array:22 [ "pii" => "S0034935614002424" "issn" => "00349356" "doi" => "10.1016/j.redar.2014.07.008" "estado" => "S300" "fechaPublicacion" => "2014-10-01" "aid" => "516" "copyright" => "Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor" "copyrightAnyo" => "2014" "documento" => "article" "crossmark" => 0 "subdocumento" => "sco" "cita" => "Rev Esp Anestesiol Reanim. 2014;61:417-21" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 960 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 636 "PDF" => 317 ] ] "itemSiguiente" => array:18 [ "pii" => "S0034935614000437" "issn" => "00349356" "doi" => "10.1016/j.redar.2014.01.007" "estado" => "S300" "fechaPublicacion" => "2014-10-01" "aid" => "432" "copyright" => "Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor" "documento" => "article" "crossmark" => 0 "subdocumento" => "fla" "cita" => "Rev Esp Anestesiol Reanim. 2014;61:422-8" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 812 "formatos" => array:3 [ "EPUB" => 4 "HTML" => 591 "PDF" => 217 ] ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original Article</span>" "titulo" => "Anesthesia for bariatric surgery: 8-Year retrospective study: Are our patients now easier to manage?" 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Acosta-Martínez, F. Sánchez-Carrillo" "autores" => array:3 [ 0 => array:2 [ "nombre" => "M." "apellidos" => "de la Matta-Martín" ] 1 => array:2 [ "nombre" => "J." "apellidos" => "Acosta-Martínez" ] 2 => array:2 [ "nombre" => "F." "apellidos" => "Sánchez-Carrillo" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0034935614000437?idApp=UINPBA00004N" "url" => "/00349356/0000006100000008/v1_201409150159/S0034935614000437/v1_201409150159/en/main.assets" ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial article</span>" "titulo" => "Playing games with the brain: The possible link between anesthesia and Alzheimer's disease revisited" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "417" "paginaFinal" => "421" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "F.A. Lobo, A. P. Saraiva" "autores" => array:2 [ 0 => array:4 [ "nombre" => "F.A." "apellidos" => "Lobo" "email" => array:1 [ 0 => "francisco.lobo@me.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" => "A." "apellidos" => "P. Saraiva" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Anesthesiology Department, Hospital Geral de Santo António, Porto, Portugal" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Anesthesiology Department, Hospital Geral de Santo António - Centro Hospitalar do Porto, Porto, Portugal" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Jugando con el cerebro: revisión del posible vínculo entre la anestesia y el Alzheimer" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">The brain is the most complex and remarkable organ in the human body: through infinite neuronal synapses and networks, neurotransmitters and neural impulses, the brain establishes in- and out-pathways receiving and sending all kind of information to command and integrating the other organs physiology. This simplistic view of the brain structure and role does not eliminate a question that we must have on our mind: does an organ so sensitive and complex enjoys to be touched and switched off by anesthetic drugs? In other words, do general anesthetic drugs jeopardize some cerebral neuronal circuits function while acting on, changing and turning off consciousness or consciousness-related pathways?<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Entities as postoperative cognitive dysfunction (POCD) and postoperative delirium may be seen as early consequences of a disrupted brain function elicited or, at least, with some contribution of anesthesia, anesthetic drugs and/or surgery. Some authors have been extensively reviewing the subject, trying to shed some light on the risk factors, the pathogenic mechanisms leading to a postoperative cognitive decline and, lately, the pathological mechanisms underlying POCD mimicking Alzheimer's Disease (AD).<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2–3</span></a> Curiously, there's a simultaneous trend among patients towards a fear about perioperative and anesthesia-related brain injury and memory loss, which was already brought to the public attention.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Several comprehensive reviews have been describing the AD<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5–6</span></a> which is estimated to affect 26.6 million people and is the most common form of dementia with higher prevalence with increasing age from 65 to 85 years old.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The large majority of cases (over 99%) are late onset and sporadic in origin, with multifactorial ethiopathology, with external factors interacting with biological or genetic susceptibility to accelerate the manifestation of the disease. Exposure to anesthesia might be such an external factor and the possibility that anesthesia/surgery may trigger or accelerate a demential process is fearful and deserves a special attention.</p><p id="par0020" class="elsevierStylePara elsevierViewall">A consensus statement coming from the First International Workshop on Anesthetics and AD held in 2008<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> provided us with an important tool for a comprehensive view of this possible link but 6 years after there are still many unanswered questions. How to look to these puzzled connections between surgery, anesthesia, anesthetic drugs, anesthesia techniques, concurrent perioperative events as hemodynamic and metabolic changes, in vitro-, animals and human studies and cognitive performance before and after surgery/anesthesia: rejecting the worst scenario or accepting that something may exist and search for protective strategies until definite evidence is proved?</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Intersection of anesthetic drugs and pathological hallmarks of AD</span><p id="par0025" class="elsevierStylePara elsevierViewall">Amyloid beta (Aβ) and tau protein fibrillar lesions are the classical hallmarks of AD.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> Briefly, mutations in the amyloid precursor protein (APP) enhance the production of a small series of soluble, unstable proteins called the amyloid-beta, which may undergo a process of association and oligomerization when exceeding some solubility threshold; these small oligomers may produce neuronal and synaptic damage, and its assembly in larger monomers results in senile plaque, the histological hallmark of AD. The other characteristic lesion of AD is the intracellular neurofibrillary tangle (NFT), composed primary by protein tau, which dephosphorylated form provides stability to microtubules (MT). When tau phosphorylation occurs, the protein detaches from microtubules and becomes cytoplasmatic; an enhanced tau hyperphosphorylation may lead to microtubules disruption but also to tau association with NFTs production.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Several experimental studies have been showing a strong association between anesthetic agents and these molecular pathways of AD. Inhalational agents may increase Aβ production, oligomerization and accumulation, promoting plaque formation in vitro and in vivo, nicely reviewed by Xie and Xu.<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Potent volatile anesthetic agents also interfere with the phosphorylation, aggregation and function of microtubule-associated tau protein<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> and concomitant cognitive impairment<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> although is unknown if the hyperphosphorylation of tau protein is induced directly by the anesthetic agents or by the anesthesia induced hypothermia or by both.<a class="elsevierStyleCrossRefs" href="#bib0055"><span class="elsevierStyleSup">11,13</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Calcium metabolism also seems to play some role on AD pathogenesis<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> and again, through this alternative pathway, anesthetic agents may interfere and strength neuronal cell damage.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Curiously, intravenous agents as propofol and thiopental are likely to be protective<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16–17</span></a> in comparison with the evidence described for potent volatile anesthetic agents, which may be significant for translational research developments.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Too many roads open to nowhere: human studies and absence of evidence</span><p id="par0045" class="elsevierStylePara elsevierViewall">Current clinical studies have failed so far to provide solid evidence that exposure to anesthesia and/or surgery is associated with an increased risk of AD.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">18–20</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Association between early POCD and anesthesia has been well documented in human studies.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21–22</span></a> This cognitive decline is usually transient and reversible, with patients recovering 3–12 months after surgery.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> However, the acute changes associated with POCD might predispose patients to chronic changes associated with dementia,<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> with a possible bimodal pattern of cognitive decline. When interpreting the clinical evidence of the association between cognitive decline and anesthesia, several barriers arise between our doubts and the scrupulous true. In a recent review, the authors address a number of inconsistencies regarding the design of these studies, such as the methodological issues (diagnosis of early and persistent POCD, learning effect, statistical analysis), the patient-related factors (age, pain, co-morbidities, vulnerability, cognitive trajectory, pathology preceding dementia) and the variety of postoperative outcomes accessed (postoperative events, quality of life, postoperative cognitive trajectory).<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> The number and significance of the possible biases accounting for all of these variables make difficult to interpret the heterogeneous results.</p><p id="par0055" class="elsevierStylePara elsevierViewall">Nevertheless, in the last few years, studies did not find a relationship between surgery, anesthesia or early POCD and dementia/AD.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">24–26</span></a> Only one study found that patients, who had undergone CABG surgery under general anesthesia, when compared to patients submitted to percutaneous angioplasty, had a higher risk to develop AD.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Biochemical markers of brain damage, neuroinflammation and, importantly, of AD as amyloid-β peptide and tau protein have been found increased after anesthesia and surgery,<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> mainly when inhalational anesthesia was employed<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> with rather intravenous anesthesia with propofol.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> It should be remarked that desflurane seems to have a different pattern than isoflurane, lowering amyloid amyloid-β peptide in CSF in humans.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Interestingly, there's also evidence of higher risk of Parkinson's disease, which has some similar features with AD,<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> among anesthesiologists as compared with internists.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Two recent Taiwanese studies, using the Taiwan's National Health Insurance Research Database (NHIRD), found an association between anesthesia and diagnosis of AD,<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">33–34</span></a> independent of the type of surgery, amount of anesthetics used, or cumulative duration of anesthesia; however, there are important limitations as highlighted by Sprung,<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> mainly related with the lack of consistency in diagnostic criteria and the possibility of inaccurate coding that can exist in such a database. A French study<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a> found similar results but still lacks scientific validation as a published study.</p><p id="par0075" class="elsevierStylePara elsevierViewall">Whether underlying diseases of patients,<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">37–39</span></a> hospitalization,<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a> surgery-related inflammatory responses<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a> or anesthetic management<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a> causes POCD or subsequent dementia, also remains unclear. Adding fuel to the fire, there's an intriguing theory advanced recently<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> suggesting that there is potential for cognitive improvement after surgery, when it improves health, quality-of-life, and decreases inflammation and pain levels.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">The present and the future: searching for the patients at risk</span><p id="par0080" class="elsevierStylePara elsevierViewall">In view of conflicting evidence, it is imperative to invest in future studies, based on scrupulous methodology, which can undoubtedly translate the association between anesthesia brain damage and AD from the biological plausibility field to the evidence based medicine. But while more and better-designed studies are being conducted, should we be adventurous and proceed with our eyes wide shut until the defendant is proved guilty as charged? Or should we be judicious and search for some protective strategies for our patients?</p><p id="par0085" class="elsevierStylePara elsevierViewall">Indeed, facing the available literature, we can identify some risk factors concerning the possible development of dementia following surgery and/or anesthesia. There are some well known risk factors for AD including advanced age, female gender, lower educational level, family history, cardiovascular diseases, diabetes mellitus, depression, and head trauma<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">44–45</span></a> and cardiac and major orthopedic surgery seem to be those most notably associated with postoperative cognitive decline.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21,46</span></a> But some other possible risk factors deserve deserve our attention: the cognitive trajectory before surgery may be an important determinant of the postoperative dysfunction,<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> with the postoperative cognitive decline reflecting a pre-existing downward tendency; or the personality trait of our patients, like neuroticism, and conscientiousness, may play an important role as showed by a metanalysis by Terracciano et al.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Another non-modifiable factor to consider is genetics. The apolipoprotein E ¿4 genotype is an important risk factor for the development of late-onset AD,<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> although there is conflicting evidence regarding its association with POCD.<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">46,49,50</span></a> Nevertheless, individuals carrying the ¿4 genotype suffering from POCD could be at higher risk of developing AD. Curiously, this genotype is associated also with the occurrence of delirium in ICU<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> and after non-cardiac surgery<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> and with higher requirements for propofol for loss of consciousness during general anesthesia induction<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a>; this association with higher anesthetic needs seems to match with the finding that transgenic AD-mice have been showing to have higher MAC values for volatile agents.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">Pain is another issue to be addressed. It has been shown in neuroimaging studies that patients with chronic pain have a decreased gray matter density in regions like the anterior <span class="elsevierStyleItalic">cingulate</span> cortex, <span class="elsevierStyleItalic">insula</span> and dorsolateral prefrontal cortex, which have an important role in the perception and integration of painful stimuli.<a class="elsevierStyleCrossRefs" href="#bib0275"><span class="elsevierStyleSup">55,56</span></a> We also know that acute pain in the postoperative period can cause delirium and POCD<a class="elsevierStyleCrossRefs" href="#bib0285"><span class="elsevierStyleSup">57,58</span></a> and that acute postoperative pain is a risk factor for the development of chronic pain.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a> Thus, postoperative non-controlled acute pain could be a risk factor for the development of permanent brain damage and optimal acute pain control and adequate selection of chronic pain patients for major procedures such as spine or joint replacement surgery are mandatory.</p><p id="par0100" class="elsevierStylePara elsevierViewall">As the peri-operative period conveys a series of aggressions to the body homeostasis, the association of surgery/anesthesia and POCD or dementia, could not only be due to the trauma stress response and anesthetics’ toxicity but also to the cumulative effect of small insults like glucose disturbances and insulin dysfunction,<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> temperature control,<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13,61</span></a> blood pressure<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">62</span></a> and adequate oxygenation.<a class="elsevierStyleCrossRefs" href="#bib0315"><span class="elsevierStyleSup">63–64</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">The present and the future, part 2: how to proceed with the old patient undergoing spine surgery next Monday morning?</span><p id="par0105" class="elsevierStylePara elsevierViewall">Following the open roads described above, we face a conflict: is there any evidence leading us to change our practice in someway or should we continue to use the drugs, anesthetic techniques and routine monitoring strategies we have been using for years?</p><p id="par0110" class="elsevierStylePara elsevierViewall">Regarding the conflicting evidence of the association of anesthesia and AD, as Woehck did addressing the approach for intraoperative carbon monoxide poisoning prevention,<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">65</span></a> we may classify the clinical anesthesiologists into three groups: the Overconcerned, the Apathetic and Negativist and the Level-headed. The Overconcerned have been anesthetizing many old patients, have managed many patients with postoperative cognitive disturbance, have heard some relatives of patients saying “Grandma has not been the same since she had anesthesia”, or is just the worrying sort. The Apathetic and Negativist may be overconfident, uninformed or simply is the modern John Henry folk (<a id="intr0005" class="elsevierStyleInterRef" href="http://en.wikipedia.org/wiki/John_Henry_(folklore"><span class="elsevierStyleUnderline">http://en.wikipedia.org/wiki/John_Henry_(folklore</span></a>)) fighting against something that may counteracts all his lifelong practice. The Level-headed anesthesiologist will keep his mind open to the possibility of the association between anesthesia/surgery and AD, but not so much for the brain not to fall out, pursuing the best care of his patients, identifying risk factors and minimizing the deleterious effects of the least worst anesthetic options.</p><p id="par0115" class="elsevierStylePara elsevierViewall">A Level-headed anesthesiologist managing an old hypertensive patient submitted to spine surgery would elaborate an anesthetic plan aiming a tailored anesthesia; in other words, he would choose total intravenous anesthesia, preferably with target-controlled infusion of propofol and remifentanil, avoiding inhalational agents,<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16,29,66</span></a> monitoring the level of consciousness depression using a processed EEG index of consciousness,<a class="elsevierStyleCrossRef" href="#bib0335"><span class="elsevierStyleSup">67</span></a> having in mind the limitations of these parameters,<a class="elsevierStyleCrossRef" href="#bib0340"><span class="elsevierStyleSup">68</span></a> and possibly brain oxygenation<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a> and some form of nociception-anti-nociception balance monitoring,<a class="elsevierStyleCrossRef" href="#bib0345"><span class="elsevierStyleSup">69</span></a> controlling tightly the temperature<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">61</span></a> and glycemia,<a class="elsevierStyleCrossRefs" href="#bib0300"><span class="elsevierStyleSup">60,70</span></a> with a multimodal postoperative analgesic plan including parecoxib.<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">71</span></a> Even if some of these attitudes in the future will be proved as useless and devoid of evidence-based benefits, the open-minded and Level-headed anesthesiologist cannot be accused today of misuse and redundancy.</p><p id="par0120" class="elsevierStylePara elsevierViewall">We were taught during the last two decades that modern Anesthesiology was reaching the maximum of safety patterns. Now, the possibility of anesthesia and/or surgery promoting or triggering AD development may be seen as a threat for this well-established highly safe and high-quality medical specialty. Some may even throw it into the big bag of medical damned lies (<a id="intr0010" class="elsevierStyleInterRef" href="http://www.theatlantic.com/magazine/archive/2010/11/lies-damned-lies-and-medical-science/308269"><span class="elsevierStyleUnderline">http://www.theatlantic.com/magazine/archive/2010/11/lies-damned-lies-and-medical-science/308269</span></a>). By the opposite, we prefer to quote George Bernard Shaw, “<span class="elsevierStyleItalic">All great truths begin as blasphemies”</span>, while hoping for better and proved epidemiological evidence establishing or not a link between anesthetic exposure and the risk of AD.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Intersection of anesthetic drugs and pathological hallmarks of AD" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Too many roads open to nowhere: human studies and absence of evidence" ] 2 => array:2 [ "identificador" => "sec0015" "titulo" => "The present and the future: searching for the patients at risk" ] 3 => array:2 [ "identificador" => "sec0020" "titulo" => "The present and the future, part 2: how to proceed with the old patient undergoing spine surgery next Monday morning?" ] 4 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:71 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Depth of anesthesia: perhaps the patient isn’t a submarine" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "J.W. 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