.

Drug-induced changes in urine color induced by drugs may have clinical significance. Pink urine syndrome (PUS), which has been associated with urinary uric acid (UA) disorders, is most frequently reported in patients with morbid obesity undergoing gastric bypass surgery and/or from propofol anesthesia use in those who potentially have preexisting UA metabolism disorders. However, PUS has rarely occurred following exposure to propofol in non-obese patients, and literature on long-term follow-up after PUS is scarce. We report a case of PUS induced by propofol in a previously healthy non-obese woman after undergoing thoracoscopic wedge resection of pulmonary nodules under general anesthesia using propofol. The patient suddenly developed pink urine 4 h after surgery. A pink sediment rapidly precipitated at the bottom of the test tube following centrifugation of the urine. Amorphous, colorless UA-like crystals were identified under a polarizing microscope. The diagnosis of PUS was confirmed by examining the urinary UA concentration. The patient recovered and as followed-up for 1 month, during which she did not experience any urinary complications. To our knowledge, this is the first report to describe in detail a case of PUS caused by propofol in a non-obese patient with follow-up. PUS is usually benign and can resolve by rapidly on administering lactated Ringer's solution; however, the potential risk of urinary complications, particularly UA lithiasis, should be fully realized.

[Tumor necrosis factor α inhibits the migration of human oligodendrocyte precursor cells in vitro].

Objective To investigate the impact of tumor necrosis factor alpha (TNF-α) on the migration ability of oligodendrocyte precursor cells (OPCs) derived from human adult neural stem cells (NSCs) for transplantation therapy. Methods Flow cytometry was performed to detect the expressions of platelet derived growth factor receptor alpha (PDGFRα) and ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1 (ST8SIA1/A2B5) in human OPCs. OPCs were cultured and incubated with 0, 10, 100, 200 ng/mL TNF-α for 18 hours. OPC viability was detected by CCK-8 assay and OPC migration was detected by TranswellTM migration assay. Results OPCs derived from human adult NSC specifically expressed PDGFRα (87.9%) and A2B5 (40.0%). Treatment with 10 ng/mL TNF-α had no impact on OPC viability while both 100 ng/mL and 200 ng/mL TNF-α treatments decreased OPC viability significantly. OPC migration was reduced significantly in 10 ng/mL TNF-α treated group compared with the blank control. Conclusion TNF-α inhibits the migration of the cultured OPCs.

Identifying the functions of two biomarkers in human oligodendrocyte progenitor cell development.

BACKGROUND: Human oligodendrocyte precursor cells (hOPCs) are an important source of myelinating cells for cell transplantation to treat demyelinating diseases. Myelin oligodendrocytes develop from migratory and proliferative hOPCs. It is well known that NG2 and A2B5 are important biological markers of hOPCs. However, the functional differences between the cell populations represented by these two biomarkers have not been well studied in depth. OBJECTIVE: To study the difference between NG2 and A2B5 cells in the development of human oligodendrocyte progenitor cells. METHODS: Using cell sorting technology, we obtained NG2+/-, A2B5+/- cells. Further research was then conducted via in vitro cell proliferation and migration assays, single-cell sequencing, mRNA sequencing, and cell transplantation into shiverer mice. RESULTS: The proportion of PDGFR-α + cells in the negative cell population was higher than that in the positive cell population. The migration ability of the NG2+/-, A2B5+/- cells was inversely proportional to their myelination ability. The migration, proliferation, and myelination capacities of the negative cell population were stronger than those of the positive cell population. The ability of cell migration and proliferation of the four groups of cells from high to low was: A2B5- > NG2- > NG2+ > A2B5+. The content of PDGFR-α+ cells and the ability of cell differentiation from high to low was: NG2- > A2B5- > A2B5+ > NG2+. CONCLUSION: In summary, NG2+ and A2B5+ cells have poor myelination ability due to low levels of PDGFR-α+ cells. Therefore, hOPCs with a higher content of PDGFR-α+ cells may have a better effect in the cell transplantation treatment of demyelinating diseases.

Study on the Safety of Human Oligodendrocyte Precursor Cell Transplantation in Young Animals and Its Efficacy on Myelination.

Oligodendrocyte precursor cells (OPCs) can differentiate into myelinating oligodendrocytes during embryonic development, thereby representing an important potential source for myelin repair or regeneration. To the best of our knowledge, there are very few OPCs from human sources (human-derived OPCs [hOPCs]). In this study, we aimed to evaluate the safety and remyelination capacity of hOPCs developed in our laboratory, transplanted into the lateral ventricles of young animals. Several acute and chronic toxicity experiments were conducted in which different doses of hOPCs were transplanted into the lateral ventricles of Sprague-Dawley rats of different ages. The toxicity, biodistribution, and tumor formation ability of the injected hOPCs were examined by evaluating the rats' vital signs, developmental indicators, neural reflexes, as well as by hematology, immunology, and pathology. In addition, the hOPCs were transplanted into the corpus callosum of the shiverer mouse to verify cell myelination efficacy. Overall, our results show that transplanted hOPCs into young mice are nontoxic to their organ function or immune system. The transplanted cells engrafted in the brain and did not appear in other organs, nor did they cause tissue proliferation or tumor formation. In terms of efficacy, the transplanted hOPCs were able to form myelin in the corpus callosum, alleviate the trembling phenotype of shiverer mice, and promote normal development. The transplantation of hOPCs is safe; they can effectively form myelin in the brain, thereby providing a theoretical basis for the future clinical transplantation of hOPCs.

Nasotracheal intubation-extubation-intubation and asleep-awake-asleep anesthesia technique for deep brain stimulation.

BACKGROUND: The asleep-awake-asleep (AAA) technique and laryngeal mask airway (LMA) is a common general anesthesia technique for deep brain stimulation (DBS) surgery. However, the LMA is not always the ideal artificial airway. In this report, we presented our experiences with nasotracheal intubation-extubation-intubation (IEI) and AAA techniques in DBS surgery for Parkinson's disease (PD) patients to meet the needs of surgery and ensure patients' safety and comfort. CASE PRESENTATION: Three PD patients scheduled for DBS surgery had to receive general anesthesia for various reasons. For the first asleep stage, general anesthesia and nasotracheal intubation was completed with routine methods. During the awake stage, we pulled the nasotracheal tube back right above the epiglottis under fiberoptic bronchoscope (FOB) guidance for microelectrode recording (MER), macrostimulation testing and verbal communication. Once monitoring is completed, we induced anesthesia with rapid sequence induction and utilized the FOB to advance the nasotracheal tube into the trachea again. To minimize airway irritations during the process, we sprayed the airway with lidocaine before any manipulation. The neurophysiologists completed neuromoinitroing successfully and all three patients were satisfied with the anesthesia provided at follow-up. CONCLUSION: Nasotracheal IEI and AAA anesthetic techniques should be considered as a viable option during DBS surgery.