Jean-François Brichant

Large-scale signatures of unconsciousness are consistent with a departure from critical dynamics.

Loss of cortical integration and changes in the dynamics of electrophysiological brain signals characterize the transition from wakefulness towards unconsciousness. In this study, we arrive at a basic model explaining these observations based on the theory of phase transitions in complex systems. We studied the link between spatial and temporal correlations of large-scale brain activity recorded with functional magnetic resonance imaging during wakefulness, propofol-induced sedation and loss of consciousness and during the subsequent recovery. We observed that during unconsciousness activity in frontothalamic regions exhibited a reduction of long-range temporal correlations and a departure of functional connectivity from anatomical constraints. A model of a system exhibiting a phase transition reproduced our findings, as well as the diminished sensitivity of the cortex to external perturbations during unconsciousness. This framework unifies different observations about brain activity during unconsciousness and predicts that the principles we identified are universal and independent from its causes.

Resting-state Network-specific Breakdown of Functional Connectivity during Ketamine Alteration of Consciousness in Volunteers

Background:Consciousness-altering anesthetic agents disturb connectivity between brain regions composing the resting-state consciousness networks (RSNs). The default mode network (DMn), executive control network, salience network (SALn), auditory network, sensorimotor network (SMn), and visual network sustain mentation. Ketamine modifies consciousness differently from other agents, producing psychedelic dreaming and no apparent interaction with the environment. The authors used functional magnetic resonance imaging to explore ketamine-induced changes in RSNs connectivity. Methods:Fourteen healthy volunteers received stepwise intravenous infusions of ketamine up to loss of responsiveness. Because of agitation, data from six subjects were excluded from analysis. RSNs connectivity was compared between absence of ketamine (wake state [W1]), light ketamine sedation, and ketamine-induced unresponsiveness (deep sedation [S2]). Results:Increasing the depth of ketamine sedation from W1 to S2 altered DMn and SALn connectivity and suppressed the anticorrelated activity between DMn and other brain regions. During S2, DMn connectivity, particularly between the medial prefrontal cortex and the remaining network (effect size &bgr; [95% CI]: W1 = 0.20 [0.18 to 0.22]; S2 = 0.07 [0.04 to 0.09]), and DMn anticorrelated activity (e.g., right sensory cortex: W1 = −0.07 [−0.09 to −0.04]; S2 = 0.04 [0.01 to 0.06]) were broken down. SALn connectivity was nonuniformly suppressed (e.g., left parietal operculum: W1 = 0.08 [0.06 to 0.09]; S2 = 0.05 [0.02 to 0.07]). Executive control networks, auditory network, SMn, and visual network were minimally affected. Conclusions:Ketamine induces specific changes in connectivity within and between RSNs. Breakdown of frontoparietal DMn connectivity and DMn anticorrelation and sensory and SMn connectivity preservation are common to ketamine and propofol-induced alterations of consciousness.

Impairment of sciatic nerve function during adductor canal block

scribe an occurrence of quadriceps muscle weakness after ACB and suggest that analgesia with ACB could be conferred by partial femoral nerve block. We would like to suggest another possible mechanism behind the analgesic benefit of ACB. Analgesia with ACB is thought to result from the block of distal terminal branches of the femoral nerve (saphenous nerve) and branches of the obturator nerve in their path underneath the sartorius muscle and through the adductor canal. However, we report an occurrence of partial

Development and validation of a morphologic obstructive sleep apnea prediction score: The DES-OSA score

BACKGROUND:Obstructive sleep apnea (OSA) is a common and underdiagnosed entity that favors perioperative morbidity. Several anatomical characteristics predispose to OSA. We developed a new clinical score that would detect OSA based on the patient’s morphologic characteristics only. METHODS:Patients (n = 149) scheduled for an overnight polysomnography were included. Their morphologic metrics were compared, and combinations of them were tested for their ability to predict at least mild, moderate-to-severe, or severe OSA, as defined by an apnea–hypopnea index (AHI) >5, >15, or >30 events/h. This ability was calculated using Cohen &kgr; coefficient and prediction probability. RESULTS:The score with best prediction abilities (DES-OSA score) considered 5 variables: Mallampati score, distance between the thyroid and the chin, body mass index, neck circumference, and sex. Those variables were weighted by 1, 2, or 3 points. DES-OSA score >5, 6, and 7 were associated with increased probability of an AHI >5, >15, or >30 events/h, respectively, and those thresholds had the best Cohen &kgr; coefficient, sensitivities, and specificities. Receiver operating characteristic curve analysis revealed that the area under the curve was 0.832 (95% confidence interval [CI], 0.762–0.902), 0.805 (95% CI, 0.734–0.876), and 0.834 (95% CI, 0.757–0.911) for DES-OSA at predicting an AHI >5, >15, and >30 events/h, respectively. With the aforementioned thresholds, corresponding sensitivities (95% CI) were 82.7% (74.5–88.7), 77.1% (66.9–84.9), and 75% (61.0–85.1), and specificities (95% CI) were 72.4% (54.0–85.4), 73.2% (60.3–83.1), and 76.9% (67.2–84.4). Validation of DES-OSA performance in an independent sample yielded highly similar results. CONCLUSIONS:DES-OSA is a simple score for detecting OSA patients. Its originality relies on its morphologic nature. Derived from a European population, it may prove useful in a preoperative setting, but it has still to be compared with other screening tools in a general surgical population and in other ethnic groups.

Prevalence, characteristics and risk factors of chronic post surgical pain after laparoscopic colorectal surgery: retrospective analysis

BACKGROUND The prevalence of chronic postsurgical pain (CPSP) is a critical medical problem with economic implications. Its prevalence after gastrointestinal surgery is not well documented, particularly when a laparoscopic approach is used. OBJECTIVE The aim of the study was to determine the prevalence, the characteristics and the risk factors for CPSP after laparoscopic colorectal surgery. DESIGN A retrospective analysis using a postal questionnaire. SETTING The study was conducted at a university teaching hospital. PATIENTS Patients who underwent laparoscopic colorectal surgery from April 2008 until December 2011 (nu200a=u200a260). No epidural analgesia was used. MAIN OUTCOME MEASURES Postoperative pain intensity, incidence and characteristics of CPSP, and impact on quality of life and sleep. RESULTS Of 199 responses, 33 patients (17%) reported chronic pain at a median [interquartile range, IQR] of 38 [27 to 55] months after laparoscopic surgery with a median intensity of 4 [3 to 5]. CPSP had a negative impact on the quality of life in 84% of patients and on sleep in 43%. CPSP required regular analgesic(s) intake in 54% patients. Using a backward stepwise multivariate logistic regression model, the following variables were determined as independent risk factors for CPSP: redo surgery for anastomotic leakage (Pu200a=u200a0.01), inflammatory bowel disease (IBD) as the indication for surgery (Pu200a=u200a0.01) and preoperative pain (Pu200a=u200a0.05). CONCLUSION The incidence of CPSP after laparoscopic colorectal surgery (17%) is similar to those reported in the literature after laparotomy. Risk factors are redo surgery for postoperative peritonitis, IBD and preoperative pain. TRIAL REGISTRATION EudraCT 2012-005712-25.

Sedation of Patients With Disorders of Consciousness During Neuroimaging: Effects on Resting State Functional Brain Connectivity.

BACKGROUND: To reduce head movement during resting state functional magnetic resonance imaging, post-coma patients with disorders of consciousness (DOC) are frequently sedated with propofol. However, little is known about the effects of this sedation on the brain connectivity patterns in the damaged brain essential for differential diagnosis. In this study, we aimed to assess these effects. METHODS: Using resting state functional magnetic resonance imaging 3T data obtained over several years of scanning patients for diagnostic and research purposes, we employed a seed-based approach to examine resting state connectivity in higher-order (default mode, bilateral external control, and salience) and lower-order (auditory, sensorimotor, and visual) resting state networks and connectivity with the thalamus, in 20 healthy unsedated controls, 8 unsedated patients with DOC, and 8 patients with DOC sedated with propofol. The DOC groups were matched for age at onset, etiology, time spent in DOC, diagnosis, standardized behavioral assessment scores, movement intensities, and pattern of structural brain injury (as assessed with T1-based voxel-based morphometry). RESULTS: DOC were associated with severely impaired resting state network connectivity in all but the visual network. Thalamic connectivity to higher-order network regions was also reduced. Propofol administration to patients was associated with minor further decreases in thalamic and insular connectivity. CONCLUSIONS: Our findings indicate that connectivity decreases associated with propofol sedation, involving the thalamus and insula, are relatively small compared with those already caused by DOC-associated structural brain injury. Nonetheless, given the known importance of the thalamus in brain arousal, its disruption could well reflect the diminished movement obtained in these patients. However, more research is needed on this topic to fully address the research question.

Obstructive Sleep Apnea and Smoking as a Risk Factor for Venous Thromboembolism Events: Review of the Literature on the Common Pathophysiological Mechanisms

Venous thromboembolism events (VTE) are a common and preventable cause of postoperative complications. Interestingly, smoking and obstructive sleep apnea syndrome (OSA) affecting a large part of our population (and especially obese patients) are two underestimated predisposing factors of VTE. Many coagulation disorders favoring thromboembolism have been identified in the case of OSA and smoking and are reviewed in this article. They can be divided into two entities: endothelial dysfunction and hemostasis disorders. Interestingly OSA and smoking share common pathways to the prothrombotic state. The interactions with others comorbidities will also be discussed. This article provides pathophysiological mechanisms of the increased risk of thromboembolism in OSA patients and smokers, which should help manage these patients more adequately during the perioperative period.

Interfascial Spread of Injectate After Adductor Canal Injection in Fresh Human Cadavers.

The adductor canal block has become a common analgesic technique in patients undergoing knee arthroplasty. Dispersion of local anesthetic outside the adductor canal through interfascial layers and blockade of smaller nerves that confer innervation to the knee could contribute to the analgesic efficacy of the adductor canal block. We studied the diffusion of local anesthetic mixed with dye after injection into the adductor canal in fresh human cadavers. In all 8 legs, injectate was found in the popliteal fossa in contact with the sciatic nerve and/or popliteal blood vessels. Interfascial spread patterns were identified.

What mediates postoperative risk in obstructive sleep apnea: airway obstruction, nocturnal hypoxia, or both?

To the Editor, Obstructive sleep apnea (OSA) is known to be an independent risk factor for postoperative complications. The apnea–hypopnea index (AHI) – i.e., the number of apnea and hypopnea events per hour of sleep during overnight polysomnographic (PSG) monitoring – has typically served to classify the severity of OSA (with severe OSA defined by an AHI[30). A recently reported matched cohort study by Mutter et al. that measured the severity of OSA by AHI during PSG monitoring appears to constitute a landmark for identifying OSA patients at risk of postoperative complications. In that study, increased severity of OSA was associated with increased risk of complications, although only the data for the severe OSA group reached statistical significance. Hypoxic events in OSA patients may have significant pathophysiological consequences. Although confirmatory prospective studies are lacking, we hypothesize that these hypoxia-mediated inflammatory modifications could increase the risk of postoperative complications, acting cumulatively with the AHI or even mediating its effects entirely. An oxygen desaturation index (ODI) can also be derived from the PSG analysis and can be used as an independent measure of hypoxia. The ODI represents the number of times per hour that the capillary blood oxygen saturation drops by C4% from baseline during overnight PSG monitoring. We recently reported the results of a study (EudraCT: 2006-006558-92) that outlined the development of the DES-OSA score (the DES part of the acronym being derived from the initials of the investigators involved in its development) in 139 patients. The Figure shows the relation between the ODI and the AHI from that study. Clearly, some, but not all, patients with severe OSA (AHI [ 30) experienced nocturnal hypoxia. In the patients with severe OSA and hypoxia, the ODI varied considerably, with minimum and maximum values of 2 and 92 events per hour, respectively, although the median [interquartile range] was only 25 [10–37] events per hour. Among patients with severe OSA, 33% encountered no (ODI 5 events per hour) or mild (ODI 5–15) nocturnal hypoxia; 29% had moderate nocturnal hypoxia (ODI 15–30); and 38% had severe nocturnal hypoxia (ODI[30). Wide variation in the preoperative and postoperative ODIs among surgical patients with and without OSA has also been noted, but the relation of the ODI to the AHI and postoperative complications was not assessed. Mutter et al. found that only severe OSA patients were at a significantly increased risk of postoperative complications. Whether hypoxemic and non-hypoxemic severe OSA patients share the same risk or only patients with both severe OSA and hypoxia are at risk is unknown. Our preliminary data suggest that future studies investigating postoperative complications in OSA patients E. P. Deflandre, MD (&) Department of Anaesthesia, Clinique Saint-Luc of Bouge, Belgium & Cabinet Medical ASTES & University of Liege, Liege, Belgium e-mail: eric.deflandre@gmail.com

Positron Emission Tomography: Basic Principles, New Applications, and Studies Under Anesthesia.

Besides electroencephalography (EEG), positron emission tomography (PET) is one of the oldest tools for the exploration of the functioning brain. PET primarily focuses on neuronal activity and metabolism in the brain. It also has potential applications in studying the neurotransmitter function in the central nervous system. PET studies have laid the foundation for understanding the fundamental properties related to motor, sensory, and some cognitive functions in physiological and pathologic states. Brain function studies with PET, EEG, magnetic resonance imaging (MRI), and other neurotechnology tools have started shedding light on hitherto unknown aspects of brain function.