Editorial article
Electroencephalography in anaesthesia; opening minds to the future
La electroencefalografía en anestesia, abriendo las mentes al futuro
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GC: control group; GPEC: treatment group.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J.B. Schuitemaker R., X. Sala-Blanch, A.P. Sánchez Cohen, L.A. López-Pantaleon, J.T. Mayoral R., M. Cubero" "autores" => array:6 [ 0 => array:2 [ "nombre" => "J.B." "apellidos" => "Schuitemaker R." ] 1 => array:2 [ "nombre" => "X." "apellidos" => "Sala-Blanch" ] 2 => array:2 [ "nombre" => "A.P." "apellidos" => "Sánchez Cohen" ] 3 => array:2 [ "nombre" => "L.A." "apellidos" => "López-Pantaleon" ] 4 => array:2 [ "nombre" => "J.T." "apellidos" => "Mayoral R." ] 5 => array:2 [ "nombre" => "M." "apellidos" => "Cubero" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "es" => array:9 [ "pii" => "S0034935618301439" "doi" => "10.1016/j.redar.2018.08.001" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935618301439?idApp=UINPBA00004N" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2341192919300010?idApp=UINPBA00004N" "url" => "/23411929/0000006600000002/v1_201902050605/S2341192919300010/v1_201902050605/en/main.assets" ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial article</span>" "titulo" => "Electroencephalography in anaesthesia; opening minds to the future" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "59" "paginaFinal" => "61" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "P.O. Sepúlveda, M. Naranjo" "autores" => array:2 [ 0 => array:4 [ "nombre" => "P.O." "apellidos" => "Sepúlveda" "email" => array:1 [ 0 => "pasevou@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "M." "apellidos" => "Naranjo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Clínica Alemana, Universidad del Desarrollo, Santiago de Chile, Chile" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Clínica de Mérida, Mérida, Yucatán, Mexico" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "La electroencefalografía en anestesia, abriendo las mentes al futuro" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Adequate anaesthesia to perform a surgical procedure has long been a matter of discussion. The first attempts to classify anaesthesia were made by Guedel in 1920 and Lundi in the 1930s. In 1968, pharmacological definitions were introduced that are still in use today, such as the minimum alveolar concentration, which is defined by immobility in response to pain stimulus. These concepts were reasonable in surgical scenarios in which the main focus was placed on monitoring vital parameters to avoid hypoxia and hypotension. Brain monitoring, nonexistent at that time, was based on maintaining haemodynamic balance and immobility to facilitate the performance of the surgical procedure.</p><p id="par0010" class="elsevierStylePara elsevierViewall">In the early 1990s, Rampil et al. demonstrated the spinal cord original of minimum alveolar concentration by showing that the concentration needed to prevent movement response to stimulus remained the same, even in an experimental group of decerebrated rats.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">1</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">This proved that movement response (both motor and haemodynamic) depends mainly on subcortical control. However, loss of consciousness is more a phenomenon of cortical and thalamocortical pathways.</p><p id="par0020" class="elsevierStylePara elsevierViewall">This notion, however, has taken some time to translate into clinical practice. Indeed, the very clinical concept of anaesthesia depth has been a source of confusion. Often considered a single phenomenon, only after much effort have clinicians been able to differentiate between cortical and subcortical components.</p><p id="par0025" class="elsevierStylePara elsevierViewall">This has been due to a poor understanding of the different brain circuits associated with consciousness or those that affect nociceptive pathways. It was necessary to combine concepts of neurophysiology, neuroanatomy and neuropharmacology in order to advance in the understanding of what we observe as electrophysiological phenomena in the EEG.</p><p id="par0030" class="elsevierStylePara elsevierViewall">An obvious example of the lack of understanding of this concept has been the exclusive use of inhaled anaesthetic agents, where prioritising the clinical concept of immobility led to anaesthesia with significant cortical activity depression.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Misunderstandings in the clinical definition of loss of consciousness or loss of response has so far led to incorrect clinical strategies, such as correcting the haemodynamic response by changing the concentration of the hypnotic drug.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Sanders et al. defined consciousness as a subjective perceptual experience, differentiating it from the concept of connection with the surroundings and capacity to respond to stimuli. Loss of connection is used in this case as a decrease in cortical input from the senses or endogenous information. This is a subcortical phenomenon caused by so-called “thalamic gating or gating of other core nuclei”, which occurs when efferents towards the cortex are blocked, generating a semi anti-nociceptive state. The loss responsiveness is the lack of response to stimulus, a phenomenon that can occur even while maintaining certain levels of consciousness, as occurs with the exclusive use of high-dose opioids.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">2</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">In an elegant multicentre study, Sebel et al. showed clearly how the bispectral index (BIS) was able to differentiate between use of subcortical and cortical drugs, with the latter affecting the BIS level.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">3</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Loss of responsiveness cannot be interpreted as unconsciousness. This was recently demonstrated by Radek et al. who concluded that patients aroused during continual TCI perfusion of propofol or dexmedetomidine, titrated to the threshold of loss of responsiveness, tended to report experiences from the unresponsive period prior to unconsciousness.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">On the other hand, from the pharmacological point of view, models that correlate effect with plasma concentrations have been, to a certain extent, useful for guiding titration. Most such models were constructed in unstable mixtures with boluses or rapid infusions, and propose that the plasma-effect gap could simply be assumed to be in equilibrium using a mathematical device that collapsed that gap (hysteresis collapse). As a result “site effect” models are associated with overestimation, and anaesthesiologists using them tend to overdose.</p><p id="par0060" class="elsevierStylePara elsevierViewall">The introduction of the EEG in 1937<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">5</span></a> prompted attempts to identify markers of unconsciousness that could guide anaesthesia. However, the inability to do online analysis and the limited capacity of computers at the time forced clinicians to look for simplifying solutions. Added to this was the fact anaesthesiologists, who were able interpret ECGs, were not trained in reading EEG.</p><p id="par0065" class="elsevierStylePara elsevierViewall">EEG studies soon showed that apart from slowing overall cortical activity, administration of anaesthetics was associated with a marked anterior shift in alpha activity (7–12<span class="elsevierStyleHsp" style=""></span>Hz).<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">6–8</span></a> This was used in the BIS<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">9</span></a> algorithm, giving the anaesthesiologist a simple solution that reduced the risk of intraoperative awakening (explicit recall). The indices created at that time involve simplified frontal lobe activity processes, which correlate frequency analysis (alpha, beta or burst suppression ratios, <span class="elsevierStyleItalic">etc.</span>) with clinical states and/or drug concentrations using different estimation techniques (for example, diffuse logic). These indices, therefore, are the product of complex statistics that assume that all anaesthetics generate the same electroencephalographic behavioural condition, and that do not include age as a covariate. In addition, they are associated with processing delays and reactions that differ at induction and emerge from anaesthesia.</p><p id="par0070" class="elsevierStylePara elsevierViewall">We now know that age does impact EEG electrical activity<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">10</span></a> and response to anaesthesia, and that each anaesthetic has its own particular electroencephalographic signature.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">11</span></a> Unfortunately, the objective of reducing the frequency of explicit intraoperative arousal was not achieved, and the research focused solely on high-risk populations, where predictive pharmacological models are even poorer in data.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">12</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">In the search for more representative mechanisms of the phenomenon of unconsciousness, a monitor was developed based on auditory evoked potentials. Schraag et al. showed that auditory evoked potentials were somewhat better than BIS at predicting unconsciousness, defined electrically as the appearance of 2 waves (P1 and N2) in mid latency evoked potentials that reflected the slowing down of activity from the geniculate body and the primary auditory cortex. This slowdown partially represents loss of the arousal required to regain consciousness, but late corticocortical potentials were already greatly diminished, creating an “excess” in that territory and the subsequent reconnection capacity of the cognitive processes.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">13</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">This monitor met with little success because it was an “all or nothing” measure of unconsciousness, and there was no linearity with plasma concentrations that is required in the administration of sedation. Moreover, the signal was extracted from subcortical activity and was, therefore, far from the corticocortical evaluation needed to identify the phenomenon of unconsciousness in earlier stages.</p><p id="par0085" class="elsevierStylePara elsevierViewall">The article by Ferreira et al. in this issue of the <span class="elsevierStyleSmallCaps">Spanish Journal of Anaesthesiology and Critical Care</span><a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">14</span></a> is an attempt to systematise the EEG indices associated with clinical unconsciousness for anaesthesia.</p><p id="par0090" class="elsevierStylePara elsevierViewall">It clearly shows that an index that simplifies cortical activity, associated with the immense variability of each monitor, is incapable of fully describing the phenomenon of anaesthesia. A simple exercise involves predicting the moment of the loss of clinical consciousness solely by observing the index; this, in the vast majority of cases, fails.</p><p id="par0095" class="elsevierStylePara elsevierViewall">One reason for the low predictive power and great variability in response observed in these monitors may be the tendency to assume unproven paradigms, such as, for example, the linearity of plasma concentration effect. We now have evidence that multiple dynamic (behavioural) states lurk under the mantle of unconsciousness, and that these do not necessarily follow a linear pattern in a wide range of drug concentrations.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">15</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">With respect to potential markers for future development, studies such as that published by Jordan et al., which reports that propofol-induced unconsciousness is associated with a reduction in lateral anteroposterior frontoparietal directional connectivity, which also involves the region of the insula. The authors used a high-density EEG and a magnetic resonance technique called symbolic transfer entropy, based on information theory, to show that this loss of electric flow is aloss-of-feedback phenomenon that is particularly important in the generation of human consciousness. It is striking to note that this is a common phenomenon in gabaergic or ketamine-based anaesthesia.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">16</span></a> Recent <span class="elsevierStyleItalic">in vitro</span> studies have uncovered other, more specific, unconsciousness markers for propofol, such as a peak-max alpha wave.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">17</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">Other challenges facing brain monitor development is to show neurophysiological states where there is no doubt that the patient is incapable of generating consciousness. We get a glimpse of this today in monitors that show a monotonous spectrogram with alpha and delta bands for gabaergic drugs, associated with SEF95 spectral frequencies under 15<span class="elsevierStyleHsp" style=""></span>Hz in healthy adults, slightly higher in children, or more compressed in older individuals.</p><p id="par0110" class="elsevierStylePara elsevierViewall">These new monitors should also be capable of early identification of drug overdosing, before the appearance of the burst-suppression ratio. The phenomenon of burst-suppression, which does not depend exclusively on drug overdosing, is particularly challenging because of its complexity.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">18</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">In our opinion, the greatest challenge involves controlling anaesthesia overdosing. Although this is poorly defined, some clinical estimates suggest that it occurs in up to 40% of cases, even in groups that regularly use BIS monitoring.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">19</span></a> Anaesthesiologists encounter an increasing number of elderly patients with particularly frail brains. This must compel us to improve our understanding of specific brain dynamics during anaesthesia in order to facilitate physiological reconnection and recovery of the connectivity of the state of consciousness, and thus reduce postoperative delirium rates and other potentially chronic cognitive alterations. The authors of a recent study propose diagnosing brain frailty on the basis of the speed of onset of slow-wave saturation.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">20</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Speculating that the assumed linearity between plasma concentration and the depressive effect of anaesthesia does not exist, the complexity of non-physiological phenomena such as burst-suppression shows that the task of identifying the adequate anaesthetic unconsciousness is still very challenging.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Sepúlveda PO, Naranjo M. La electroencefalografía en anestesia, abriendo las mentes al futuro. Rev Esp Anestesiol Reanim. 2019;66:59–61.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:20 [ 0 => array:3 [ "identificador" => "bib0105" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Anesthetic potency (MAC) is independent of forebrain structures in the rat" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "I.J. Rampil" 1 => "P. Mason" 2 => "H. 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