The Reliability of Measuring Early Brain Edema with Computed Tomography.

BACKGROUND: Postoperative brain edema is a common complication in patients with high-grade glioma after craniotomy. Both Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are applied to diagnose brain edema. Usually, MRI is considered to be better than CT for identifying brain edema. However, MRI is not generally applied in diagnosing acute cerebral edema in the early postoperative stage. Whether CT is reliable in detecting postoperative brain edema in the early stage is unknown. OBJECTIVE: This study aimed at investigating the agreement and correlation between CT and MRI for measuring early postoperative brain edema. METHODS: Patients with high-grade glioma who underwent craniotomy in the Beijing Tiantan hospital from January 2017 to October 2018 were retrospectively analyzed. The region of interest and operative cavity were manually outlined, and the volume of postoperative brain edema was measured on CT and MRI. Pearson correlation testing and the Intraclass Correlation Coefficient (ICC) were used to evaluate the association and agreement between CT and MRI for detecting the volume of postoperative brain edema. RESULTS: Twenty patients were included in this study. The interrater agreement was perfect for detecting brain edema (CT: κ=1, ICC=0.977, P<0.001; MRI: κ=0.866, ICC=0.963, P<0.001). A significant positive correlation and excellent consistency between CT and MRI were found for measuring the volume of brain edema (rater 1: r=0.97, ICC=0.934, P<0.001; rater 2: r=0.97, ICC=0.957, P<0.001). CONCLUSION: Substantial comparability between CT and MRI is demonstrated for detecting postoperative brain edema. It is reliable to use CT for measuring brain edema volume in the early stage after surgery.

Awake craniotomy for auditory brainstem implant in patients with neurofibromatosis type 2: Four case reports.

BACKGROUND: The auditory brainstem implant (ABI) is a significant treatment to restore hearing sensations for neurofibromatosis type 2 (NF2) patients. However, there is no ideal method in assisting the placement of ABIs. In this case series, intraoperative cochlear nucleus mapping was performed in awake craniotomy to help guide the placement of the electrode array. CASE SUMMARY: We applied the asleep-awake-asleep technique for awake craniotomy and hearing test via the retrosigmoid approach for acoustic neuroma resections and ABIs, using mechanical ventilation with a laryngeal mask during the asleep phases, utilizing a ropivacaine-based regional anesthesia, and sevoflurane combined with propofol/remifentanil as the sedative/analgesic agents in four NF2 patients. ABI electrode arrays were placed in the awake phase with successful intraoperative hearing tests in three patients. There was one uncooperative patient whose awake hearing test needed to be aborted. In all cases, tumor resection and ABI were performed safely. Satisfactory electrode effectiveness was achieved in awake ABI placement. CONCLUSION: This case series suggests that awake craniotomy with an intraoperative hearing test for ABI placement is safe and well tolerated. Awake craniotomy is beneficial for improving the accuracy of ABI electrode placement and meanwhile reduces non-auditory side effects.

Perioperative massive cerebral stroke in thoracic patients: Report of three cases.

BACKGROUND: Perioperative stroke is a rare but devastating complication. The risk factors for massive cerebral stroke in surgical patients include older age, male sex, prior cerebrovascular disease, hypertension, renal failure, smoking, diabetes mellitus, and atrial fibrillation. CASE SUMMARY: We describe two cases of perioperative massive cerebral stroke following thoracic surgery and one case following bronchoscopy. Neurologic symptoms, including changes in mental status and hemiplegia, occurred within 10 h after surgery in the three patients. All three patients died after the surgery. CONCLUSION: Perioperative massive cerebral stroke may be more likely to occur in thoracic surgical patients if there are pre-existing factors including previous stroke, hypotension, and hypoxemia. Sufficient pain control after surgery and timely neurology consultation and management are helpful for the diagnosis and control of stroke in high-risk patients.

Association between neutrophil-to-lymphocyte ratio and major postoperative complications after carotid endarterectomy: A retrospective cohort study.

BACKGROUND: Carotid artery cross-clamping during carotid endarterectomy (CEA) may damage local cerebral perfusion and induce cerebral ischemia-reperfusion injury to activate local inflammatory responses. Neutrophil-to-lymphocyte ratio (NLR) is an indicator that reflects systemic inflammation. However, the correlation between NLR and complications after CEA remains unclear. AIM: To investigate the association between NLR and major complications after surgery in patients undergoing CEA. METHODS: This retrospective cohort study included patients who received CEA between January 2016 and July 2018 at Beijing Tiantan Hospital. Neutrophil and lymphocyte counts in whole blood within 24 h after CEA were collected. The primary outcome was the composite of major postoperative complications including neurological, pulmonary, cardiovascular and acute kidney injuries. The secondary outcomes included infections, fever, deep venous thrombosis, length of hospitalization and cost of hospitalization. Statistical analyses were performed using EmpowerStats software and R software. RESULTS: A total of 224 patients who received CEA were screened for review and 206 were included in the statistical analyses; of whom, 40 (19.42%) developed major postoperative complications. NLR within 24 h after CEA was significantly correlated with major postoperative complications (P = 0.026). After confounding factors were adjusted, the odds ratio was 1.15 (95%CI: 1.03-1.29, P = 0.014). The incidence of major postoperative complications in the high NLR group was 8.47 times that in the low NLR group (P = 0.002). CONCLUSION: NLR is associated with major postoperative complications in patients undergoing CEA.

Changes in Rat Brain MicroRNA Expression Profiles Following Sevoflurane and Propofol Anesthesia.

BACKGROUND: Sevoflurane and propofol are widely used anesthetics for surgery. Studies on the mechanisms of general anesthesia have focused on changes in protein expression properties and membrane lipid. MicroRNAs (miRNAs) regulate neural function by altering protein expression. We hypothesize that sevoflurane and propofol affect miRNA expression profiles in the brain, expect to understand the mechanism of anesthetic agents. METHODS: Rats were randomly assigned to a 2% sevoflurane group, 600 µg·kg - 1·min - 1 propofol group, and a control group without anesthesia (n = 4, respectively). Treatment group was under anesthesia for 6 h, and all rats breathed spontaneously with continuous monitoring of respiration and blood gases. Changes in rat cortex miRNA expression profiles were analyzed by miRNA microarrays and validated by quantitative real-time polymerase chain reaction (qRT-PCR). Differential expression of miRNA using qRT-PCR among the control, sevoflurane, and propofol groups were compared using one-way analysis of variance (ANOVA). RESULTS: Of 677 preloaded rat miRNAs, the microarray detected the expression of 277 miRNAs in rat cortex (40.9%), of which 9 were regulated by propofol and (or) sevoflurane. Expression levels of three miRNAs (rno-miR-339-3p, rno-miR-448, rno-miR-466b-1FNx01) were significantly increased following sevoflurane and six (rno-miR-339-3p, rno-miR-347, rno-miR-378FNx01, rno-miR-412FNx01, rno-miR-702-3p, and rno-miR-7a-2FNx01) following propofol. Three miRNAs (rno-miR-466b-1FNx01, rno-miR-3584-5p and rno-miR-702-3p) were differentially expressed by the two anesthetic treatment groups. CONCLUSIONS: Sevoflurane and propofol anesthesia induced distinct changes in brain miRNA expression patterns, suggesting differential regulation of protein expression. Determining the targets of these differentially expressed miRNAs may help reveal both the common and agent-specific actions of anesthetics on neurological and physiological function.

Propofol ameliorates calpain-induced collapsin response mediator protein-2 proteolysis in traumatic brain injury in rats.

BACKGROUND: Collapsin response mediator protein-2 (CRMP2), a multifunctional cytosolic protein highly expressed in the brain, is degraded by calpain following traumatic brain injury (TBI), possibly inhibiting posttraumatic neurite regeneration. Lipid peroxidation (LP) is involved in triggering postinjury CRMP2 proteolysis. We examined the hypothesis that propofol could attenuate LP, calpain-induced CRMP2 degradation, and brain injury after TBI. METHODS: A unilateral moderate controlled cortical impact injury was induced in adult male Sprague-Dawley rats. The animals were randomly divided into seven groups: Sham control group, TBI group, TBI + propofol groups (including propofol 1 h, 2 h, and 4 h groups), TBI + U83836E group and TBI + fat emulsion group. The LP inhibitor U83836E was used as a control to identify that antioxidation partially accounts for the potential neuroprotective effects of propofol. The solvent of propofol, fat emulsion, was used as the vehicle control. Ipsilateral cortex tissues were harvested at 24 h post-TBI. Immunofluorescent staining, Western blot analysis, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling were used to evaluate LP, calpain activity, CRMP2 proteolysis and programmed cell death. The data were statistically analyzed using one-way analysis of variance and a paired t-test. RESULTS: Propofol and U83836E significantly ameliorated the CRMP2 proteolysis. In addition, both propofol and U83836E significantly decreased the ratio of 145-kDa αII-spectrin breakdown products to intact 270-kDa spectrin, the 4-hydroxynonenal expression and programmed cell death in the pericontusional cortex at 24 h after TBI. There was no difference between the TBI group and the fat emulsion group. CONCLUSIONS: These results demonstrate that propofol postconditioning alleviates calpain-mediated CRMP2 proteolysis and provides neuroprotective effects following moderate TBI potentially by counteracting LP and reducing calpain activation.

Effect of epidural analgesia with 0.075% ropivacaine versus 0.1% ropivacaine on the maternal temperature during labor: a randomized controlled study.

BACKGROUND: A wealth of evidence has indicated that labor epidural analgesia is associated with an increased risk of hyperthermia and overt clinical fever. Recently, evidence is emerging that the epidural analgesia-induced fever is associated with the types of the epidural analgesia and the variations in the epidural analgesia will affect the incidence of fever. The aim of the present study was to investigate the effects of epidural analgesia with 0.075% or 0.1% ropivacaine on the maternal temperature during labor. METHODS: Two hundred healthy term nulliparas were randomly assigned to receive epidural analgesia with either 0.1% ropivacaine or 0.075% ropivacaine. Epidural analgesia was initiated with 10 ml increment of the randomized solution and 0.5 µg/ml sufentanyl after a negative test dose of 5 ml of 1.5% lidocaine, and maintained with 7 ml bolus doses of the above mentioned mixed analgesics every 30 minutes by the patient-controlled epidural analgesia. The measurements included the maternal oral temperature, visual analog scale pain scores, labor events and neonatal outcomes. RESULTS: Epidural analgesia with 0.075% ropivacaine could significantly lower the mean maternal temperature at 4 hours after the initiation of analgesia and the oxytocin administration during labor compared with the one with 0.1% ropivacaine. Moreover, 0.075% ropivacaine treatment could provide satisfactory pain relief during labor and had no significant adverse effects on the labor events and neonatal outcomes. CONCLUSION: Epidural analgesia with 0.075% ropivacaine may be a good choice for the epidural analgesia during labor.

[Clinical analysis of trigemino-cardiac reflex during surgery for patients with skull base tumors].

OBJECTIVE: To investigate the clinical features, risky factors and outcome of the trigemino-cardiac reflex (TCR) during surgery for skull base tumors. METHODS: Two hundred and sixty-two neurosurgical patients with skull base tumors underwent general anesthesia and open surgery from October 2009 to December 2011 in department of neurosurgery of Beijing Tiantan Hospital. The occurrence of TCR and the type of tumor, the surgical approach as well as the postoperative complication relative to TCR was evaluated retrospectively. RESULTS: Seventeen patients occurred TCR events intraoperatively (6.5%). There were 8 men and 9 women with an average age of 40.5 years. Eleven of them (64.7%) underwent schwannoma surgery. Regarding with the surgical procedure, the suboccipital retrosigmoidal approach and the middle fossa transtentorial approach were most commonly associated with TCR in this series (88.2%). The heart rate and blood pressure returned to the patient's normal baseline level after cessation of the surgical manipulation. There was no TCR-relative complication in cardiovascular system. The postoperative course is uneventful in all 17 patients. CONCLUSIONS: TCR may occur during surgery for skull base tumor, especially when performing schwannoma surgery and suboccipital retrosigmoidal or middle fossa transtentorial approach. Accurate recognition and management of TCR during skull base surgery often carry on favorable outcome.

[Effects of total intravenous anesthesia on evoked potentials during aneurysm clip placement surgery].

OBJECTIVE: To explore the influences of total intravenous anesthesia (TIVA) on the feasibility and success rate of monitoring the evoked potentials (EP) and examine the correlations between EP changes and clinical outcomes in intracranial aneurysm surgery. METHODS: Thirty-one patients undergoing intracranial aneurysm surgery received TIVA. TIVA was maintained with a target controlled infusion (TCI) of propofol and a continuous infusion of remifentanyl. The bilateral SEP (somatosensory evoked potential) and MEP (motor evoked potentials) were monitored intra-operatively. And the changes of evoked potential and success rate were recorded. The preoperative and postoperative neurological outcomes and radiological manifestations were compared. RESULTS: Bilateral SEP was detected in all cases. And the control side MEP was unsuccessfully monitored. Three patients had postoperative neurological deficits. The amplitudes of MEP and SEP declined simultaneously and failed to revert back to the baseline levels in 1 case. There was postoperative hemiplegia. And computed tomography showed multiple sites of ischemic brain infarction. CONCLUSION: The administration of TIVA with propofol and remifentanyl enables successful SEP and MEP monitoring during intracranial aneurysm surgery. This protocol may detect early cerebral ischemia and reduce the incidence of ischemic stroke.

Comparison of the effects of etomidate and propofol combined with remifentanil and guided by comparable BIS on transcranial electrical motor-evoked potentials during spinal surgery.

BACKGROUND: Transcranial electrical motor-evoked potentials (TceMEPs) can provide early warning of possible motor compromise during surgery. There are fewer reports comparing the effects of etomidate and propofol infusion on TceMEPs when used for the maintenance of anesthesia and guided by comparable values of bispectral index (BIS) during spinal surgery. METHODS: Thirty-three patients scheduled for spinal surgery were randomly divided into 2 groups: propofol (PR, n=18) and etomidate (ER, n=15). Anesthesia was maintained with either propofol or etomidate combined with remifentanil. The infusion rates for propofol or etomidate were guided by the BIS value, which was maintained between 40 and 45. TceMEPs were conducted by stimulating needles placed at C1 and C2; recordings were made by measuring myogenic responses from the upper extremity abductor pollicis brevis muscles using needle electrodes. The threshold for eliciting a response, amplitudes, and latencies of TceMEPs, were recorded at 30, 60, 90, and 120 minutes after the induction of anesthesia. The cortisol levels were measured at 2 and 24 hours after induction. RESULTS: The voltage threshold needed to enlist TceMEPs in the ER group was significantly lower than that in the PR group (142±20 vs. 172±23 V, P=0.005). The amplitudes of TceMEPs were higher in the ER group than those in the PR group (P<0.05), whereas the latencies were shorter in the ER group than those in the PR group (P<0.05) at all study time points. Cortisol levels at all study time points were within the normal range. CONCLUSIONS: Etomidate has more favorable effects than propofol during the monitoring of TceMEPs under comparable BIS levels.

[Effect of electroacupuncture on Sevoflurane anesthesia in patients undergoing resection of supratentorial tumor].

OBJECTIVE: To observe the supplementary analgesic effect of electroacupuncture and its influence on the maintenance of anesthesia and the speed of recovery of patients undergoing craniotomy. METHODS: Eighty cases of supratentorial tumor resection were randomly divided into group A and group S, 40 cases in each group. All the patients were anesthetized with 2% Sevoflurane. The patients in group A received electroacupuncture at Hegu (LI 4) and Waiguan (TE 5), Jinmen (BL 63) and Taichong (LR 3), Zusanli (ST 36) and Qiuxu (GB 40) from anesthesia beginning to the end of operation, and in group S without electroacupuncture. The end-tidal Sevoflurane concentration, minimum alveolar concentration (MAC), bispectral index (BIS) and the information during anesthesia recovery stage were recorded, respectively. RESULTS: The end-tidal concentration and MAC of Sevoflurane in group A at all times were significant lower than those in group S (P<0.05, P<0.01) with a Sevoflurane saving of 9.62% on average. The BIS in group A during a few phases were higher than that in group S (all P<0.05). During anesthesia recovery stage, the time of each phase in group A was significantly shorter than that in group S (all P<0.01). No dysphoria and one case with nausea and vomiting were shown in group A, but in group S, 2 patients had dysphoria and 3 patients had nausea and vomiting. CONCLUSION: Electroacupuncture combined with Sevoflurane anesthesia can decrease the dosage of Sevoflurane, shorten the recovery time of anesthesia and improve the quality of anesthesia recovery of the patients undergoing resection of supratentorial tumor.

Postischemic brain injury is attenuated in mice lacking the beta2-adrenergic receptor.

BACKGROUND: Several beta-adrenergic receptor (betaAR) antagonists have been shown to have neuroprotective effects against cerebral ischemia. However, clenbuterol, a beta(2)AR agonist, was shown to have neuroprotective activity by increasing nerve growth factor expression. We used beta(2)AR knockout mice and a beta(2) selective antagonist to test the effect of loss of beta(2)ARs on outcome from transient focal cerebral ischemia. METHODS: Ischemia was induced by the intraluminal suture method, for 60 min of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. Neurological score was determined at 24 h reperfusion and infarct size was determined by cresyl violet or 2,3,5-triphenyltetrazolium chloride staining. beta(2)AR knockout mice and wild-type congenic FVB/N controls were studied, as well as 2 groups of wild type mice given either ICI 118,551 (0.2 mg/kg) or 0.9% saline intraperitoneally 30 min before MCAO (n = 10 per group). Changes in expression of heat shock protein (Hsp)72 after ischemia were examined by immunohistochemistry and western blots. RESULTS: Compared with wild type littermates, infarct volume was decreased by 22.3% in beta(2)AR knockout mice (39.7 +/- 10.7 mm(3) vs 51.0 +/- 11.4 mm(3), n = 10/group, P = 0.034) after 60 min of MCAO followed by 24 h reperfusion. Pretreatment with a beta(2)AR selective antagonist, ICI 118,551, also decreased infarct size significantly, by 25.1%, compared with the saline control (32.8 +/- 11.9 mm(3) vs 43.8 +/- 10.3 mm(3), n = 10/group, P = 0.041). Neurological scores were also significantly improved in mice lacking the beta(2)AR or pretreated with ICI 118,551. After cerebral ischemia, total levels of Hsp72 and the number of Hsp72 immunopositive cells were greater in mice lacking beta(2) AR. CONCLUSION: Brain injury is reduced and neurological outcome improved after MCAO in mice lacking the beta(2)AR, or in wild type mice pretreated with a selective beta(2)AR antagonist. This is consistent with a shift away from prosurvival signaling to prodeath signaling in the presence of beta(2)AR activation in cerebral ischemia. Protection is associated with higher levels of Hsp72, a known antideath protein. The effect of beta(2)AR signaling in the setting of cerebral ischemia is complex and warrants further study.

Regulation of apoptotic and inflammatory cell signaling in cerebral ischemia: the complex roles of heat shock protein 70.

Although heat shock proteins have been studied for decades, new intracellular and extracellular functions in a variety of diseases continue to be discovered. Heat shock proteins function within networks of interacting proteins; they can alter cellular physiology rapidly in response to stress without requiring new protein synthesis. This review focuses on the heat shock protein 70 family and considers especially the functions of the inducible member, heat shock protein 72, in the setting of cerebral ischemia. In general, inhibiting apoptotic signaling at multiple points and up-regulating survival signaling, heat shock protein 70 has a net prosurvival effect. Heat shock protein 70 has both antiinflammatory and proinflammatory effects depending on the cell type, context, and intracellular or extracellular location. Intracellular effects are often antiinflammatory with inhibition of nuclear factor-kappaB signaling. Extracellular effects can lead to inflammatory cytokine production or induction of regulatory immune cells and reduced inflammation.

[The effect of isoflurane induced hypotension on intraoperative cerebral vasospasm in intracranial aneurysm surgery].

OBJECTIVE: To evaluate whether isoflurane induced hypotension increases the incidence of cerebral vasospasm in intracranial aneurysm surgery. METHODS: Thirty consecutive patients undergoing intracranial aneurysmal surgery without preexisting cerebral ischemia were prospectively randomized into 2 groups: isoflurane induced hypotension group (group A, n = 15) and isoflurane maintained anesthesia group (group B, n = 15). The patients in the group A were performed isoflurane induced hypotension after dura opening by increasing the inhaled concentration of isoflurane to decrease the mean arterial pressure (MAP) by 30 - 40 percent of that of baseline value. After the aneurysm was clipped, the concentration of inhaled isoflurane was decreased so as to stop blood pressure reduction. The patient in group B was given 1 minimum alveolar concentration (MAC) of isoflurane during the whole procedure. The indicators of blood circulation were measured before blood pressure reduction, 30 minutes after blood pressure reduction, just after the clipping of the aneurysm, and 30 minutes after stopping blood pressure reduction. The S100B protein level in cerebrospinal fluid was observed before the controlled hypotension and 0, 2, and 4 h after the aneurysm was clipped. Assessment of the mean blood flow velocity of parent artery and its main branches was performed by microvascular ultrasonics before and after the aneurysm was clipped. The patients were followed-up for one week after the operation to observe the neurological complication. RESULTS: The MAP was decreased from 95 mm Hg +/- 12 mm Hg to 59 mm Hg +/- 5 mm Hg 30 minutes after the induced hypotension, and resumed to 75 mm Hg +/- 8 mm Hg 30 minutes after the aneurysm was clipped. Compared with those in the group B, both the total systemic vascular resistance and myocardial contract acceleration were decreased in group A, whereas the cardiac output and heart rate remained stable. (2) 4 hours after the aneurysm was clipped the S100B protein level in CSF was increased significantly in both groups, and that in the group A being significantly higher than that in the group B (t = 2.854, P < 0.01). (3) In the group A, the mean arterial flow velocity of distal parent vessels increased by more than 30 percent in 8 out of the 15 patients and 3 of these 8 patients suffered from neurological deficits postoperatively. However, the mean arterial flow velocity of distal parent vessels in the group B increased by more than 30 percent in only 3 of the 15 patients and 2 of these 3 patients suffered from neurological deficits postoperatively. CONCLUSION: Isoflurane controlled hypotension may increase the incidence of cerebral vasospasm. Isoflurane induced hypotension for intracranial aneurysm surgery should be cautioned.

[The effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery].

OBJECTIVE: To evaluate the effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery. METHODS: Thirty consecutive patients under-going intracranial aneurysmal surgery were prospectively randomized into two groups: Isoflurane (group A, n = 15) and nimodipine (group B, n = 15). The patients in group A were maintained with 1 minimum alveolar concentration (MAC) isoflurane anesthesia during the whole procedure. The patients in group B were given nimodipine infusion continuously (20 microg.kg(-1).h(-1)) after induction of anesthesia and anesthetized with 1 MAC isoflurane. S100B levels in cerebrospinal fluid were determined before aneurysm clipping and 0, 2, 4 h after aneurysm clipping by enzyme linked immunosorbent assay. Assessment of mean blood flow velocity of parent arterial and arterial branches were performed before and after aneurysm clipping. RESULTS: (1) S100B in cerebrospinal fluid was increased significantly at 4 h after aneurysm was clipped in group A (F = 4.11, P < 0.05). However, S100B in cerebrospinal fluid was stable in group B in the whole procedure. (2) Mean arterial flow velocity of parent vessels in group B was lower significantly than that in group A (t = 2.08, P < 0.05). However, mean arterial flow velocity of distal vessels in both groups has no significant difference. CONCLUSION: Intraoperative nimodipine infusion may prevent cerebral vasospasm during intracranial aneurysm surgery.