[Interest of a biopsychosocial approach in the management of a patient with chronic pain : a narrative review]. / Intérêt d'une approche biopsychosociale dans la prise en charge d'un patient souffrant de douleurs chroniques : une revue narrative.

Pain is generally perceived as a sensory, emotional and cognitive aggression by the patient who suffers from it and as the enemy that must be defeated by the physician. It may become chronic, and the passage from the acute phase to the chronic phase cannot be explained in a single way. Indeed, multiple factors come into play: biological, psychological and socio-professional. The patient's quality of life then deteriorates and places him/her in a vicious cycle of pain. The assessment of the different components of pain (sensory, emotional, cognitive and behavioural) and its maintenance factors allow for the implementation of therapeutic strategies, both physical and psychological, adapted to every patient. Due to the complexity of chronic pain management, a multidisciplinary strategy is being developed, with a global approach according to the biopsychosocial perspective, including non-pharmacological approaches, with the objective of allowing the patient to be autonomous in the management of his/her symptoms.

La douleur est généralement perçue comme une agression sensorielle, émotionnelle et cognitive par le patient qui en souffre, et comme l'ennemi que le médecin doit vaincre. Elle peut se chroniciser, et le passage de la phase aiguë à la phase chronique ne peut s'expliquer d'une façon unique. En effet, de multiples facteurs biologiques, psychologiques et socio-professionnels entrent en jeu. La qualité de vie du patient se dégrade alors et le place dans un véritable cercle vicieux de la douleur. L'évaluation des différentes composantes de la douleur (sensorielle, émotionnelle, cognitive et comportementale) et de ses facteurs de maintien permet de mettre en place des stratégies thérapeutiques, aussi bien sur le plan physique que psychologique, adaptées à chaque patient. Du fait de la complexité de la prise en charge de la douleur chronique, se développe une méthode pluridisciplinaire, dans une perspective d'approche globale selon le modèle biopsychosocial, incluant également des approches non médicamenteuses avec comme objectif, notamment, de permettre au patient une autonomie dans la gestion de sa symptomatologie.

[Intracerebroventricular infusion of morphine, bupivacaine and clonidine for the management of refractory neoplasic pain in a palliative care setting : a case report]. / Administration intracérébroventriculaire de morphine, bupivacaïne et clonidine pour la gestion de la douleur réfractaire d'origine néoplasique en soins palliatifs.

Intracerebroventricular (ICV) infusion of morphine is a well-known technique to relieve intractable neoplasic pain when conventional analgesic strategies reach their limits. Through this case report, we present indications, assets, and drawbacks of this procedure in such conditions. We also describe the adaptation of the systemic analgesic treatment to allow discharge from the hospital to home settings. Thanks to the ICV infusion of a mixture of morphine, bupivacaine and clonidine, the patient was weaned from oral opioid medications and reached an acceptable level of comfort. This allowed him to be discharged from the hospital to go back home with a specific setting of mobile palliative care structure. The patient's family followed training about the device to prevent any technical trouble and to react in case of unwanted events.

L'administration de morphine intracérébroventriculaire (ICV) est une technique bien connue pour traiter les douleurs néoplasiques insoutenables lorsqu'un traitement antalgique conventionnel atteint ses limites. A travers un cas clinique, nous présentons les indications, les atouts et les inconvénients de cette procédure dans de telles conditions. Nous décrivons aussi l'adaptation du traitement antalgique per os après implantation du cathéter. Grâce à l'infusion ICV d'un mélange de morphine, de bupivacaïne et de clonidine, le patient a été sevré totalement des dérivés opioïdes oraux et a atteint un niveau de confort acceptable pour rentrer à domicile avec une structure mobile de soins palliatifs mise en place. L'entourage du patient a bénéficié de séances d'information pour prévenir les problèmes techniques liés au dispositif et pour réagir en cas d'incident.

Propofol-induced unresponsiveness is associated with impaired feedforward connectivity in cortical hierarchy.

BACKGROUND: Impaired consciousness has been associated with impaired cortical signal propagation after transcranial magnetic stimulation (TMS). We hypothesised that the reduced current propagation under propofol-induced unresponsiveness is associated with changes in both feedforward and feedback connectivity across the cortical hierarchy. METHODS: Eight subjects underwent left occipital TMS coupled with high-density EEG recordings during wakefulness and propofol-induced unconsciousness. Spectral analysis was applied to responses recorded from sensors overlying six hierarchical cortical sources involved in visual processing. Dynamic causal modelling (DCM) of induced time-frequency responses and evoked response potentials were used to investigate propofol's effects on connectivity between regions. RESULTS: Sensor space analysis demonstrated that propofol reduced both induced and evoked power after TMS in occipital, parietal, and frontal electrodes. Bayesian model selection supported a DCM with hierarchical feedforward and feedback connections. DCM of induced EEG responses revealed that the primary effect of propofol was impaired feedforward responses in cross-frequency theta/alpha-gamma coupling and within frequency theta coupling (F contrast, family-wise error corrected P<0.05). An exploratory analysis (thresholded at uncorrected P<0.001) also suggested that propofol impaired feedforward and feedback beta band coupling. Post hoc analyses showed impairments in all feedforward connections and one feedback connection from parietal to occipital cortex. DCM of the evoked response potential showed impaired feedforward connectivity between left-sided occipital and parietal cortex (T contrast P=0.004, Bonferroni corrected). CONCLUSIONS: Propofol-induced loss of consciousness is associated with impaired hierarchical feedforward connectivity assessed by EEG after occipital TMS.

Frontal alpha-delta EEG does not preclude volitional response during anaesthesia: prospective cohort study of the isolated forearm technique.

BACKGROUND: The isolated forearm test (IFT) is the gold standard test of connected consciousness (awareness of the environment) during anaesthesia. The frontal alpha-delta EEG pattern (seen in slow wave sleep) is widely held to indicate anaesthetic-induced unconsciousness. A priori we proposed that one responder with the frontal alpha-delta EEG pattern would falsify this concept. METHODS: Frontal EEG was recorded in a subset of patients from three centres participating in an international multicentre study of IFT responsiveness following tracheal intubation. Raw EEG waveforms were analysed for power-frequency spectra, depth-of-anaesthesia indices, permutation entropy, slow wave activity saturation and alpha-delta amplitude-phase coupling. RESULTS: Volitional responses to verbal command occurred in six out of 90 patients. Three responses occurred immediately following intubation in patients (from Sites 1 and 2) exhibiting an alpha-delta dominant (delta power >20 dB, alpha power >10 dB) EEG pattern. The power-frequency spectra obtained during these responses were similar to those of non-responders (P>0.05) at those sites. A further three responses occurred in (Site 3) patients not exhibiting the classic alpha-delta EEG pattern; these responses occurred later relative to intubation, and in patients had been co-administered ketamine and less volatile anaesthetic compared with Site 1 and 2 patients. None of the derived depth-of-anaesthesia indices could robustly discrimate IFT responders and non-responders. CONCLUSIONS: Connected consciousness can occur in the presence of the frontal alpha-delta EEG pattern during anaesthesia. Frontal EEG parameters do not readily discriminate volitional responsiveness (a marker of connected consciousness) and unresponsiveness during anaesthesia. CLINICAL TRIAL REGISTRATION: NCT02248623.

Brain functional connectivity differentiates dexmedetomidine from propofol and natural sleep.

BACKGROUND: We used functional connectivity measures from brain resting state functional magnetic resonance imaging to identify human neural correlates of sedation with dexmedetomidine or propofol and their similarities with natural sleep. METHODS: Connectivity within the resting state networks that are proposed to sustain consciousness generation was compared between deep non-rapid-eye-movement (N3) sleep, dexmedetomidine sedation, and propofol sedation in volunteers who became unresponsive to verbal command. A newly acquired dexmedetomidine dataset was compared with our previously published propofol and N3 sleep datasets. RESULTS: In all three unresponsive states (dexmedetomidine sedation, propofol sedation, and N3 sleep), within-network functional connectivity, including thalamic functional connectivity in the higher-order (default mode, executive control, and salience) networks, was significantly reduced as compared with the wake state. Thalamic functional connectivity was not reduced for unresponsive states within lower-order (auditory, sensorimotor, and visual) networks. Voxel-wise statistical comparisons between the different unresponsive states revealed that thalamic functional connectivity with the medial prefrontal/anterior cingulate cortex and with the mesopontine area was reduced least during dexmedetomidine-induced unresponsiveness and most during propofol-induced unresponsiveness. The reduction seen during N3 sleep was intermediate between those of dexmedetomidine and propofol. CONCLUSIONS: Thalamic connectivity with key nodes of arousal and saliency detection networks was relatively preserved during N3 sleep and dexmedetomidine-induced unresponsiveness as compared to propofol. These network effects may explain the rapid recovery of oriented responsiveness to external stimulation seen under dexmedetomidine sedation. TRIAL REGISTRY NUMBER: Committee number: 'Comité d'Ethique Hospitalo-Facultaire Universitaire de Liège' (707); EudraCT number: 2012-003562-40; internal reference: 20121/135; accepted on August 31, 2012; Chair: Prof G. Rorive. As it was considered a phase I clinical trial, this protocol does not appear on the EudraCT public website.

Pre-Operative Ability of Clinical Scores to Predict Obstructive Sleep Apnea (OSA) Severity in Susceptible Surgical Patients.

BACKGROUND: Severe obstructive sleep apnea (OSA) is an independent risk factor for perioperative complications. Clinical scores such as Snoring, Tiredness, Observed apnea, high blood Pressure, Body Mass Index (BMI) higher than 35 kg m-2, Age older than 50 years, Neck circumference larger than 40 cm, and male gender (STOP-Bang), perioperative sleep apnea prediction (P-SAP), and OSA50 have been proposed for detecting OSA. We recently proposed a new score based on morphological metrics only, the DES-OSA score. This study compared the DES-OSA score to the three other ones with regard to their ability to detect OSA. Obese patients are particularly at risk of OSA. METHODS: Following informed consent and institutional review board (IRB) approval, 1584 consecutive adults were. Should the STOP-Bang be indicative of increased risk of severe OSA, the patient was referred to complementary polysomnography (PSG). Eventual already existing recent PSG data were also collected. The abilities of the four scores to predict OSA severity were compared using sensitivity, specificity, Cohen's kappa coefficient (CKC), and area under ROC curve (AUROC) analysis. RESULTS: PSG was performed in 150 patients. For detecting severe OSA, OSA50 had the highest sensitivity [value (95 % CI) 0.98 (0.90-1)]. STOP-Bang was significantly less sensitive than P-SAP and OSA50. In that respect, DES-OSA was significantly more specific than the three other ones [0.75 (0.65-0.83)]. The AUROC of DES-OSA was significantly the largest [0.9 (0.84-0.95)]. The highest CKC at detecting severe OSA was 0.62 (0.49-0.74) for DES-OSA. Similar results were obtained for moderate to severe OSA prediction. CONCLUSIONS: DES-OSA, which is the only exclusively morphological score available, appears to surpass the three other scores in their ability to predict moderate to severe and severe OSA, at least in our setting and in our screened population. CLINICAL TRIAL REGISTRATION: ClinicalTrial.gov NCT02051829.

Influence of premedication with alprazolam on the occurence of obstructive apneas. A prospective randomized double-blind study.

Postoperative development or worsening of obstructive sleep apnea is a potential complication of anesthesia. The objective of this study was to study the effects of a premedication with alprazolam on the occurrence of apneas during the immediate postoperative period. Fifty ASA 1 - 2 patients undergoing a colonoscopy were recruited. Patients with a history of obstructive sleep apnea (OSA) were excluded. Recruited patients were randomly assigned to one of two groups: in Group A, they received 0.5 mg of alprazolam orally one hour before the procedure; and in Group C, they received placebo. Anesthesia technique was identical in both groups. Patients were monitored during the first two postoperative hours to establish their AHI (apnea hypopnea index, the number of apneas and hypopneas per hour). Nine patients were excluded (4 in group A and 5 in group C) due to technical problems or refusal. Interestingly, premedication by alprazolam did not change intra-operative propofol requirements. During the first two postoperative hours, the AHI was significantly higher in group A than in group C (Group A: 20.33 ± 10.97 h-1, C: 9.63 ± 4.67 h-1). These apneas did not induce significant arterial oxygen desaturation, or mandibular instability. Our study demonstrates that a premedication with 0.5 mg of alprazolam doesn't modify intra-operative anesthetic requirements during colonoscopy, but is associated with a higher rate of obstructive apneas during at least three and a half hours after ingestion. No severe side effects were observed in our non-obese population. Our results must be confirmed on a larger scale.

Combined minimally invasive techniques to cure accidental dural tears occurring during spine surgery: epidural blood patch associated with cerebrospinal fluid drainage and ventral bed rest.

We report the case of a 70-year-old man, with increased anesthetic risk, who beneficiated from a lumbar laminarthrectomy from lumbar vertebra 4 (L4) to sacral 1 (S1). A dural tear facing L5-S 1 levels occurred during surgery and was repaired intra-operatively. Postoperatively, back and radicular pain symptoms appeared along with a pseudo-meningocele. Successful treatment was only achieved after performing an epidural blood patch and closed subarachnoid drainage. This well-known but infrequent management was undertaken after a first epidural blood patch attempt, and after two unsuccessful surgical choking procedures. Management is here described, and discussed at the light of existing literature.

Two different techniques of facial mask induction of anesthesia in children provide identical intubation conditions despite different anesthetic depth.

BACKGROUND: Sevoflurane induction in chil- dren is performed using different techniques. Constricted, centered, and symmetrical pupils (CCSP) are classically the endpoint to be achieved before laryngoscopy is performed. OBJECTIVES: We investigated whether two different inhalation induction techniques with the same clinical end- point provided similar intubating conditions and comparable depth of anesthesia as assessed by the Bispectral Index (BIS). METHODS: Following IRB approval, and informed parental consent, 20 children were recruited. They were sched- uled for general anesthesia with tracheal intubation, and randomly assigned to Group 1, where the practitioner used 6% inspired sevoflurane in 50% 02/N20, and no manually assisted ventilation, or Group 2, where inspired sevoflurane was 8% in 50% 02/N20, and ventilation was manually supported upon loss of consciousness. BIS values were blinded. Laryngoscopy was performed after CCSP. Intubation conditions scoring was based on jaw relaxation (mobile = 1, partially mobile = 2, fixed = 3), position of vocal cords (open = 1, half-closed = 2, closed = 3), and cough (no cough = 1, 1 or 2 coughing efforts = 2, persistent coughing = 3). A total score > 3 corresponded to non-optimal conditions. RESULTS: Upon CCSP, BIS values were significantly lower in Group 1 [mean (SD) : 30 (8) - 48 (18), p <0.001], despite significantly higher end-tidal sevoflurane concentration in Group 2 [mean (SD) : 5.0 (0.7) - 6.2 (0.5) ; p <0.001]. Time to CCSP was slightly shorter in Group 2. Intubation conditions were always optimal except for one patient of Group 1. DISCUSSION: Both induction techniques achieve good intubating conditions. Possible explanations for the between-group BIS difference include variable appreciation of the CCSP endpoint, different induction lengths or sevoflurane equilibration times, or sevoflurane-induced increase in electroencephalogram power. A better indicator of the best time to intubate is needed to avoid too deep anesthesia in children.

Physiological Signal Processing for Individualized Anti-nociception Management During General Anesthesia: a Review.

OBJECTIVE: The aim of this paper is to review existing technologies for the nociception / anti-nociception balance evaluation during surgery under general anesthesia. METHODS: General anesthesia combines the use of analgesic, hypnotic and muscle-relaxant drugs in order to obtain a correct level of patient non-responsiveness during surgery. During the last decade, great efforts have been deployed in order to find adequate ways to measure how anesthetic drugs affect a patient's response to surgical nociception. Nowadays, though some monitoring devices allow obtaining information about hypnosis and muscle relaxation, no gold standard exists for the nociception / anti-nociception balance evaluation. Articles from the PubMed literature search engine were reviewed. As this paper focused on surgery under general anesthesia, articles about nociception monitoring on conscious patients, in post-anesthesia care unit or in intensive care unit were not considered. RESULTS: In this article, we present a review of existing technologies for the nociception / anti-nociception balance evaluation, which is based in all cases on the analysis of the autonomous nervous system activity. Presented systems, based on sensors and physiological signals processing algorithms, allow studying the patients' reaction regarding anesthesia and surgery. CONCLUSION: Some technological solutions for nociception / antinociception balance monitoring were described. Though presented devices could constitute efficient solutions for individualized anti-nociception management during general anesthesia, this review of current literature emphasizes the fact that the choice to use one or the other mainly relies on the clinical context and the general purpose of the monitoring.

Preoperative adherence to continuous positive airway pressure among obstructive sleep apnea patients.

BACKGROUND: Obstructive Sleep Apnea (OSA) increases the perioperative risk of complications. Chronic use of Continuous Positive Airway Pressure (CPAP) by patients decreases the importance of comorbidities caused by the OSA. However, many patients do not adhere to the treatment. Given the postoperative complications, it is important for the anesthesiologist to identify non-adherent patients. This prospective study was designed to identify factors that would predict patient adherence. METHODS: Ninety patients who were treated by CPAP for more than one year were recruited. Among them, and based on objective criteria such as length of use of CPAP during the night, 75 were considered as being adherent to CPAP, while the other 15 were not. Sixty-two potential causes of non-adherence were investigated (some have not been tested before), and further divided into five categories. Those categories included cultural, intellectual, or economic factors, OSA comorbidities, patient belief about health, ENT-related problems, and pathophysiological features estimating the degree of improvement afforded by CPAP introduction. RESULTS: Multivariate binary logistic regression analysis identified one criterion of non-adherence to treatment, namely the feeling of breathlessness, and three criteria of adherence, namely awareness of the risk of complications, awareness of treatment efficacy, and feeling of being less tired with CPAP therapy. CONCLUSIONS: These four new criteria should preoperatively be sought, in order to detect non-adherent patients more efficiently.

[The value of electroencephalography monitoring and analysis during anesthesia]. / Intérêt de la surveillance et de l'analyse de l'électroencéphalogramme au cours de l'anesthésie.

Electroencephalography (EEG) records brain electrical activity at the scalp level. As a functional and non invasive witness of brain activity, EEG has long raised the interest of researchers and practitioners, notably in the domain of anesthesia. Thanks to technical advances, this complex signal can now be dissected, and a huge amount of information can be extracted from it. This information gives the opportunity to quantify theeffects of general anesthesia on the brain, and provides a better understanding of the underlying mechanisms.

Preeclampsia: an update.

Preeclampsia was formerly defined as a multisystemic disorder characterized by new onset of hypertension (i.e. systolic blood pressure (SBP) ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 mmHg) and proteinuria (> 300 mg/24 h) arising after 20 weeks of gestation in a previously normotensive woman. Recently, the American College of Obstetricians and Gynecologists has stated that proteinuria is no longer required for the diagnosis of preeclampsia. This complication of pregnancy remains a leading cause of maternal morbidity and mortality. Clinical signs appear in the second half of pregnancy, but initial pathogenic mechanisms arise much earlier. The cytotrophoblast fails to remodel spiral arteries, leading to hypoperfusion and ischemia of the placenta. The fetal consequence is growth restriction. On the maternal side, the ischemic placenta releases factors that provoke a generalized maternal endothelial dysfunction. The endothelial dysfunction is in turn responsible for the symptoms and complications of preeclampsia. These include hypertension, proteinuria, renal impairment, thrombocytopenia, epigastric pain, liver dysfunction, hemolysis-elevated liver enzymes-low platelet count (HELLP) syndrome, visual disturbances, headache, and seizures. Despite a better understanding of preeclampsia pathophysiology and maternal hemodynamic alterations during preeclampsia, the only curative treatment remains placenta and fetus delivery. At the time of diagnosis, the initial objective is the assessment of disease severity. Severe hypertension (SBP ≥ 160 mm Hg and/or DBP ≥ 110 mmHg), thrombocytopenia < 100.000/µL, liver transaminases above twice the normal values, HELLP syndrome, renal failure, persistent epigastric or right upper quadrant pain, visual or neurologic symptoms, and acute pulmonary edema are all severity criteria. Medical treatment depends on the severity of preeclampsia, and relies on antihypertensive medications and magnesium sulfate. Medical treatment does not alter the course of the disease, but aims at preventing the occurrence of intracranial hemorrhages and seizures. The decision of terminating pregnancy and perform delivery is based on gestational age, maternal and fetal conditions, and severity of preeclampsia. Delivery is proposed for patients with preeclampsia without severe features after 37 weeks of gestation and in case of severe preeclampsia after 34 weeks of gestation. Between 24 and 34 weeks of gestation, conservative management of severe preeclampsia may be considered in selected patients. Antenatal corticosteroids should be administered to less than 34 gestation week preeclamptic women to promote fetal lung maturity. Termination of pregnancy should be discussed if severe preeclampsia occurs before 24 weeks of gestation. Maternal end organ dysfunction and non-reassuring tests of fetal well-being are indications for delivery at any gestational age. Neuraxial analgesia and anesthesia are, in the absence of thrombocytopenia, strongly considered as first line anesthetic techniques in preeclamptic patients. Airway edema and tracheal intubation-induced elevation in blood pressure are important issues of general anesthesia in those patients. The major adverse outcomes associated with preeclampsia are related to maternal central nervous system hemorrhage, hepatic rupture, and renal failure. Preeclampsia is also a risk factor for developing cardiovascular disease later in life, and therefore mandates long-term follow-up.

The M3 from the international point of view.

Deciding to cease treatment in intensive care unit patients whose prognosis is hopeless allows programming the moment of death, and hence, post mortem transplantable organ donation. Such organ donations are more frequent in Anglo-Saxon countries. In the context of growing organ needs, they have significantly increased the number of organs that are available for transplant. Progressive experience has shown that crystal-clear procedures must be set up in order to avoid lack of understanding, opposition, or even conflict between involved medical teams and immediate relatives of potential donors. The decision of organ transplantation must totally be separated from the decision of treatment cessation. Supportive treatment cessation must be done according to previously established procedures. Medications that are compatible with organ transplantation must be listed. Finally, the needs of patient relatives must be met.

Neural correlates of consciousness during general anesthesia using functional magnetic resonance imaging (fMRI).

This paper reviews the current knowledge about the mechanisms of anesthesia-induced alteration of consciousness. It is now evident that hypnotic anesthetic agents have specific brain targets whose function is hierarchically altered in a dose-dependent manner. Higher order networks, thought to be involved in mental content generation, as well as sub-cortical networks involved in thalamic activity regulation seems to be affected first by increasing concentrations of hypnotic agents that enhance inhibitory neurotransmission. Lower order sensory networks are preserved, including thalamo-cortical connectivity into those networks, even at concentrations that suppress responsiveness, but cross-modal sensory interactions are inhibited. Thalamo-cortical connectivity into the consciousness networks decreases with increasing concentrations of those agents, and is transformed into an anti-correlated activity between the thalamus and the cortex for the deepest levels of sedation, when the subject is non responsive. Future will tell us whether these brain function alterations are also observed with hypnotic agents that mainly inhibit excitatory neurotransmission. The link between the observations made using fMRI and the identified biochemical targets of hypnotic anesthetic agents still remains to be identified.

Effect of a fluid challenge on the Surgical Pleth Index during stable propofol-remifentanil anaesthesia.

BACKGROUND: The Surgical Pleth Index (SPI), derived from pulse amplitude and heartbeat interval, is proposed to monitor anti-nociception during anaesthesia. Its response to noxious stimulation can be affected by the intravascular volume status. This study investigated the effect of a fluid challenge (FC) on SPI during steady-state conditions. METHODS: After Institutional Review Board approval, 33 consenting patients undergoing neurosurgery received a 4 ml/kg starch FC over less than 5 min under stable surgical stimulation conditions and stable propofol (Ce(PPF) ) and remifentanil (Ce(REMI) ) effect-site concentrations as estimated by target-controlled infusion systems. Intravascular volume status was assessed using the Delta Down (DD). We looked at the SPI response to FC according to DD, Ce(PPF) , and Ce(REMI) . RESULTS: Following FC, SPI did not change in 16, increased in 12, and decreased in 3 patients. Ce(REMI) poorly affected the SPI response to FC. In normovolaemic patients, the probability of an SPI change after FC was low under common Ce(PPF) (0.9 to 3.9 µg/ml). A decrease in SPI was more probable with worsening hypovolaemia and lowering Ce(PPF) , while an increase in SPI was more probable with increasing Ce(PPF) . SPI changes were only attributable to modifications in pulse wave amplitude and not in heart rate. CONCLUSIONS: During stable anaesthesia and surgery, SPI may change in response to FC. The effect of FC on SPI is influenced by volaemia and Ce(PPF) through pulse wave amplitude modifications. These situations may confound the interpretation of SPI as a surrogate measure of the nociception-anti-nociception balance.

Linking sleep and general anesthesia mechanisms: this is no walkover.

This review aims at defining the link between physiological sleep and general anesthesia. Despite common behavioral and electrophysiological characteristics between both states, current literature suggests that the transition process between waking and sleep or anesthesia-induced alteration of consciousness is not driven by the same sequence of events. On the one hand, sleep originates in sub-cortical structures with subsequent repercussions on thalamo-cortical interactions and cortical activity. On the other hand, anesthesia seems to primarily affect the cortex with subsequent repercussions on the activity of sub-cortical networks. This discrepancy has yet to be confirmed by further functional brain imaging and electrophysiological experiments. The relationship between the observed functional modifications of brain activity during anesthesia and the known biochemical targets of hypnotic anesthetic agents also remains to be determined.