Intraoperative Brainstem Auditory Evoked Potentials and Postoperative Nausea and Vomiting After Microvascular Decompression.

BACKGROUND: We performed this study to investigate the effect of intraoperative brainstem auditory evoked potential (IBAEP) changes on the development of postoperative nausea and vomiting (PONV) after microvascular decompression (MVD) for neurovascular cross compression. METHODS: A total of 373 consecutive cases were treated with MVD. The use of rescue antiemetics after surgery was used as an objective indicator of PONV. IBAEP monitoring was routinely performed in all. RESULTS: The use of rescue antiemetics was significantly associated with female sex (OR = 3.427; 95% CI, 2.077-5.654; P < 0.001), PCA use (OR = 3.333; 95% CI, 1.861-5.104; P < 0.001), and operation time (OR = 1.017; 95% CI, 1.008-1.026; P < 0.001). A Wave V peak delay of more than 1.0 milliseconds showed a significant relation with the use of rescue antiemetics (OR = 1.787; 95% CI, 1.114-2.867; P = 0.016) and a strong significant relation with the use of rescue antiemetics more than 5 times (OR = 2.426; 95% CI, 1.372-4.290; P = 0.002). CONCLUSIONS: A wave V peak delay of more than 1.0 milliseconds might have value as a predictor of PONV after MVD. More detailed neurophysiological studies will identify the exact pathophysiology underlying PONV after MVD.

Erratum: Correction of Affiliations in the Article "Preoperative Prognostic Nutritional Index Is a Prognostic Indicator of Cancer-Specific Survival in Patients Undergoing Endometrial Cancer Surgery".

This corrects the article on p. e163 in vol. 38, PMID: 37270918.

Preoperative Prognostic Nutritional Index Is a Prognostic Indicator of Cancer-Specific Survival in Patients Undergoing Endometrial Cancer Surgery.

BACKGROUND: The prognostic nutritional index (PNI) reflects systemic inflammation and nutritional status. This study aimed to evaluate the effect of preoperative PNI on postoperative cancer-specific survival in patients with endometrial cancer (EC). METHODS: Demographic, laboratory, and clinical data were retrospectively collected from 894 patients who underwent surgical resection of EC. Preoperative PNIs were determined from the serum albumin concentration and total lymphocyte count, which were measured within 1 month before surgery. Patients were classified into high PNI (n = 619) and low PNI (n = 275) groups according to the preoperative PNI cut-off value of 50.6. The stabilized inverse probability of treatment weighting (IPTW) method was used to reduce bias: a weighting cohort divided into high PNI (n = 615.4) and low PNI (n = 272.3) groups. The primary outcome measure was postoperative cancer-specific survival. RESULTS: The postoperative cancer-specific survival rate was higher in the high PNI group than the low PNI group in the unadjusted cohort (93.1% vs. 81.5%; proportion difference [95% confidence interval; 95% CI], 11.6% [6.6-16.6%]; P < 0.001) and in the IPTW-adjusted cohort (91.4% vs. 86.0%; 5.4% [0.8-10.2%]; P = 0.021). In the multivariate Cox proportional hazard regression model in the IPTW-adjusted cohort, high preoperative PNI (hazard ratio [95% CI], 0.60 [0.38-0.96]; P = 0.032) was an independent determinant of postoperative cancer-specific mortality. The multivariate-adjusted restricted cubic spline curve for the Cox regression model showed a significant negative association between preoperative PNI and postoperative cancer-specific mortality (P < 0.001). CONCLUSION: High preoperative PNI was associated with improved postoperative cancer-specific survival in patients undergoing surgery for EC.

The novel prognostic value of postoperative follow-up lateral spread response after microvascular decompression for hemifacial spasm.

OBJECTIVE: The lateral spread response (LSR) is an aberrant electrophysiological response in which a stimulus on one branch of the facial nerve spills over to other branches of the nerve, which can be captured by electrodes near each branch. The authors performed this study to evaluate the prognostic value of the follow-up LSR with a sufficient time interval from intraoperative LSR (IO-LSR) after microvascular decompression (MVD) for hemifacial spasm (HFS), excluding the interference of various intraoperative situations. METHODS: A total of 247 patients treated with MVD for HFS between June 2011 and March 2019 were enrolled in this study. The IO-LSR was routinely evaluated in all patients. The LSR was checked again on postoperative day (POD) 2 after surgery (POD2-LSR). A total of 228 patients (92.3%) were considered cured at the last clinical follow-up. RESULTS: The IO-LSR disappeared in 189 patients (76.5%), and among them, 181 patients (95.8%) were cured 1 year after surgery. The POD2-LSR disappeared in 193 patients (78.1%), and 185 patients (95.9%) among them were cured. Among the 189 patients in which the IO-LSR disappeared, the POD2-LSR reappeared in 26 patients (13.8%). In contrast, the POD2-LSR disappeared in 30 (51.7%) of 58 patients for whom the IO-LSR continued at the end of surgery. When classified into groups according to the status of the IO-LSR and POD2-LSR, in the group of patients in whom both LSRs disappeared, the cure rate was 98.2%, which was significantly higher than that of the other 3 groups (p < 0.05, Cochran-Armitage trend test). The use of both LSRs was found to be significantly associated with better predictability (p < 0.05, McNemar's test). CONCLUSIONS: Postoperative follow-up LSR examination may be beneficial in predicting clinical outcomes after MVD for HFS, especially when considered together with IO-LSR.

The 5% Lidocaine Patch for Decreasing Postoperative Pain and Rescue Opioid Use in Sternotomy: A Prospective, Randomized, Double-blind Trial.

PURPOSE: Poststernotomy pain (PSP), a primary concern after sternotomy, can negatively affect patients' satisfaction with surgery and quality of life. Many clinical trials have been conducted to examine the usefulness of lidocaine patches (LPs) for postoperative pain control for multiple types of surgery; however, the results of these trials are inconsistent. In addition, little is known about the use of LPs after cardiac procedures that require sternotomy. This prospective, double-blind, placebo-controlled trial aimed to determine the efficacy of the 5% LP application at the sternotomy site for reducing PSP and rescue opioid consumption. METHODS: The patients were randomly assigned to receive either the 5% LP or the placebo patch on each side of the incision site immediately after the surgery. The intensity of pain at 6, 12, 24, and 48 h after the patch application; the total dose of rescue opioids; incidence of nausea, vomiting, and sleep disturbance; and use of antiemetics were compared between the 2 groups. FINDINGS: Fifty-seven (31 in the LP group and 26 in the placebo group) patients were included. The pain intensity was significantly lower in the LP group at each time point (66%-68% pain reduction, P < 0.001, interaction of time × treatment P = 0.69). In addition, the total dose of rescue opioids used for 48 h was significantly lower in the L group (27.2% reduction, P = 0.008). No significant differences were found in other outcome variables between the 2 groups. IMPLICATIONS: The application of a 5% LP on each side of the sternotomy site can reduce PSP and additional opioid use without significant adverse effects in patients undergoing sternotomy. Thus, it can be considered as a standard and routine modality along with other analgesic medications for the management of PSP. Clinical Trial Registry in South Korea identifier: KCT0000476.

The Effect of a Transdermal Scopolamine Patch on Postoperative Nausea and Vomiting after Retromastoid Craniectomy with Microvascular Decompression: A Preliminary Single Center, Double-Blind, Randomized Controlled Trial.

Background: We performed this prospective double-blind randomized controlled trial to identify the effect of a preoperative prophylactic transdermal scopolamine (TDS) patch on postoperative nausea and vomiting (PONV) after retromastoid craniectomy with microvascular decompression (RMC-MVD). Methods: We recruited 38 patients undergoing RMC-MVD and randomized them into two groups: the TDS group (n = 19, application of the TDS patch) and placebo group (n = 19, application of a sham patch). Nausea (as a self-reported 100-mm visual analog scale (VAS) score; range, 0 (no nausea) to 10 (worst nausea)), vomiting, and the use of antiemetics were the primary endpoints. Results: There was no significant difference in terms of the incidence of PONV (73.7% in the TDS group and 78.9% in the placebo group; p = 1.00) between the groups. However, the mean nausea VAS score was significantly different at arrival to the general ward (0.93 ± 1.71 in the TDS group vs. 2.52 ± 2.85 in the placebo group; p = 0.046), and throughout the study period (0.03 ± 0.07 in the TDS group vs. 0.44 ± 0.71 in the placebo group; p = 0.029). Rescue antiemetics were more frequently used in the placebo group than in the TDS group (9 (47.4%) vs. 2 (10.5%), respectively; p = 0.029). The mean number of antiemetics used throughout the study period was significantly higher in the placebo group than in the TDS group (1.37 ± 2.19 vs. 0.16 ± 0.50, respectively; p = 0.029). Conclusions: The preoperative prophylactic use of a TDS patch was safe and effective in the management of PONV after RMC-MVD in terms of the severity of PONV and the use of rescue antiemetics.

A critical role of glutamate transporter type 3 in the learning and memory of mice.

Hippocampus-dependent learning and memory are associated with trafficking of excitatory amino acid transporter type 3 (EAAT3) to the plasma membrane. To assess whether this trafficking is an intrinsic component of the biochemical responses underlying learning and memory, 7- to 9-week old male EAAT3 knockout mice and CD-1 wild-type mice were subjected to fear conditioning. Their hippocampal CA1 regions, amygdalae and entorhinal cortices were harvested before, or 30 min or 3 h after the fear conditioning stimulation. We found that EAAT3 knockout mice had worse contextual and tone-related learning and memory than did the wild-type mice. The expression of EAAT3, glutamate receptor (GluR)1 and GluR2 in the plasma membrane and of phospho-GluR1 (at Ser 831) and phospho-CaMKII in the hippocampus of the wild-type mice was increased at 30 min after the fear conditioning stimulation. Similar biochemical changes occurred in the amygdala. Fear conditioning also increased the expression of c-Fos and activity-regulated cytoskeleton-associated protein (Arc) in the CA1 regions and of Arc in the entorhinal cortices of the wild-type mice. These biochemical responses were attenuated in the EAAT3 knockout mice. These results suggest that EAAT3 plays a critical role in learning and memory. Our results also provide initial evidence that EAAT3 may have receptor-like functions to participate in the biochemical reactions underlying learning and memory.

A peroxisome proliferator-activated receptor gamma agonist attenuates neurological deficits following spinal cord ischemia in rats.

OBJECTIVE: Neuroprotective effects of the peroxisome proliferator-activated receptor gamma (PPARγ) agonist in cerebral ischemia have been reported, but the effect of a PPARγ agonist on spinal cord ischemia has not been investigated. The objective of this study was to investigate the effect of a PPARγ agonist on spinal cord ischemia. Pioglitazone, a PPARγ agonist, was administered in a rat model of spinal cord ischemia, and the extent of neurological damage and histological alterations were assessed. METHODS: Forty-five rats were randomly enrolled into one of the three groups: (1) pioglitazone group (group PIO): rats were treated with pioglitazone 24 hours before ischemia; (2) control group (group C): rats were treated with the same volume of saline 24 hours before ischemia; and (3) sham group (group sham): rats were treated with the same volume of saline 24 hours before the sham surgery. Spinal cord ischemia was induced using a balloon-tipped catheter placed on the proximal descending aorta. Neurologic function was assessed using the motor deficit index (0 = normal, 6 = complete paralysis) during the 48 hours after reperfusion. Histological and biochemical evaluations were then performed. RESULTS: Compared with group C, group PIO presented with lower motor deficit index 48 hours after reperfusion (5.0 [4.0-6.0] vs 3.0 [2.0-3.0]; group C vs group PIO, respectively; P < .001). Group PIO presented with a higher number of normal motor neurons (10.7 [8.1-11.9] vs 14.7 [14.0-15.3]; group C vs group PIO, respectively; P = .009) and a smaller area of infarcts (48.4% [46.3%-54.0%] vs 16.8% [11.5%-18.3%]; group C vs group PIO, respectively; P = .009) when compared with group C. The degree of inflammatory reactions, assessed by microglia activities, was significantly reduced in group PIO. Oxidative stress level, assessed using malonydialdehyde assay, was significantly reduced in group PIO relative to group C (192.21% [173.5%-206.4%] of sham vs 141.1% [131.7%-152.1%] of sham; group C vs group PIO, respectively; P = .007). The sham group exhibited no abnormality upon neurological or histological examination. CONCLUSIONS: PPARγ agonist pioglitazone pretreatment significantly reduces infarct volume and attenuates neurological deficits following spinal cord ischemia. The possible mechanism of neuroprotection by PPARγ agonist may involve modulation of inflammatory reaction and oxidative stress.

Effects of isoflurane on learning and memory functions of wild-type and glutamate transporter type 3 knockout mice.

OBJECTIVES: General anesthetics may contribute to the post-operative cognitive dysfunction. This study was designed to determine the effects of isoflurane on the learning and memory of healthy animals or animals with a decreased brain antioxidative capacity. METHODS: Seven- to nine-week-old female CD-1 wild-type mice or glutamate transporter type 3 (EAAT3) knockout mice whose brains have a decreased glutathione level were exposed to or were not exposed to 1.3% isoflurane for 2 h. They were subjected to fear conditioning or Barnes maze tests 1 week later. KEY FINDINGS: The EAAT3 knockout mice had less freezing behaviour than the wild-type mice in tone-related fear. Isoflurane did not affect the freezing behaviour of the wild-type and EAAT3 knockout mice. The time for the wild-type and EAAT3 knockout mice to identify the target hole in the training sessions and memory test with the Barnes maze was not affected by isoflurane. However, the EAAT3 knockout mice took longer to identify the target hole than the wild-type mice in these tests. CONCLUSIONS: These results suggest that EAAT3 knockout mice have significant cognitive impairment. Isoflurane may not significantly affect the cognition of wild-type and EAAT3 knockout mice in a delayed phase after isoflurane exposure.