The role of dexmedetomidine in neurosurgery.

Dexmedetomidine can be used for sedation and analgesia and has been approved for this use by the European Medicines Agency since 2017. It causes an arousable state of sedation, which is beneficial during neurosurgical procedures that require the patient to cooperate with neurological tests (i.e. tumor surgery or implantation of deep brain stimulators). During procedures where monitoring of somatosensory evoked potentials and/or motor evoked potentials is required, dexmedetomidine can be used as an adjunct to general anesthesia with GABAergic drugs to decrease the dose of the latter when these drugs impair the monitoring signals. The use of dexmedetomidine has also been associated with neuroprotective effects and a decreased incidence of delirium, but studies confirming these effects in the peri-operative (neuro-)surgical setting are lacking. Although dexmedetomidine does not cause respiratory depression, its hemodynamic effects are complex and careful patient selection, choice of dose, and monitoring must be performed.

Effect of Compound Muscle Action Potential After Peripheral Nerve Stimulation Normalization on Anesthetic Fade of Intraoperative Transcranial Motor-Evoked Potential.

PURPOSE: Anesthetic fade refers to the time-dependent decrease in the amplitude of the intraoperative motor-evoked potential. It is thought to be caused by the accumulation of propofol. The authors examined whether normalization by the compound muscle action potential (CMAP) after peripheral nerve stimulation could compensate for anesthetic fade. METHODS: In 1,842 muscles in 578 surgeries, which did not exhibit a motor-neurologic change after the operation, the motor-evoked potential amplitude was normalized by the CMAP amplitude after peripheral nerve stimulation, and the CMAP amplitude and operation times were analyzed. RESULTS: The amplitudes of both motor-evoked potential and CMAP increased over time after peripheral nerve stimulation because of the disappearance of muscle-relaxant action. Especially, after peripheral nerve stimulation, CMAP significantly increased from the beginning to the end of the operation. Anesthetic fade in transcranial motor-evoked potential monitoring seemed to occur at more than 235 minutes of surgery based on the results of a receiver operating characteristic analysis of the operation time and relative amplitudes. Although the mean amplitude without CMAP normalization at more than 235 minutes was significantly lower than that at less than 235 minutes, the mean amplitude with normalization by CMAP after peripheral nerve stimulation at more than 235 minutes was not significantly different from that at less than 235 minutes. CONCLUSIONS: Compound muscle action potential after peripheral nerve stimulation normalization was able to avoid the effect of anesthetic fade. Anesthetic fade was seemed to be caused by a decrease in synaptic transmission at the neuromuscular junction because of propofol accumulation by this result.

Epidural Administration of Ropivacaine Reduces the Amplitude of Transcranial Electrical Motor-Evoked Potentials: A Double-Blinded, Randomized, Controlled Trial.

BACKGROUND: An epidurally administered local anesthetic acts primarily on the epidural nerve roots and can act directly on the spinal cord through the dural sleeve. We hypothesized that epidurally administered ropivacaine would reduce the amplitude of transcranial electrical motor-evoked potentials by blocking nerve conduction in the spinal cord. Therefore, we conducted a double-blind, randomized, controlled trial. METHODS: Thirty adult patients who underwent lung surgery were randomly allocated to 1 of 3 groups, based on the ropivacaine concentration: the 0.2% group, the 0.375% group, and the 0.75% group. The attending anesthesiologists, neurophysiologists, and patients were blinded to the allocation. The epidural catheter was inserted at the T5-6 or T6-7 interspace by a paramedian approach, using the loss of resistance technique with normal saline. General anesthesia was induced and maintained using propofol and remifentanil. Transcranial electrical motor-evoked potentials were elicited by a train of 5 pulses with an interstimulus interval of 2 milliseconds by using a constant-voltage stimulator and were recorded from the tibialis anterior muscle. Somatosensory-evoked potentials (SSEPs) were evoked by electrical tibial nerve stimulation at the popliteal fossa. After measuring the baseline values of these evoked potentials, 10 mL of epidural ropivacaine was administered at the 0.2%, 0.375%, or 0.75% concentration. The baseline amplitudes and latencies recorded before administering ropivacaine were defined as 100%. Our primary end point was the relative amplitude of the motor-evoked potentials at 60 minutes after the epidural administration of ropivacaine. We analyzed the amplitudes and latencies of these evoked potentials by using the Kruskal-Wallis test and used the Dunn multiple comparison test as the post hoc test for statistical analysis. RESULTS: The data are expressed as the median (interquartile range). Sixty minutes after epidurally administering ropivacaine, the motor-evoked potential amplitude was lower in the 0.75% group (7% [3%-18%], between-group difference P < .001) and in the 0.375% group (52% [43%-59%]) compared to that in the 0.2% group (96% [89%-105%]). The latency of SSEP was longer in the 0.75% group compared to that in the 0.2% group, but the amplitude was unaffected. CONCLUSIONS: Epidurally administered high-dose ropivacaine lowered the amplitude of motor-evoked potentials and prolonged the onset latencies of motor-evoked potentials and SSEPs compared to those in the low-dose group. High-dose ropivacaine can act on the motor pathway through the dura mater.

The Effects of Nicotine on Cortical Excitability After Exercise: A Double-Blind Randomized, Placebo-controlled, Crossover Study.

PURPOSE: The use of smokeless tobacco/nicotine products is common among athletes, but clear evidence for their positive or negative effect on sports performance is lacking. Nicotine is a psychoactive substance involved in numerous neuronal processes including cortical excitability. The aim of this study was to evaluate its effect on cortical excitability associated with aerobic exercise in nicotine-naive healthy volunteers. METHODS: Ten nicotine-naive healthy volunteers were recruited for this double-blind, randomized, crossover study to compare the effect of snus (8 mg nicotine), an oral, smokeless tobacco product, to placebo on cortical excitability before and after aerobic exercise. Transcranial magnetic stimulation (TMS) was used to measure changes in corticomotor excitability (motor-evoked potentials, MEPs) and electromyography of leg muscles during maximal voluntary contractions (MVC) to assess changes in muscle contractions. Before and after aerobic exercise and with or without nicotine treatment, MEPs and MVCs were measured. RESULTS: Analysis of TMS data showed lower motor cortex activation (lower MEP amplitude) after snus administration compared with placebo, whereas electromyography data showed no difference in muscle contraction between snus and placebo treatment. CONCLUSIONS: These findings suggest a general reduction in cortical excitability, without no relevant effect on physical performance.

Neuroanesthesia Guidelines for Optimizing Transcranial Motor Evoked Potential Neuromonitoring During Deformity and Complex Spinal Surgery: A Delphi Consensus Study.

STUDY DESIGN: Expert opinion-modified Delphi study. OBJECTIVE: We used a modified Delphi approach to obtain consensus among leading spinal deformity surgeons and their neuroanesthesiology teams regarding optimal practices for obtaining reliable motor evoked potential (MEP) signals. SUMMARY OF BACKGROUND DATA: Intraoperative neurophysiological monitoring of transcranial MEPs provides the best method for assessing spinal cord integrity during complex spinal surgeries. MEPs are affected by pharmacological and physiological parameters. It is the responsibility of the spine surgeon and neuroanesthesia team to understand how they can best maintain high-quality MEP signals throughout surgery. Nevertheless, varying approaches to neuroanesthesia are seen in clinical practice. METHODS: We identified 19 international expert spinal deformity treatment teams. A modified Delphi process with two rounds of surveying was performed. Greater than 50% agreement on the final statements was considered "agreement"; >75% agreement was considered "consensus." RESULTS: Anesthesia regimens and protocols were obtained from the expert centers. There was a large amount of variability among centers. Two rounds of consensus surveying were performed, and all centers participated in both rounds of surveying. Consensus was obtained for 12 of 15 statements, and majority agreement was obtained for two of the remaining statements. Total intravenous anesthesia was identified as the preferred method of maintenance, with few centers allowing for low mean alveolar concentration of inhaled anesthetic. Most centers advocated for <150 µg/kg/min of propofol with titration to the lowest dose that maintains appropriate anesthesia depth based on awareness monitoring. Use of adjuvant intravenous anesthetics, including ketamine, low-dose dexmedetomidine, and lidocaine, may help to reduce propofol requirements without negatively effecting MEP signals. CONCLUSION: Spine surgeons and neuroanesthesia teams should be familiar with methods for optimizing MEPs during deformity and complex spinal cases. Although variability in practices exists, there is consensus among international spinal deformity treatment centers regarding best practices. LEVEL OF EVIDENCE: 5.

Transplantation of IFN-γ Primed hUCMSCs Significantly Improved Outcomes of Experimental Autoimmune Encephalomyelitis in a Mouse Model.

The aim of this study was to investigate potential therapeutic effects of IFN-γ primed human umbilical cord mesenchymal stem cell (IFN-γ-hUCMSCs) transplantation on experimental autoimmune encephalomyelitis (EAE) in mice. In this study, EAE mouse model was established by MOG35-55 immunization method. Outcomes of the EAE mice in terms of body weight and clinical symptoms were analyzed. Electromyography (EMG) was performed to evaluate nerve conduction. ELISA was applied to quantify inflammatory cytokine levels in serum. Our results showed that IFN-γ could up-regulate protein expression of indoleamine 2, 3-dioxygenease 1 (IDO1), an important molecule released by MSCs to exert their immune suppressive activity (p < 0.01). In this study treatment efficacy for EAE was compared between transplantation of hUCMSCs alone and the IFN-γ-hUCMSCs which were cultured in the presence of IFN-γ for 48 h prior to be harvested for transplantation. Compared with hUCMSCs alone and control (PBS transfusion) group, transplantation of the IFN-γ-hUCMSCs could significantly alleviate the body weight loss and clinical symptoms of EAE mice (p < 0.05). Consistently EMG latency was significantly improved in treatment groups (p < 0.001), and the IFN-γ-hUCMSCs group was even better than the hUCMSCs group (p < 0.05). Moreover, the concentrations of IL-17A and TNF-α in serum of the mice treated by IFN-γ-hUCMSCs were significantly lower than hUCMSCs alone and controls, respectively (p < 0.05). In few of the roles of IL-17A and TNF-α in the pathogenesis of EAE, IFN-γ-hUCMSCs treatment associated-suppression of IL-17A and TNF-α expression may contribute in part to their therapeutic effects on EAE. In sum, our study highlights a great clinical potential of IFN-γ-hUCMSCs for multiple sclerosis (MS) treatment.

Effect of chronic nicotine consumption on motor cortical excitability: A transcranial magnetic stimulation study.

OBJECTIVES: Transcranial magnetic stimulation (TMS) allows exploration of the mode of action of neuroactive substances in the human brain, and allows evaluation of neuronal networks, which might be involved in the action of nicotine. The aim of the present study was to explore motor cortex excitability in chronic smokers and non-smokers using TMS. METHODS: The study included 50 healthy subjects, of whom 25 were chronic smokers and 25 were age- and sex-matched non-smokers. Number of cigarettes per day and duration of smoking in years were documented. Serum level of cotinine was measured. Resting and active motor threshold (RMT, AMT) and input-output curves (I/O) were performed to assess corticospinal excitability. The duration of the contralateral silent period (cSP) at different ranges of stimulation intensities and ipsilateral silent period (iSP) were used as measures of inhibition. RESULTS: There were no significant differences either in RMT or AMT between groups. I/O curve showed a significant intensity×group interaction (P=0.008). This was attributable to significantly higher amplitudes of MEP among smokers than non-smokers especially at 130, 140 and 150% of RMT (P=0.0001 and P=0.03 and 0.02 respectively). The mean duration of the cSP at different intensities and iSP duration were similar in both groups. Nicotine level and smoking index were correlated respectively with rMT and iSP (P=0.03 and 0.01). CONCLUSION: The present results confirm previous findings by Grundey et al. (2013) that chronic nicotine consumption is characterized by hyperexcitability of corticospinal output. We speculate that it is a secondary adaptation to long-term nicotine use with high inter-individual variance.

Evaluation of the effects of erythropoietin and interleukin-6 in rats submitted to acute spinal cord injury.

OBJECTIVE: To evaluate the effects of interleukin-6 (IL-6) and erythropoietin (EPO) in experimental acute spinal cord injury (SCI) in rats. METHODS: Using standardized equipment, namely, a New York University (NYU) Impactor, a SCI was produced in 50 Wistar rats using a 10-g weight drop from a 12.5-mm height. The rats were divided into the following 5 groups of 10 animals each: "Group EPO", treated with erythropoietin only; "Group EPO + IL-6", treated with both substances; "Group IL-6", receiving IL-6 administration only; "Group Placebo", receiving a placebo solution; and "Group Sham", submitted to an incomplete procedure (only laminectomy, without SCI). All drugs and the placebo solution were administered intraperitoneally for three weeks. The animals were followed up for 42 days. Functional motor recovery was monitored by the Basso, Beattie, and Bresnahan (BBB) scale on days 2, 7, 14, 21, 28, 35 and 42. Motor-evoked potential tests were performed on the 42nd day. Histological analysis was performed after euthanasia. RESULTS: The group receiving EPO exhibited superior functional motor results on the BBB scale. IL-6 administration alone was not superior to the placebo treatment, and the IL-6 combination with EPO yielded worse results than did EPO alone. CONCLUSIONS: Using EPO after acute SCI in rats yielded benefits in functional recovery. The combination of EPO and IL-6 showed benefits, but with inferior results compared to those of isolated EPO; moreover, isolated use of IL-6 resulted in no benefit.

Effect of Dexmedetomidine Combined Anesthesia on Motor evoked Potentials During Brain Tumor Surgery.

BACKGROUND: Dexmedetomidine (DEX) is used as an adjunct to total intravenous anesthesia. However, its effect on intraoperative neurophysiologic monitoring (IOM) during brain tumor surgery remains controversial. The aim of this study was to explore the effect of DEX on IOM during brain tumor surgery. METHODS: Seventy-eight consecutive patients (DEX group, n = 40; control group, n = 38), who underwent brain tumor surgery with IOM, were retrospectively reviewed. The outcomes included the predictability, laterality of alterations, and stimulation parameters of transcranial motor evoked potentials (tcMEPs) and somatosensory evoked potentials (SSEPs). RESULTS: The predictability of tcMEPs for postoperative motor outcomes showed a higher false-positive rate in the DEX group than in the control group (27.5% vs. 5.3%, P = 0.047). Bilateral alterations were observed only in the DEX group (31.3%; P = 0.053). Compared with the control group, the DEX group required significantly higher intensity (377.5 ± 48.0 vs. 347.1 ± 30.0 mV; P = 0.001) and repetition rate (6.0 ± 0.2 vs. 5.7 ± 0.5 pulse/train; P = 0.001) of transcranial electric stimulation to evoke adequate tcMEPs. The SSEP results were comparable between both groups. In the DEX group, false-positive tcMEPs changes occurred 222.2 ± 70.5 minutes (range, 95-342 minutes) after the induction of anesthesia. In addition, the patients who were administered DEX under bispectral index monitoring (n = 12) showed a significantly higher false-positive rate than shown by the control group (50.5% vs. 5.3%; P = 0.003). CONCLUSIONS: This study showed that DEX had significant effects on tcMEPs during IOM in brain tumor surgery. Because the high false-positive rate could decrease the accuracy of IOM, outcomes after using DEX should be cautiously interpreted.

Effect of caffeine on long-term potentiation-like effects induced by quadripulse transcranial magnetic stimulation.

Caffeine, an adenosine receptor antagonist, is known to affect sleep-awake cycles, the stress response, and learning and memory. It has been suggested that caffeine influences synaptic plasticity, but the effects of caffeine on synaptic plasticity in the human brain remain unexplored. The present study aimed to investigate the effects of caffeine on long-term potentiation (LTP)-like effects in the primary motor cortex of healthy humans. Twelve healthy participants (six women and six men; mean age: 44.8 ± 1.5 years) underwent quadripulse magnetic stimulation with an inter-stimulus interval of 5 ms (QPS5) to induce LTP-like effects, 2 h after administration of either a caffeine (200 mg) or placebo tablet in a double-blind crossover design. We recorded motor-evoked potentials (MEPs) before and after QPS5. The degree of MEP enhancement was compared between the placebo and caffeine conditions. Neither active nor resting motor thresholds were influenced by caffeine administration. Following caffeine administration, the degree of potentiation significantly decreased in "significant responders", whose average MEP ratios were greater than 1.24 in the placebo condition. The observed reduction in potentiation following caffeine administration is consistent with the A2A receptor antagonistic effect of caffeine. This is the first report of an effect of caffeine on neural synaptic plasticity in the human brain, which is consistent with the caffeine-induced plasticity reduction observed in primate studies. Because we studied only a small number of subjects, we cannot firmly conclude that caffeine reduces LTP in humans. The present results will, however, be helpful when considering further or new clinical uses of caffeine.

Evaluation of the effects of erythropoietin and interleukin-6 in rats submitted to acute spinal cord injury

OBJECTIVE: To evaluate the effects of interleukin-6 (IL-6) and erythropoietin (EPO) in experimental acute spinal cord injury (SCI) in rats. METHODS: Using standardized equipment, namely, a New York University (NYU) Impactor, a SCI was produced in 50 Wistar rats using a 10-g weight drop from a 12.5-mm height. The rats were divided into the following 5 groups of 10 animals each: "Group EPO", treated with erythropoietin only; "Group EPO + IL-6", treated with both substances; "Group IL-6", receiving IL-6 administration only; "Group Placebo", receiving a placebo solution; and "Group Sham", submitted to an incomplete procedure (only laminectomy, without SCI). All drugs and the placebo solution were administered intraperitoneally for three weeks. The animals were followed up for 42 days. Functional motor recovery was monitored by the Basso, Beattie, and Bresnahan (BBB) scale on days 2, 7, 14, 21, 28, 35 and 42. Motor-evoked potential tests were performed on the 42nd day. Histological analysis was performed after euthanasia. RESULTS: The group receiving EPO exhibited superior functional motor results on the BBB scale. IL-6 administration alone was not superior to the placebo treatment, and the IL-6 combination with EPO yielded worse results than did EPO alone. CONCLUSIONS: Using EPO after acute SCI in rats yielded benefits in functional recovery. The combination of EPO and IL-6 showed benefits, but with inferior results compared to those of isolated EPO; moreover, isolated use of IL-6 resulted in no benefit.

Nicotine modulates human brain plasticity via calcium-dependent mechanisms.

KEY POINTS: Nicotine (NIC) modulates cognition and memory function by targeting the nicotinic ACh receptor and releasing different transmitter systems postsynaptically. With both NIC-generated mechanisms, calcium influx and calcium permeability can be regulated, which is a key requirement for the induction of long-term potentiation, comprising the physiological basis of learning and memory function. We attempt to unmask the underlying mechanism of nicotinic effects on anodal transcranial direct current stimulation (tDCS)-induced long-term potentiation-like plasticity based on the hypothesis of calcium-dependency. Abolished tDCS-induced neuroplasticity as a result of NIC administration is reversed by calcium channel blockade with flunarizine in a dose-dependent manner. The results of the present study suggest that there is a dose determination of NIC/NIC agonists in therapeutical settings when treating cognitive dysfunction, which partially explains the heterogeneous results on cognition observed in subjects in different experimental settings. ABSTRACT: Nicotine (NIC) modulates neuroplasticity and improves cognitive performance in animals and humans mainly by increased calcium permeability and modulation of diverse transmitter systems. NIC administration impairs calcium-dependent plasticity induced by non-invasive brain stimulation with transcranial direct current stimulation (tDCS) in non-smoking participants probably as a result of intracellular calcium overflow. To test this hypothesis, we analysed the effect of calcium channel blockade with flunarizine (FLU) on anodal tDCS-induced cortical excitability changes in healthy non-smokers under NIC. We applied anodal tDCS combined with NIC patch and FLU at three different doses (2.5, 5 and 10 mg) or with placebo medication. NIC abolished anodal tDCS-induced neuroplasticity. Under medium dosage (but not under low and high dosage) of FLU combined with NIC, plasticity was re-established. For FLU alone, the lowest dosage weakened long-term potentiation (LTP)-like plasticity, whereas the highest dosage again abolished tDCS-induced plasticity. The medium dosage turned LTP-like plasticity in long-term depression-like plasticity. The results of the present study suggest a key role of calcium influx and calcium levels in nicotinic effects on LTP-like plasticity in humans. This knowledge might be relevant for the development of new therapeutic strategies in cognitive dysfunction.

An evaluation of anesthetic fade in motor evoked potential monitoring in spinal deformity surgeries.

BACKGROUND: Intraoperative neuromonitoring using motor evoked potentials (MEP) satisfactorily detects motor tract integrity changes during spinal surgery. However, monitoring is affected by "anesthetic fade," in which the stimulation threshold increases because the waveform amplitude decreases with the accumulation of propofol. Therefore, the purpose of this study was to clarify the effect of anesthetic fade on transcranial MEPs by investigating the time-dependent changes of amplitude during spinal deformity surgeries. METHODS: We retrospectively reviewed medical records of 142 spinal deformity patients (66 patients with idiopathic scoliosis, 28 with adult spinal deformities, 19 with neuromuscular scoliosis, 17 with syndromic scoliosis, and 12 with congenital scoliosis). The average age was 28 years (range, 5 to 81 years). MEPs were recorded bilaterally from the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles during spinal deformity surgeries. The Wilcoxon signed-rank test was used to investigate the time-dependent changes of amplitude after propofol infusion to evaluate anesthetic fade effects. RESULTS: The average time to baseline from initial propofol infusion was 113 min (range, 45 to 182 min). In the ADM, the amplitude was 52% at 1 h after initial propofol infusion, 102% at 2 h, 105% at 3 h, 101% at 4 h, 86% at 5 h, and 81% at 6 h. Compared to the 2-h time point, MEP decreased significantly by 16% at 5 h (P < 0.0005) and by 21% at 6 h (P < 0.05). In the AH, the amplitude was 49% at 1 h after initial infusion of propofol, 102% at 2 h, 102% at 3 h, 92% at 4 h, 71% at 5 h, and 63% at 6 h. Compared to the 2-h time point, MEP decreased significantly by 10% at 4 h (P < 0.005), by 31% at 5 h (P < 0.0000005), and by 39% at 6 h (P < 0.05). CONCLUSIONS: MEP amplitude significantly decreased in the upper limbs at 5 and 6 h and in the lower limbs at 4, 5, and 6 h after the initial infusion of propofol, respectively. The influence of anesthetic fade could influence false positive MEPs during long spinal surgeries.

Electrophysiological characterisation of central sensitisation in canine spontaneous osteoarthritis.

In man, central sensitisation (CS) contributes to the pain of osteoarthritis (OA). Dogs with spontaneous OA may also exhibit CS. Electrophysiological reflex measurements are more objective than behavioural assessments and can be used to evaluate CS in preclinical and clinical studies. It was hypothesised that dogs suffering from OA would exhibit electrophysiological characteristics indicative of CS, associated with reduced diffuse noxious inhibitory controls (DNICs). One hundred and seventeen client-owned dogs were recruited to the study. Hind limb nociceptive withdrawal reflex thresholds, stimulus response, and temporal summation characteristics were recorded, during alfaxalone anaesthesia, from 46 OA dogs, 29 OA dogs receiving nonsteroidal anti-inflammatory drugs (OANSAIDs), and 27 breed- and weight-matched control dogs. Efficacy of DNIC was evaluated in 12 control and 11 of the OA dogs, by application of a mechanical conditioning stimulus to the contralateral forelimb. Nociceptive withdrawal reflex thresholds were higher in OA compared with control dogs (P = 0.02). Stimulus response characteristics demonstrated an augmented response in OANSAID dogs compared with OA (P < 0.001) and control (P < 0.001) dogs. Temporal summation demonstrated exaggerated C-fibre-mediated responses in both OA (P < 0.001) and OANSAID (P = 0.005) groups, compared with control animals. Conditioning stimulus application resulted in inhibition of test reflex responses in both OA and control animals (P < 0.001); control animals demonstrated greater inhibition compared with OA (P = 0.0499). These data provide evidence of neurophysiological changes consistent with CS in dogs with spontaneous OA and demonstrate that canine OA is associated with reduced DNIC.

Marked attenuation of the amplitude of transcranial motor-evoked potentials after intravenous bolus administration of ketamine: a case report.

BACKGROUND: It is believed that ketamine does not affect motor-evoked potential amplitude, whereas various anesthetic drugs attenuate the amplitude of transcranial motor-evoked potential. However, we encountered a patient with marked attenuation of motor-evoked potential amplitude after intravenous bolus administration of ketamine. CASE PRESENTATION: A 15-year-old Japanese girl with a diagnosis of adolescent idiopathic scoliosis was admitted to our hospital to undergo posterior spinal fusion at T4-L3. After induction of general anesthesia using a continuous infusion of propofol and remifentanil, we confirmed that transcranial electrical motor-evoked potentials were being recorded correctly. Ketamine 1.25 mg/kg was administered intravenously for intraoperative and postoperative analgesia. About 3 minutes later, the motor-evoked potential amplitude was markedly attenuated. No other drugs were administered except for ketamine. The patient's vital signs were stable, and the surgery had not yet started. The motor-evoked potential amplitude was recovered at about 6 minutes after administration of ketamine. The surgery was performed uneventfully, and the patient had no neurologic deficit when she emerged from general anesthesia. CONCLUSIONS: Although there is a widely held belief in the field of anesthesiology that ketamine does not affect motor-evoked potential amplitude, it has been suggested that ketamine could affect its monitoring.

Capsaicin-enriched diet ameliorates autoimmune neuritis in rats.

BACKGROUND: Autoimmune neuropathies are common PNS disorders and effective treatment is challenging. Environmental influence and dietary components are known to affect the course of autoimmune diseases. Capsaicin as pungent component of chili-peppers is common in human nutrition. An influence of capsaicin on autoimmune diseases has been postulated. METHODS: We tested capsaicin in the animal model of experimental autoimmune neuritis (EAN) in Lewis rat. Rats were immunized with P2-peptide and were treated with capsaicin in different preventive settings. Electrophysiological, histological, and molecular biological analyses of the sciatic nerve were performed to analyze T-cell and macrophage cell count, TRPV1, and cytokine expression. Moreover, FACS analyses including the intestinal immune system were executed. RESULTS: We observed an immunomodulatory effect of an early preventive diet-concept, where a physiological dosage of oral capsaicin was given 10 days before immunization in EAN. A reduced inflammation of the sciatic nerve was significant detectable clinically, electrophysiologically (CMAPs reduced in control group p < 0.01; increase of nerve conduction blocks in control group p < 0.05), histologically (significant reduction of T-cells, macrophages and demyelination), and at cytokine level. In contrast, this therapeutic effect was missing with capsaicin given from the day of immunization onwards. As possible underlying mechanism, we were able to show changes in the expression of the capsaicin receptor in the sciatic nerve and the small intestine, as well as altered immune cell populations in the small intestine. CONCLUSION: This is the first report about the immunomodulatory effect of the common nutrient, capsaicin, in an experimental model for autoimmune neuropathies.

Regenerative potential of chitosan-coated poly-3-hydroxybutyrate conduits seeded with mesenchymal stem cells in a rat sciatic nerve injury model.

OBJECTIVES: A number of chemical and biological factors, including mesenchymal stem cells (MSCs), have been developed to enhance nerve regeneration by introduction through a variety of nerve conduits. This study was designed to assess the efficacy of using chitosan-coated poly-3-hydroxybutyrate (PHB) nerve conduits seeded with human bone marrow-derived MSCs (hMSC-bm) to augment repair in an experimental rat model of sciatic nerve injury. METHODS: A total of 30 rats were randomly assigned to one of three groups (n = 10). In each rat, a 10 mm segment of the sciatic nerve was removed and was replaced by a chitosan-coated PHB conduit seeded with hMSC-bm (PHB/chitosan-hMSC-bm group), a chitosan-coated PHB conduit (PHB/chitosan group), or an autograft (autograft group) as the control. The results were evaluated 8 weeks postoperatively by observation, electromyography and histologic examination with light microscopy and immunostaining. RESULTS: Histologic examination showed that both PHB/chitosan-hMSC-bm conduits and PHB/chitosan conduits led the damaged axons through the injured area. When the effects were compared, the results with the PHB/chitosan-hMSC-bm conduits were superior to those with the PHB/chitosan conduits (p < 0.05) but not as successful as with the autologous nerve grafts (p < 0.05). CONCLUSION: PHB/chitosan-hMSC-bm nerve conduits may be a useful artificial guide for nerve regeneration.

Predictive Value of Intraoperative Facial Motor Evoked Potentials in Vestibular Schwannoma Surgery Under 2 Anesthesia Protocols.

OBJECTIVE: We sought to validate the feasibility of facial motor evoked potential (FMEP) in facial nerve (FN) monitoring during vestibular schwannoma (VS) surgery under 2 anesthesia protocols and to examine its value for postoperative prognosis. METHODS: This prospective study included 106 patients with VS who underwent microsurgical excision between May 2014 and November 2016 at the Beijing Tiantan Hospital, Capital Medical University, China. All patients were investigated for FMEP elicited by transcranial electrical stimulation in the contralateral facial motor cortex. The patients randomly received total intravenous anesthesia or combined intravenous-inhalation anesthesia. Postoperative FN function was evaluated 7-10 days after surgery (short-term) and at the last follow-up (long-term) using the House-Brackmann (HB) grading system. HB grades 1 and 2 were deemed satisfactory, whereas HB grades 3-6 were deemed unsatisfactory. The value of the final-to-start FMEP ratio for predicting short-term and long-term postoperative FN functions was examined. RESULTS: Valid FMEPs were obtained in 97 patients, which were recorded from the mentalis muscle. The FMEP amplitude ratio was significantly correlated with short-term and long-term postoperative FN functions. Receiver operating characteristic curve analysis showed that the FMEP ratio cut-off values of 77.4% (area under the curve = 0.797) and 56.9% (area under the curve = 0.900) predicted satisfactory FN function 7-10 days after surgery and at the last follow-up, respectively. No statistically significant difference was found in FMEP quantitative parameters between the 2 anesthesia protocols. CONCLUSION: The FMEP amplitude ratio is a valuable predictor for postoperative FN function. FMEP ratio ≥57% is predictive of satisfactory long-term FN function.