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by Neuroskeptic in Neuroskeptic
Every time we blink, a wave of activity sweeps through our brain - and this could be a serious problem for some fMRI researchers.French neuroscientists Hupé et al report on A BOLD signature of eyeblinks in the visual cortex. They found that spontaneous blinks are associated with a neural activation pattern over the occipital cortex areas responsible for processing vision.In many ways this is not surprising - when you blink, everything goes dark, and then lights up again, all within a fraction of second, which means that blinks are a kind of very dramatic visual stimulus, equivalent to a big black object suddenly appearing and then vanishing again. However, it's long been believed that blink suppression mechanisms in the eye and brain somehow block out the responses that would otherwise happen during a blink.Don't be so sure, say Hupé et al. In an elegant experiment, they showed volunteers a standard set of visual stimuli during fMRI scanning, while recording blinks using an eye tracking camera. Then they simply treated the blinks as events, and used standard analysis methods to find neural activation associated with them.Blinks caused a significant BOLD response over a number of "visual" areas.Compared to the "real" visual stimuli in the task, the blink signal was less extensive, but no less strong.So what? The great majority of fMRI experiments don't use eyetracking to measure blinks, so this study raises the scary possibility that blinks could lie behind some of the "stimulus-related" activations that we all know and love. It would be a problem if subject blinks were correlated with the stimuli or tasks, which they might be, because blink rate may vary with our psychological state.I don't think we should be too worried yet. The blink blobs were essentially confined to parts of the visual cortex. So any study that's not focussed on vision is probably in the clear (although that's just the average response: in some individual subjects, the activations were a lot wider.)However, as the authors point out, there is a risk that alterations in blink rate, caused, perhaps, by emotional or cognitive stress, might be wrongly "found" to be causing visual cortex activation, which might call into question claims of "top-down" influences on early visual cortex... oh dear.... Read more »
Hupé, J., Bordier, C., & Dojat, M. (2012) A BOLD signature of eyeblinks in the visual cortex. NeuroImage. DOI: 10.1016/j.neuroimage.2012.03.001
by Neuroskeptic in Neuroskeptic
Diagnosed rates of ADHD in American children have skyrocketed in the past 20 years, and use of medication such as Ritalin and Adderall has increased by an even greater amount.So says a report just out in Clinical Pediatrics, using data from the major US National Ambulatory Medical Care Survey (NAMCS). The rate of office based visits (i.e. visits when a doctor saw or treated a patient, outside of a hospital) was the main outcome measure. The authors looked at the number of visits reporting a diagnosis of ADHD, and also the number of ADHD visits also involving psychostimulant medication, for kids aged 5 to 18.See above - that's a big increase, and a lot of visits (remember the Y axis is visits per 1000 children per year.) One thing to remember is that the increase might not mean that there are more patients with ADHD - it could reflect more visits per patient, but that seems unlikely to account for all of it.A few thoughts -The rise of ADHD parallels the recent increase in autism diagnoses. Yet people don't seem to be talking about it to the same extent. We're always hearing about "the autism epidemic", the "Age of Autism". Why aren't we equally concerned about the ADHD 'epidemic'? Why don't we have minor celebs railing about vaccine-damaged ADHD children?Next - like autism - it seems likely that much or all of the increase is due to changes in awareness and willingness to diagnose the disorder. If so, logically, ADHD must either be being seriously overdiagnosed now, or was being seriously underdiagnosed previously. Or both.This is especially true of boys. Rates in girls rose pretty much steadily for 15 years but in boys, there have been swings up and down, although the overall trend is still upward. It's always possible that this is a quirk of the NAMCS dataset, but if not, it suggests that ADHD diagnosis in boys is especially prone to changes in diagnostic fashion.It's tempting, actually, to see the recent fall in boys with ADHD as a consequence of the rise of autism diagnoses over the same period. Autism is predominantly diagnosed in boys and the two disorders are often comorbid.Maybe, boys are now getting autism diagnoses which are then felt to explain their behaviour, meaning that they don't "need" an ADHD diagnosis, which previously they would have got. But that's just my speculation, and it's probably reading too much into the data, because there was also a peak in 1994 which I can't see any explanation for.Sclar DA, Robison LM, Bowen KA, Schmidt JM, Castillo LV, and Oganov AM (2012). Attention-Deficit/Hyperactivity Disorder Among Children and Adolescents in the United States: Trend in Diagnosis and Use of Pharmacotherapy by Gender. Clinical pediatrics PMID: 22399571... Read more »
Sclar DA, Robison LM, Bowen KA, Schmidt JM, Castillo LV, & Oganov AM. (2012) Attention-Deficit/Hyperactivity Disorder Among Children and Adolescents in the United States: Trend in Diagnosis and Use of Pharmacotherapy by Gender. Clinical pediatrics. PMID: 22399571
by Neuroskeptic in Neuroskeptic
A "phantom limb" is the sensation that an amputated limb (or other body part) is still present.They can be distressing, especially when they're accompanied by pain in the "limb" which is not uncommon. The leading theory of why they happen is that the brain areas that used to receive sensations from the lost appendage respond to input "spilling over" from nearby brain regions.Anyway, a phantom limb is bad enough, but a paper just out reports on the case of a phantom finger that was never there in the first place.A woman, RN, was born with an abnormally short right arm; her right hand was also malformed, with a shortened thumb, no index finger, and immobile ring and middle fingers. Only the little finger was present and correct.At the age of 18, she then had the misfortune to suffer a car crash; the injuries meant that her right hand had to be amputated. She soon found herself experiencing a phantom hand - with all five fingers. Three of them felt like they were normal length; the "thumb" and "index finger" felt shorter than normal, but remember that the original hand had no index finger at all.RN also suffered from phantom pains and was distressed by the fact that the "hand" felt like it was bent into an impossible posture. Fortunately, the mirror box technique was able to set things right; while the phantom was still there, it was no longer painful, and all the fingers were the right length.This is a remarkable case. The authors of the paper, Paul McGeoch and V. S. Ramachandran (perhaps the best known phantom-limb expert) say that it could mean that we're born with an innate, hard-wired "body plan" in the brain, regardless of the way our body actually develops -While RN’s phocomelic[abnormal] hand was present she did not experience any phantom sensations. Thus, although severely deformed, the mere presence of the hand was sufficient to inhibit the innate representation of her normal hand and prevent any phantom sensations from emerging, presumably from tactile, proprioceptive and visual feedback... the amputation of her hand appears to have disinhibited these suppressed finger representations in her sensory cortex and allowed the emergence of phantom fingers that had never existed in her actual hand. They do consider alternative explanations though -Clearly it is beholden on us to consider whether RN’s descriptions do not describe a genuine sensory experience, but rather are confabulatory in origin. We do not believe this to be the case, since if she were confabulating then it would seem unlikely that she should report that her phantom hand had five fingers, but that they were not all of normal length; if this were simply ‘wishful thinking’ then she would likely claim to have five normal length fingers. This appears a persuasive, although not definitive argument, against confabulation. Seems like a fair assessment.I don't even know what you'd call the phantom "index finger". A pseudo-phantom? A phantom phantom? McGeoch, P., and Ramachandran, V. (2012). The appearance of new phantom fingers post-amputation in a phocomelus Neurocase, 18 (2), 95-97 DOI: 10.1080/13554794.2011.556128... Read more »
McGeoch, P., & Ramachandran, V. (2012) The appearance of new phantom fingers post-amputation in a phocomelus. Neurocase, 18(2), 95-97. DOI: 10.1080/13554794.2011.556128
by Neuroskeptic in Neuroskeptic
Not one but two new papers have appeared from the Carlos Zarate group at NIMH reporting that a single injection of the drug ketamine has rapid, powerful antidepressant effects.One placebo-controlled study found a benefit in depressed bipolar patients who were already on mood stabilizers. The other found benefits in treatment-resistant major depression, though ketamine wasn't compared to placebo that time. Here's the bipolar trial: There have now been several studies finding dramatic antidepressant effects of ketamine, a compound that all journalists seem contractually bound to call either a or a "club drug" or a "horse-tranquilizer". Great news?If you believe it. But hold your, er, horses... there's a problem. As I said almost 3 years ago about one of the earlier ketamine trials:In theory, the trial was double blind - neither the patients nor the doctors knew whether they were getting ketamine or placebo. But you'll know when you've been injected with 0.5mg/kg ketamine. You get high. That's why people take it [recreationally]. The study can't really be called double blind. To their credit, Zarate et al did acknowledge this, and suggested that in future ketamine could be compared to another drug which produces noticeable effects. But they really should have done that to begin with.It's now 2012, and there have still not been any published studies comparing ketamine to an active comparator i.e. a different drug that produces noticable psychoactive effects, to avoid unblinding. This means it's 12 years since the initial pilot report on ketamine in depression, and 6 years since the first large trial appeared.The authors of the 2006 paper themselves wrote that "limitations in preserving study blind may have biased patient reporting... One potential study design in future studies with ketamine might be to include an active comparator" and suggested amphetamine for the big role.Good idea. But six years later, we're still waiting. Which is really a bit silly. There have been dozens of papers written about the possible antidepressant effects of ketamine, from human trials to mouse work. That's a lot of research dollars (and dead mice) on something that might just be an active placebo.Looking at the registered ketamine research on clinicaltrials.gov, I found that four active-comparator ketamine trials are in the pipeline (1,2,3,4), plus one cancelled (5). Only one is for depression though. The others being for OCD, cocaine dependence and suicidal ideation.In all of these trials a benzodiazepine is the active comparator. Is that a good idea? Well, it's certainly better than nothing, but I wonder.An active comparator has to "make an impression" on the patient equal to that produced by the real drug. The null hypothesis, remember, is that ketamine has no specific antidepressant effect. That means it produces improvement through a combination of a) the placebo effect (expectation) and b) non-specific psychoactive changes.More on that second one: any psychoactive drug might relieve depression by "taking your mind off it" and a change in mental state, as provided by a drug, also provides a demonstration that "I won't always feel this way". By showing that states of consciousness are products of brain chemistry, almost any drug could therefore offer a "glimmer of hope" to the depressed. If all this sounds very subjective, it is, but that's the point. Psychiatry is.Would a benzo make as big an impression as 0.5 mg/kg ketamine IV? It's impossible to predict, really; so we'd need to ask people about the subjective strength of the drug effect. Personally, I worry that a lot of people just get sleepy on benzos and don't really feel much, so I'd prefer they used something a bit more hard-hitting like amphetamine, but maybe that's just me.There's a deeper problem though. Suppose our ketamine-benzo trial finds no difference between ketamine and benzo. A critic could say, ah, but maybe it was just a "failed trial", so it doesn't overturn the positive studies. The patients weren't properly diagnosed, or weren't depressed enough, or were too depressed, etc.Nitpicking such differences between studies is a well-practiced art.Critics could complain in other ways if the study did find a benefit of ketamine. As I see it, the only way to settle this once and for all is to do a three-way randomized controlled trial - inactive placebo vs. active comparator vs. ketamine.That way, if it's a failed trial, we'd know: there'd be no difference between ketamine and the inactive placebo. If there was a difference, but the active comparator was just as good as ketamine, that means it was all about nonspecific effets. Finally, if ketamine was better than the other two conditions, we could be pretty confident it was really working.Also important is the question of volunteer expertise; subjects shouldn't be able to tell what drug they're on, but people who'd taken ketamine and/or the comparator drug before might be able to do that, so you'd want naive volunteers.In conclusion: It's possible that ketamine has no specific antidepressant effects. To find out we ideally need a three-way trial, with both active and inactive comparators, careful monitoring of subjective drug effects and patient knowledge and expectations. Until that happens, I will be skeptical of ketamine in depression.This is not because I just think it's impossible. Ketamine profoundly affects the brain in ways that we don't understand. I've suffered depression and I know it can come and go in a matter of minutes. So I think it's entirely possible that it works - but it's also possible that it's a nonspecific effect.Look. I really want to know the answer to this. Both as a neuroscientist, and as a depression sufferer, this is very important to me. That's why we urgently need a good trial.Link: See also the discussion and the comments over at The Neurocritic and this Scientific American piece which is pretty good except that it doesn't cover the active placebo issue. Zarate CA Jr, Brutsche NE, Ibrahim L, Franco-Chaves J, Diazgranados N, Cravchik A, Selter J, Marquardt CA, Liberty V, and Luckenbaugh DA (2012). Replication of Ke... Read more »
Zarate CA Jr, Brutsche NE, Ibrahim L, Franco-Chaves J, Diazgranados N, Cravchik A, Selter J, Marquardt CA, Liberty V, & Luckenbaugh DA. (2012) Replication of Ketamine's Antidepressant Efficacy in Bipolar Depression: A Randomized Controlled Add-On Trial. Biological psychiatry. PMID: 22297150
Ibrahim, L., DiazGranados, N., Franco-Chaves, J., Brutsche, N., Henter, I., Kronstein, P., Moaddel, R., Wainer, I., Luckenbaugh, D., Manji, H.... (2012) Course of Improvement in Depressive Symptoms to a Single Intravenous Infusion of Ketamine vs Add-on Riluzole: Results from a 4-Week, Double-Blind, Placebo-Controlled Study. Neuropsychopharmacology. DOI: 10.1038/npp.2011.338
by Neuroskeptic in Neuroskeptic
The British Journal of Social Psychology has published a fiery rebuke to psychologists who argue that belief in free will makes people more ethical.Recent much-publicized studies have claimed that scepticism about free will makes people behave less morally. "Disbelief in Free Will Increases Aggression and Reduces Helpfulness" as the title of one of hese papers puts it.In his article (free pdf), British 'independent researcher' James B. Miles says that these experiments are flawed, because they didn't distinguish between determinism (lack of free choice) and fatalism (lack of the ability to change events).More fundamentally, though, Miles says that free will is used to justify things, such as punishment and poverty, that would otherwise be seen as scandalous -Western law recognizes that the penal system is so harmful to the existing life and future opportunities of persons that to convict requires evidence beyond a reasonable doubt. Yet libertarians provide no objective evidence whatsoever for the existence of free will, and therefore no apparent justification for the mass poverty and brutal punishments that belief in libertarian free will often brings with it. The leading legal theorist Stephen J. Morse freely admits that harsh prison conditions and execution are only morally tolerable where the presumption of free choice exists......In June 2009, the Joseph Rowntree Foundation published research showing that up to 83% of Britons think that ‘virtually everyone’ remains in poverty in Britain not as the result of socialmisfortune or biological handicap but through choice (Bamfield & Horton, 2009, p. 23; 69% of those surveyed agreed with the statement and an additional 14% were unsure but did not disagree.) Because of their belief in the fairness of ‘deserved inequalities’, such respondents were discovered to have become almost completely unconcerned with the idea of promoting greater equality while at the same time asserting that Britain was a beacon of fairness that offered opportunities for all......Free will may just be the primary excuse many use to legitimize a contempt for the poor that would exist independent of their professed belief in free will, but free will assertion nonetheless provides the ethical fig leaf for such contempt that would be far harder to rationalize (and therefore tolerate) without the myth of free will. This is a polemical piece (remarkably so, for an academic journal), and clearly this is only one side of the story, but it's hard to deny that he has a point: there's a dark side to the belief in free will. If you doubt free will, and yet praise the myth of it, as some scientists seem to be doing, you need to accept that you're condemning some people (prisoners, most obviously) to suffer as a result "through no fault of their own".Personally, I think the great majority of people do believe in free will and always will - the arguments against it have been around for millenia, they're as convincing as they'll ever be, and they haven't convinced most people, however irrational that might make most people. So I think the debate over belief in free will is academic; it's not going away. Miles JB (2011). 'Irresponsible and a Disservice': The integrity of social psychology turns on the free will dilemma. The British journal of social psychology / the British Psychological Society PMID: 22074173... Read more »
Miles JB. (2011) 'Irresponsible and a Disservice': The integrity of social psychology turns on the free will dilemma. The British journal of social psychology / the British Psychological Society. PMID: 22074173
by Neuroskeptic in Neuroskeptic
Is research on the global distribution of mental health problems a kind of modern-day missionary work?Maybe, says Australia's Dr Stephen Rosenman in a provocative paper: Cause for caution: culture,sensitivity and the World Mental Health Survey Initiative.The World Mental Health Survey (WMHS) is a huge World Health Organization project that aims to measure the rates of various psychiatric disorders in countries around the world. The WMHS has produced a great deal of data, but Rosenman points out that this assumes that people all over the world suffer from the same psychiatric disorders (and display them in the same ways) as the Americans and Europeans about whom the diagnostic manual was originally written.The surveys translated the diagnostic criteria into the local languages, of course, but that doesn't mean they were appropriate to the local cultures.He suggests that all this is a bit like missionaries who went around translating the Bible and trying to convince people to read it -Looked at with a less admiring eye, the [WMHS] resembles in some ways the missionary movements of the last two centuries. Like the missionaries, the organisers are committed, selfless people of extraordinary goodwill who have come to poor countries from cultures at the apogee of their wealth, prestige and intellectual power. They bring an evolved and highly developed system of thought. They set about delivering the fruits of that to the people. The survey initiative has engaged the leaders of the profession in the countries and, in a sense, has converted them to this view of psychopathology. It is difficult to know if their success is due to the power of the ideas they brought, or the power and prestige of the cultures they came from, or from their technique of taking over both the centre and the contours of the beliefs of a culture. Missionaries brought a ‘colonisation of consciousness’... etc.He does goes on to say though, "I do not want to push the missionary analogy too far" which is wise I think; there are important differences and other analogies are equally apt.The paper's a good read though. It refers to Crazy Like Us, a book I'm fond of.Although Rosenman doesn't cite another important source (cough cough): he points out that the WMHS national estimates of rates of depression don't correlate at all with national suicide rates, which is seriously odd - According to the CIDI [the psychiatric interview used in the WMHS], Japan, for example, has one-third the rate of mood disorders (3.1%) seen in the USA (9.6%). At the same time, Japan’s suicide rate (20.3/100,000) is twice that of the USA (10.8/100,000). Suicide rates seem to have almost no relationship with CIDI diagnoses of affective disorder... Suicide, of course, is complexly shaped by the culture but are we to believe that answers to the CIDI are any less culturally determined and which is to be considered the better index of disorder?I made the very same point using the very same datasets in 2009 (although I looked at 'all mental illness' rather than 'mood disorders').Rosenman, S. (2012). Cause for caution: culture, sensitivity and the World Mental Health Survey Initiative Australasian Psychiatry, 20 (1), 14-19 DOI: 10.1177/1039856211430149... Read more »
Rosenman, S. (2012) Cause for caution: culture, sensitivity and the World Mental Health Survey Initiative. Australasian Psychiatry, 20(1), 14-19. DOI: 10.1177/1039856211430149
by Neuroskeptic in Neuroskeptic
Canadian Neuroscientists Jacqueline Snow et al propose a new method of making brain scanning studies a bit more realistic.Typically, in an fMRI or other neuroimaging study, any visual stimuli shown to the volunteer are just pictures on a screen. Sometimes videos will be used, but in almost all cases they're just 2D images. Is that adaquate? People have hoped so.Snow et al's data suggest that it might not be.They created a contraption for presenting subjects with real objects during a scan. See above. Now, to the uninitiated this might not seem like a big deal, but those with MRI experience will appreciate how impressive this is.Everything from the angle of the volunteer's head to the LED lighting is an achivement, given the nature of MRI. The stimuli were controlled by one of the researchers, who had to sit next to the scanner, in total darkness, and operate the turntable with the help of some glow-in-the-dark stickers.Having built this device, they then used it to compare the brain's responses to real objects vs photos of those same objects. The experiment was designed to test fMRI adaptation - the phenemenon whereby if you present the same stimuli repeatedly, the neural responses are reduced.fMRI adaptation has been found to happen in many studies using 2D pictures, but Snow et al show that the effect was much smaller, maybe entirely absent, when people were repeatedly shown real objects: this graph shows the BOLD neural response in the lateral occipital complex. Seeing the same pictures over and over led to a weaker response, as expected; but seeing the same 3D objects didn't:This is a good study and an important result, which suggests that the much-studied fMRI adaptation might not be a universal phenemonon. And the potential implications are big, as the authors write:Finally, our preliminary fMRI results raise the provocative suggestion that the presence of real-world objects (i.e., as indicated initially via stereoscopic cues) invokes qualitatively different computations to those elicited by 2D images. Researchers in the field of behavioral psychophysics have expressed long-standing concern about the extent to which pictures of objects capture the properties of their real-world counterparts (i.e., their ecological validity), with reservations as to their appropriateness as stimuli with which to examine the nature of human object perception...Snow, J., Pettypiece, C., McAdam, T., McLean, A., Stroman, P., Goodale, M., and Culham, J. (2011). Bringing the real world into the fMRI scanner: Repetition effects for pictures versus real objects Scientific Reports, 1 DOI: 10.1038/srep00130... Read more »
Snow, J., Pettypiece, C., McAdam, T., McLean, A., Stroman, P., Goodale, M., & Culham, J. (2011) Bringing the real world into the fMRI scanner: Repetition effects for pictures versus real objects. Scientific Reports. DOI: 10.1038/srep00130
by Neuroskeptic in Neuroskeptic
In all the fuss over the pressure for scientists to publish positive results, we may have been missing an equally dangerous kind of publication bias operating in the opposite direction.So say Luijendijk and Koolman in the Journal of Clinical Epidemiology: The incentive to publish negative studies: how beta-blockers and depression got stuck in the publication cycle.The background here is the possible link between beta blockers and depression. Beta blockers are drugs widely used to treat high blood pressure. Some studies have reported that they raise the risk of depression, though many others found no link. Propranolol is said by some to be the worst offender because it's best at entering the brain.Luijendijk and Koolman say that beta blocker-depression studies have appeared in the form of "publication cycles" - first a positive study appears, and then negative ones follow. Then another study finds a positive link using a different method - and rebuttals, using those methods, soon appear. They sketch out several such positive-negative cycles based on different methods and particular hypotheses.Now, there's two ways to look at this. You could explain this in terms of standard positive publication bias. Maybe lots of people looked into a possible link, the ones who found nothing didn't publish. Then someone, by chance, did find an association with depression, and they published it. Once that happens, the question became a hot topic so the unpublished negative studies were dusted off and submitted.But there's a more worrying possibility. What if the original positive studies were correct, and the subsequent negative studies were the product of an inverse publication bias in favor of contrarian negative results?The publication cycles in the literature about beta-blockers and depression seem to suggest thatthe very publication of positive studies, whether true or false, increases the incentive to publish negative results, whether true or false... [in the case in question] the first as well as a significant number of subsequent negative studies were published in high-impact journals (8 of 19 journals with 2009 impact factor greater than 4.0). Third, power analysis showed thatd in two cycles, the first negative studies were underpowered... If a true-positive study stimulated the publication of one or more false-negative studies, again an invalid picture of the true association would emerge. Publication of false-negative studies may thus give rise to publication bias, just like publication of false-positive studies. Research groups usually compete to get the first positive study published in a high-impact journal. It has been suggested that it could also be worthwhile to aim at getting the first study that challenges the former published.This is not an entirely new idea. It was described in the classic Why Most Published Research Findings Are False, but only in passing.To be honest it's impossible to know, in any particular case, whether inverse publication bias is at work. Depending upon whether you think beta blockers cause depression (and that's still controversial), your interpretation of the biases in the literature will probably differ.However, I think the basic idea is important. Publication bias isn't a bias in favor of positive results per se. It's a bias towards "interesting" results - which in most cases means positive ones, but could equally well include negative ones, in certain contexts. In some ways, this could be a good thing, if the negative and positive biases eventually cancelled out, leaving a neutral playing field; but there's no guarantee that would ever happen.As for how to fix publication bias - my opinions on that question are well known...Luijendijk, H., and Koolman, X. (2012). The incentive to publish negative studies: how beta-blockers and depression got stuck in the publication cycle Journal of Clinical Epidemiology DOI: 10.1016/j.jclinepi.2011.06.022... Read more »
Luijendijk, H., & Koolman, X. (2012) The incentive to publish negative studies: how beta-blockers and depression got stuck in the publication cycle. Journal of Clinical Epidemiology. DOI: 10.1016/j.jclinepi.2011.06.022
by Neuroskeptic in Neuroskeptic
Fighting "the stigma of mental illness" is big business at the moment. But does "the stigma" really exist?As I said back in 2010 :There is a stigma of schizophrenia, and there's a stigma of depression, etc. but they're not the same stigma. We're told it's a myth that "the mentally ill are violent" - [but] no-one thinks depressed or anorexic people are violent. They think (roughly) that people with psychosis are. They have other equally silly opinions about each diagnosis, but there's no monolithic "stigma of mental illness".Now a paper has come out which explores this idea in some detail: Stereotypes of mental disorders differ in competence and warmth. The title says it all : people have stereotypical views of people suffering from different mental disorders, but these stereotypes vary substantially.The authors use the "Stereotype Content Model" framework, which despite the fancy name is very simple. On this view stereotypes are characterised by two dimensions, "competence" and "warmth". These are pretty self-explanatory. Warmth is whether you're seen as nice and friendly, or hostile and dangerous. Competence is whether you're thought to be good at it.We all know that warmth and competence are distinct and indeed orthogonal concepts, and they crop up in other languages and in popular culture.Anyway, in two Mechanical Turk online surveys of American adults, they first showed that respondants felt that "people with mental illness" were generally low on both warmth and competence compared to other social and ethnic groups, a position also shared by the homeless, poor, and welfare recipients.However in the second study, they asked about specific diagnoses, and this revealed a more complex pattern. I've shown the results above (colors are mine). There seemed to be four clusters. Mental retardation and Alzheimer's were perceived as warm, but incompetent; sociopaths and violent criminals were the opposite.Schizophrenia clustered with homelessness and addiction in a worst-of-both-worlds category of low warmth and competence, while what could broadly be called "emotional" disorders, like bipolar, depression and anxiety, were rated more favorably. For what its worth, OCD was the least bad diagnosis.These are interesting results. The only oddity about the method was that people weren't actually asked what they thought about these people; they were asked “In general, how much do Americans believe that..." This is, apparantly, standard procedure in this kind of stereotype research, but it seems a little strange to me.Sadler, M., Meagor, E., and Kaye, K. (2012). Stereotypes of mental disorders differ in competence and warmth Social Science and Medicine DOI: 10.1016/j.socscimed.2011.12.019... Read more »
Sadler, M., Meagor, E., & Kaye, K. (2012) Stereotypes of mental disorders differ in competence and warmth. Social Science . DOI: 10.1016/j.socscimed.2011.12.019
by Neuroskeptic in Neuroskeptic
In my previous post, on the paper A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage by Michael B. Lewis, I wrongly stated that it was unclear from the paper whether the research assistant who selected the Facebook images was blind to the hypothesis of the study.In fact, the paper did state that they were "a naive research assistant", something I missed. Apologies for this avoidable mistake. I've corrected the post.I'd also like to take this opportunity to remind everyone that sometimes comments will get caught in the Blogger spam filter, especially if they're long or contain links, but it can happen to any comment. If your comment doesn't appear immediately, don't worry, I will manually approve such comments as soon as possible. Lewis, M. (2012). A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage PLoS ONE, 7 (2) DOI: 10.1371/journal.pone.0031703... Read more »
Lewis, M. (2012) A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage. PLoS ONE, 7(2). DOI: 10.1371/journal.pone.0031703
by Neuroskeptic in Neuroskeptic
There are some papers that you can tell are going to be hot potatoes just from the titles. This is one of them: A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage.Coming so soon after The Unconquered World, you'd be forgiven for thinking I am taking this blog in a more linkbaiting direction because I'm planning to introduce ads. I'm really not, it's just a coincidence.The paper claims that white women are on average more attractive than black, while East Asians are prettier still. For men, however, the positions were reversed (and the effects were even stronger.)Saying that black women are on average less attractive than others was what got evolutionary psychologist and blogger Satoshi Kanazawa into spot of bother last year. The current paper agrees with Kanazawa on that point (though doesn't cite him)... although it also declares Kanazawa to be part of the least attractive race for males, so I don't know how happy he'll be about it.Author Michael B. Lewis of Cardiff University took 600 Facebook photos "from people who were members of groups associated with further and higher education bodies either in the UK (for White faces), sub-Saharan Africa (for Black faces) and East Asia (for Asian faces)."Photos with a "weird expression" and people who "looked" under 18 or over 30 were excluded. The actual ages were not checked. Hmm.A panel of 40 British students (half male) were asked to rate all of the opposite-sex faces for attractiveness from 1 to 10. The ethnicity of the rater made no difference to the results but there were only 5 black and 6 Asian students out of 40 though:After this we get some models proposing how these data might relate to British and American inter-racial marriage patterns, and some evolutionary speculation regarding why this might have evolved - Asia was cold so men were in short supply, that kind of thing - but that's all assuming the basic data are solid.There are many possible objections to the methodology here, some of which are addressed in the paper, but there's one massive one that isn't -It's not stated how the Facebook images were gathered. All we're told is that "a research assistant" got the images from higher education institutions. Were they, consciously or subconsciously, picking photos that fitted the expected pattern?We're not told whether or not this individual was aware of the hypothesis of the study when they chose the pics. If they were aware, it's a fatal confound; even if not, they might have been selecting in line with their own preferences or some other bias. Clearly, there's much room for cherry picking the examples, based on whether they "looked" too young or old, or had a "weird" expression. Was anything done to guard against that?Link: Also blogged about here.Lewis, M. (2012). A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage PLoS ONE, 7 (2) DOI: 10.1371/journal.pone.0031703... Read more »
Lewis, M. (2012) A Facial Attractiveness Account of Gender Asymmetries in Interracial Marriage. PLoS ONE, 7(2). DOI: 10.1371/journal.pone.0031703
by Neuroskeptic in Neuroskeptic
An important new study shows how being awake causes progressive changes to the brain. This could shed light on the function of sleep - but it also raises warnings for neuroscientists.Italian researchers Huber et al report that Human Cortical Excitability Increases with Time Awake. The experiment was conceptually simple - they measured cortical excitability when people were well rested and then looked to see how it changed as they were kept awake for over 24 hours.The participants woke up at 7 am on Day 1 and were kept awake all of that day, all of the subsequent night, and all of Day 2. The excitability measurements spanned a period of 30 hours, from 9 am to 3 pm the next day. They were finally allowed to go to sleep on the next night and one final session took place on Day 3. I hope they got well paid for taking part.The results showed a nice linear increase in excitability with increasing time spent awake. Sleep put this back to normal - mostly:"Excitability" was measured using electroencephalography (EEG) combined with transcranial magnetic stimulation (TMS). Essentially, they zapped the brain (left frontal cortex) with a strong magnetic pulse, and measured the electrical activity that this provoked in the brain.It was a small study but the findings look solid, with all six participants showing clearly higher stimulation-evoked potentials after sleep deprivation. EEG cortical theta band activity was also correlated with time spent awake, replicating previous findings. The authors say that these data fit with the idea that the function of sleep is to prevent the brain from becoming too excitable. I previously described this as the "defragmentation" hypothesis of sleep.The theory goes that while we're awake, our brains are constantly forming new and stronger synaptic connections, as we learn and remember. Most of the new connections are excitatory. However this creates a problem because the brain must maintain a delicate balance between excitation and inhibition. Too much neural excitation and you'll have a seizure, amongst other things. So some researchers believe that during sleep, the brain "prunes" the new excitatory connections in such a way that the information they store is preserved, but the overall excitability is reset.These data are the first clear-cut human evidence in favor of the theory. Most of the previous work was in animals.So sleep researchers will be very interested by this paper, but all neuroscientists should take note. If being awake changes cortical excitability, it means that the time of day that you conduct your experiments could have an impact on your results. EEG researchers should pay particular notice, but it could well be that these changes also affect the fMRI signal.This could be a serious confounding factor in your data. Suppose, for example, that your healthy controls are more likely to have jobs than your patients with, say, autism or depression - which is sadly all too common. Now people with jobs would naturally prefer to attend your study later in the day, after work, leaving those with more flexible schedules to come in bright and early... you see the problem.Huber, R., Maki, H., Rosanova, M., Casarotto, S., Canali, P., Casali, A., Tononi, G., and Massimini, M. (2012). Human Cortical Excitability Increases with Time Awake Cerebral Cortex DOI: 10.1093/cercor/bhs014... Read more »
Huber, R., Maki, H., Rosanova, M., Casarotto, S., Canali, P., Casali, A., Tononi, G., & Massimini, M. (2012) Human Cortical Excitability Increases with Time Awake. Cerebral Cortex. DOI: 10.1093/cercor/bhs014
by Neuroskeptic in Neuroskeptic
The latest February 2012 issue of the British Journal of Psychiatry features a paper about the association between child abuse and later mental health problems. I haven't read it yet, but it looks pretty good.However, it also includes an editorial from John Read and Richard Bentall which argues that: Just 20 years ago, however, it would have been difficult to get the paper published. Mental health professions have been slow, even resistant, to recognise the role of childhood adversities in psychiatric disorder... Until very recently the hypothesis that abuse in childhood has a causal role in psychosis was regarded by many biologically oriented psychiatrists as heresy...Really? I checked the BJP from exactly 20 years ago. The February 1992 issue contained:A paper about child sexual abuse in female psychiatric patients.A letter praising a different article, on the same topic.A review of 11 studies on psychosocial family interventions as treatments for schizophrenia.A paper looking at the effect of the social environment on symptoms of schizophrenia.Four strikes and they're out. It's not true that this kind of thing wasn't being discussed 20 years ago.Such grandstanding is bad for science. Few would deny that psychiatry in recent years has undervalued psychosocial factors and overvalued genetics and neuroscience, but it's actually quite a complicated story, not a Punch and Judy show with bad guys on one side and good guys on the other.Rhetorical flourishes like this editorial certainly get attention but in the long run, down that road lies madness.Read, J., and Bentall, R. (2012). Negative childhood experiences and mental health: theoretical, clinical and primary prevention implications The British Journal of Psychiatry, 200 (2), 89-91 DOI: 10.1192/bjp.bp.111.096727... Read more »
Read, J., & Bentall, R. (2012) Negative childhood experiences and mental health: theoretical, clinical and primary prevention implications. The British Journal of Psychiatry, 200(2), 89-91. DOI: 10.1192/bjp.bp.111.096727
by Neuroskeptic in Neuroskeptic
So it seems as though the "connectome" is the latest big thing in neuroscience. This is the brain's wiring diagram, in terms of the connections between neurons and on a larger scale, between brain regions.We certainly won't understand the brain without getting to grips with the connections but equally, it's not the whole story. I previously emphasised that the brain is not made of soup; it's not made of spaghetti, either.Connectomics does however unquestionably provide some of the prettiest images in neuroscience. And they just got prettier, with a new technique for visualizing connections, just revealed in Neuroimage: Circular representation of human cortical networks for subject and population-level connectomic visualization.See above. It's a rather lovely vista (for which the authors Irimia et al share credit with the folks behind the Circos visualization tool they used).All you need are some MRI scans, and a lot of image processing, and you can produce one of these "Connectograms". But what does it mean? Here's the authors' description:The outermost ring shows the various brain regions arranged by lobe (fr — frontal; ins — insula; lim — limbic; tem — temporal; par — parietal; occ — occipital; nc — non-cortical; bs — brain stem; CeB — cerebellum) and further ordered anterior-to-posterior. The color map of each region is lobe-specific and maps to the color of each regional parcellation.In other words, the outer ring is just a list of brain regions, each with an assigned colour. The inner rings tell us about those regions: Proceeding inward towards the center of the circle, these measures are: total GM volume, total area of the surface associated with the GM–WM interface (at the base of the cortical ribbon), mean cortical thickness, mean curvature and connectivity per unit volume. For non-cortical regions, only average regional volume is shown.So each of the five inner rings displays data about one aspect of brain anatomy, for each of the regions. The colors are a heat map of the numbers.Finally, the lines between regions represent the degrees of connectivity between regions via white matter tracts, as measured with diffusion tensor imaging:The links represent the computed degrees of connectivity between segmented brain regions. Links shaded in blue represent DTI tractography pathways in the lower third of the distribution of FA, green lines the middle third, and red lines the top third (see text for details). You can also make a pooled connectogram of the average neuroanatomy across a group of people. Still, it remains to be seen whether these are as useful as they are beautiful.Irimia A, Chambers MC, Torgerson CM, and Van Horn JD (2012). Circular representation of human cortical networks for subject and population-level connectomic visualization. NeuroImage PMID: 22305988... Read more »
Irimia A, Chambers MC, Torgerson CM, & Van Horn JD. (2012) Circular representation of human cortical networks for subject and population-level connectomic visualization. NeuroImage. PMID: 22305988
by Neuroskeptic in Neuroskeptic
Imagine that there was a blood test that could detect depression. Wouldn't that be useful?It depends.Ridge Diagnostics are a US company who offer such a test. They've just published some results of the technology in Molecular Psychiatry. In two samples of patients with major depressive disorder (MDD), they report differences in the"MDDScore", between the patients and healthy controls.The MDDScore is an aggregate value, calculated from the levels of 9 metabolites in blood serum. They're all well-known molecules, including hormones, such as cortisol and prolactin. The novelty is in how they're put together to make the MDDScore. We're given equations - but the key variables are not provided, because they're proprietary:Long-term Neuroskeptic readers will recall that this "secret ingredients" approach to publishing science was also adopted by another company offering a different depression test.Anyway, the performance of the test was impressive. In both the pilot and the replication samples, the MDDScore was significantly higher in the depressed people than in the controls. In both cases, the test had a sensitivity of over 91% and a specificity of over 81%, which is pretty good. Ridge Diagnostics are already offering the MDDScore clinically. For $745 a pop.However...Although there were two depressed patient groups (n=36 and 34), there was only one set of controls (n=43); both patient samples were compared to it. This means the second, "replication", test was not fully independent of the first one. If the first finding was a fluke caused by the control group having weird results by chance, for instance, then the second study would just repeat the fluke.The patients were significantly older, and with a higher BMI, than the controls. They did control for these variables, which is good, but this raises the question of whether these folks differed in other ways, that they didn't measure, and hence couldn't control for.In both samples, the patients had a very significantly higher MDDScore than the controls (p less than 0.0001, both times). But in both cases, the difference in levels of EGF (epidermal growth factor) was almost as strong: p=0.0003 and p less than 0.0001, respectively. Other metabolites weren't far behind. Testing for EGF would almost certainly be cheaper than getting an MDDScore.Finally, all these data demonstrate is that the test can distinguish between people with MDD and entirely healthy people. But how often are doctors going to need to do that? More likely, they'll want to distinguish depression from other things that are often confused with it, such as: bipolar disorder, anxiety disorders, chronic fatigue syndrome, bereavement, "stress", and all manner of physical illnesses e.g. thyroid problems. Daniel Carlat said last year that If the test cannot distinguish different psychiatric problems, then the MDDScore is simply a non-specific "biomarker" for emotional difficulties of all stripes, and would be essentially useless. How disorder-specific is the MDDScore? This paper doesn't tell us. And to date, this is the only published paper mentioning the MDDScore. The website mentions some conference presentations, but none have yet appeared in a peer reviewed journal.Ridge Diagnostics have an interesting history. But that's another story - stay tuned for Part 2.Papakostas, G., Shelton, R., Kinrys, G., Henry, M., Bakow, B., Lipkin, S., Pi, B., Thurmond, L., and Bilello, J. (2011). Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a Pilot and Replication Study Molecular Psychiatry DOI: 10.1038/mp.2011.166... Read more »
Papakostas, G., Shelton, R., Kinrys, G., Henry, M., Bakow, B., Lipkin, S., Pi, B., Thurmond, L., & Bilello, J. (2011) Assessment of a multi-assay, serum-based biological diagnostic test for major depressive disorder: a Pilot and Replication Study. Molecular Psychiatry. DOI: 10.1038/mp.2011.166
by Neuroskeptic in Neuroskeptic
According to a new study, students with a family history of autism tend to major in math and science, while substance abuse and depression are more common in the ancestors of humanities fans.In an online survey, over 1,000 new Princeton undergrads were asked about their intended major and whether anyone in their family had been diagnosed with one of 16 neurological and psychiatric disorders. More details here.Of the 16 maladies, 5 were so rare that there wasn't enough data to analyze. Of the remaining 11, there were significant differences between the three types of students in four. The categories being humanities, social sciences, and "technical" i.e. science, engineering and maths. Social science majors were in the middle, except for autism.See the graph I made above.It's an interesting study. The autism result seems tenuous though because only 24 of 1077 students reported any autism in their immediate family. That's 3% of "technical" students and 1% of others, so not very many. The authors excluded schizophrenia and epilepsy from the analysis on the grounds of being too rare - and they had 18 each. Substance abuse and depression had over 150 each, so those differences are rather more solid.The authors note that this fits with various previous studies and they discuss their findings in Baron-Cohen-esque terms:It has been suggested that autism represents an extreme manifestation of a ‘‘systemizing’’ nature. Since ASDs have complex inheritance, shared genetic variation between close relatives might establish a continuous phenotype which in milder forms confers interest or benefits in understanding highly structured fields... Similarly, affective disorders may represent an extreme phenotype of emotional lability that, in milder forms, is commensurate with interest in the humanities.Hmm. OK, but does that really make sense? Sure, it fits with the popular image of the Geeky Scientist vs the Tortured Artist - but that's not science, that's stereotypes. Why would emotional lability make you favor the humanities, exactly?Imagine if the stereotype was the Geeky Artist vs the Tortured Scientist (and there really have been plenty of both, over the years). Couldn't we rationalize that equally well?"People with autistic traits are drawn to study the humanities because they wish to learn about humans and their emotions, something they find hard to do in day-to-day life... While emotionally volatile people like science and maths because they offer a calming sense of order and stability..."Campbell BC, and Wang SS (2012). Familial Linkage between Neuropsychiatric Disorders and Intellectual Interests. PloS one, 7 (1) PMID: 22291951... Read more »
Campbell BC, & Wang SS. (2012) Familial Linkage between Neuropsychiatric Disorders and Intellectual Interests. PloS one, 7(1). PMID: 22291951
by Neuroskeptic in Neuroskeptic
Two years ago, neuroscientists were shaken by the appearance of a draft paper showing that half of the published work in a particular field had fallen prey to a major statistical error.Originally called "Voodoo Correlations in Social Neuroscience", it ended up with the less snappy name of Puzzlingly high correlations in fMRI studies of emotion, personality, and social cognition. I prefer the old title.The error in question is now known variously as the "circular analysis problem", "non-independence problem" or "double-dipping" although I still call it the "voodoo problem". In a nutshell it arises whenever you take a large set of data, search for data points which are statistically significantly different from some baseline (null hypothesis), and then go on to perform further statistics only on those significant data points.The problem is that when you picked out the statistically significant observations, you selected the data points that were especially "good", so if you then do some more analyses only on those data, you are almost guaranteed to find something "good". To avoid this you need to make sure that your second analysis is truly independent of your first one.Anyway, Vul and Pashler, the main authors of the original voodoo article, have just written a short piece in NeuroImage offering some reflections on the paper and the aftermath. They don't make any major new arguments but it's a good read. Particularly fun is their explanation of what inspired them to look into the voodoo problem:In early 2005 a speaker in our department reported that BOLD activity in a small region of the brain can account for the great majority of the variance in speed with which subjects walk out of the experiment several hours later (this finding was never published as far as we know). The implications of this result struck us as puzzling, to say the least: Are walking speeds really so reliable that most of their variability can be predicted? Does a focal cortical region determine walking speeds? Are walking speeds largely predetermined hours in advance? These implications all struck us as far-fetched...But they reveal that it was one paper in particular that set them off voodoo-hunting Our interest in probing the matter was further whetted by an episode occurring a short while later: Grill-Spector et al. (2006) reported that individual voxels in face selective regions have a variety of stable stimulus preferences; in a critical commentary, Baker et al. (2007) found that the analysis used to ascertain this fact implicitly built these conclusions into the method, such that the same analysis applied to noise data (voxels from the nasal cavity) revealed a similar variety of stable preferences. It occurred to us that a similar circularity might underlie the puzzlingly high correlations.To their credit, Grill-Spector et al quickly accepted Baker et al's criticism and admitted that some of their original conclusions had been wrong.Vul, E., and Pashler, H. (2012). Voodoo and circularity errors NeuroImage DOI: 10.1016/j.neuroimage.2012.01.027... Read more »
Vul, E., & Pashler, H. (2012) Voodoo and circularity errors. NeuroImage. DOI: 10.1016/j.neuroimage.2012.01.027
by Neuroskeptic in Neuroskeptic
People who take their medication as directed are less likely to die - even when that "medication" is just a sugar pill.This is the surprising finding of a paper just published, Adherence to placebo and mortality in the Beta Blocker Evaluation of Survival Trial (BEST).BEST was a clinical trial of beta blockers, drugs used in certain kinds of heart disease. The patients were aged about 60 and they all suffered from heart failure. Everyone was randomly assigned to get a beta blocker or placebo, then followed up for 3 years to see how they did.Here's the big finding: in the placebo group of 1174 patients, the people who took all of their placebo pills on time (the good adherers), were significantly less likely to die than the patients who missed lots of doses. People who took over 75% as directed were 40% less likely to die than those with less than 75% adherence:That's pretty interesting. The pills were placebos - they can't have had any benefit. So what's going on? It gets even better. You might be tempted to write off these results as obvious: "Clearly, people who follow the study instructions are just 'healthy' people in other ways - maybe they take more exercise, eat better, etc. and that's what protects them."Certainly, that's what I'd have said.... Read more »
Pressman, A., Avins, A., Neuhaus, J., Ackerson, L., & Rudd, P. (2012) Adherence to placebo and mortality in the Beta Blocker Evaluation of Survival Trial (BEST). Contemporary Clinical Trials. DOI: 10.1016/j.cct.2011.12.003
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One of these two images contains a hidden picture of a face. Which one?This was the question faced by participants in a remarkable psychology experiment just published, Measuring Internal Representations from Behavioral and Brain Data. Five healthy volunteers were presented with a series of random black and white grid patterns. Each grid square was either black or white, and this was randomly determined on each trial.There was no pattern to the images, they were completely random. But the subjects were told that half of the patterns contained a hidden face, and that their job was to work out which ones did. Each subject saw over 10,000 random images and they took about 1 second to judge each one. The volunteers "detected" a face in 44% of the images. Somehow, all five of them convinced themselves that they were seeing faces in many of the grids. The authors say thatUpon completion of the experiment we debriefed observers, and all expressed shock that no face was ever presented.That's strange enough in itself, but here's the really clever bit. The authors compared the patterns which were declared to contain a face, to the ones that were reported as empty. The image below shows the average "face" grid, minus the average "non face" grid, for each individual subject: As you can see, this reveals...a face! Kind of. The top half shows the raw average; the bottom half shows the statistically significant differences from random noise.In Subjects 1 and 2, the face is pretty clear, with eyes, a nose and a mouth. For 3 and 4, it's less coherent, but you might be able to see it if you look hard enough. For Subject 5, not really. What this means is that people (at least, most of them) were not just seeing faces in any noise. They tended to see faces when the random patterns happened to resemble a kind of primitive face, but it was a different face for each person. The authors say that these strange faces correspond to the individual's internal representations, or models, of "a face", that each subject was "seeing" in the noise.Finally, the whole experiment was conducted while EEG data was being recorded from the participant's brains. The EEG results revealed that there was a clear difference in the neural activity associated with "face" compared to "nonface" stimuli - except in Subject 5, who you'll remember had the least coherent "internal face".What's exciting about this approach is that it investigates perception in a purely "top down" way. Normally, when we look at anything, what we end up perceiving is a product of "bottom up" influences - the raw data - and "top down" ones - what we expect to see. In this experiment, there was no real "bottom up" data; it was all "top down".This is a form of pareidolia - perceiving familiar things in random stimuli. Seeing the face of Jesus in your sock, that kind of thing. It works for sounds too: in the famous White Christmas Experiment, people report "hearing" music in pure white noise - when told to expect it. Real-life examples of this include the "Islam Is The Light" doll, and my personal favorite, the singing paedophile Christmas mouse.Finally, I wonder what embodied cognition theorists make of this paper. Because this paper claims to be "Measuring Internal Representations from Behavioral and Brain Data"; embodied cognition (at least the radical kind) is the theory that "internal representations" either don't exist, or at least don't explain anything about human cognition.Smith, M., Gosselin, F., and Schyns, P. (2012). Measuring Internal Representations from Behavioral and Brain Data Current Biology DOI: 10.1016/j.cub.2011.11.061... Read more »
Smith, M., Gosselin, F., & Schyns, P. (2012) Measuring Internal Representations from Behavioral and Brain Data. Current Biology. DOI: 10.1016/j.cub.2011.11.061
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Dodgy science is being smuggled into medical journals thanks to a loophole in the regulations, say Italian psychiatrists Barbui and Cipriani in an important article.They focus on agomelatine, a recently-approved antidepressant. But their point applies to all of medicine, not just psychiatry.Here's the problem. Nowadays, major medical journals have rules governing systematic reviews and meta-analyses of clinical trial data. If you want to review the evidence about how well a certain drug works, or its safety, you've got to do it properly. You have to consider all of the data, not just focus on the results that suit you. And so on.However, these rules don't apply to "narrative" review papers, which is a broad term meaning any kind of article meant to give a discussion of the pharmacology, history, chemistry etc. behind a particular drug. For a narrative review, there are no rules.In particular, you can write about the clinical trial data in such articles with no restrictions. Unlike in a proper systematic review, you can cherry-pick trials and so on to your heart's content. Some narrative reviews have so much clinical data in them that they end up being, in effect, a bad systematic review. One that would never have been deemed acceptable as a systematic review.Barbui and Cipriani argue that narrative reviews are often used in this way, namely to paint drugs in a positive light. In the case of agomelatine, they mention a number of recent narrative reviews which were supposedly about the drug's mechanism of action, but which actually contained extensive (but biased) reviews of the clinical trial data.It's not hard to see how pharmaceutical companies might take advantage of this process. However, the problem is surely not limited to agomelatine. It's a loophole that affects every branch of medicine:Most medical journals require adherence to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). It is an evidence-based minimum set of items for reporting in systematic reviews and meta-analyses. Adherence to PRISMA is not required in review articles dealing with basic science issues as these articles are not focused on clinical trials.In practice, however, the agomelatine case indicates that clinical data are regularly included and reviewed with no reference to the rigorous requirements of the PRISMA approach. These articles have this way became a modern Trojan horse for reintroducing the brave old world of narrative-based medicine into medical journals.How do we stop this? It's simple, the authors say: just make all references to clinical data subject to PRISMA, or other accepted regulations, whatever the supposed 'primary focus' of the paper:We argue that medical journals should urgently apply this higher standard of reporting, which is already available, easy to implement and inexpensive, to any form of clinical data presentation.Of course, there are plenty of good narrative reviews that really do cover the pharmacology or other science in a useful way. The problem is not narrative reviews as such, but the way they're used.Barbui, C., and Cipriani, A. (2012). Agomelatine and the brave old world of narrative-based medicine Evidence-Based Mental Health, 15 (1), 2-3 DOI: 10.1136/ebmh.2011.100485... Read more »
Barbui, C., & Cipriani, A. (2012) Agomelatine and the brave old world of narrative-based medicine. Evidence-Based Mental Health, 15(1), 2-3. DOI: 10.1136/ebmh.2011.100485
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