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May 7, 2012
10:07 AM
315 views

Child Bipolar Disorder Still Rare

by Neuroskeptic in Neuroskeptic

Bipolar disorder usually strikes between the ages of 15 and 25, and is extremely rare in preteens, according to a major study: Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patientsThe findings are old hat. It's long been known that manic-depression most often begins around the age of 20, give or take a few years. Onset in later life is less common while earlier onset is very unusual.The main graph could have been lifted from any psychiatry textbooks of the last century:The red bars are the data. Ignore the black line, that just shows an imaginary 'even' distribution over the lifespan.Why am I blogging about these remarkably unremarkable results? Because they undermines the theory, popular in certain quarters but highly controversial, that 'child bipolar' or 'pediatric bipolar' is a major health problem.The study confirmed that early-onset bipolar I does exist, but just 5% of the bipolar I patients had an onset before the age of 15. Assuming a lifetime prevalence of 1% for bipolar I disorder, which is about right, that makes about 0.05%, 1 in 2000 kids, about the same prevalence as Down's Syndrome. Even that's an overestimate, though, because this sample was enriched for early-onset cases: some of the participating clinics were child and adolescent only.There's a few caveats. This was a retrospective study, that took adults diagnosed bipolar, and asked when their symptoms first appeared. It's possible that early onset cases were under-sampled, if they were less likely to survive to adulthood, or get treated. The generally milder bipolar II might also be different from the bipolar I studied here. But in general, these numbers support the traditional view that childhood bipolar is just not very prevalent.Baldessarini, R., Tondo, L., Vázquez, G., Undurraga, J., Bolzani, L., Yildiz, A., Khalsa, H., Lai, M., Lepri, B., Lolich, M., Maffei, P., Salvatore, P., Faedda, G., Vieta, E., and; Tohen, M. (2012). Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patients World Psychiatry, 11 (1), 40-46 DOI: 10.1016/j.wpsyc.2012.01.006... Read more »

Baldessarini, R., Tondo, L., Vázquez, G., Undurraga, J., Bolzani, L., Yildiz, A., Khalsa, H., Lai, M., Lepri, B., Lolich, M.... (2012) Age at onset versus family history and clinical outcomes in 1,665 international bipolar-I disorder patients. World Psychiatry, 11(1), 40-46. DOI: 10.1016/j.wpsyc.2012.01.006

May 5, 2012
04:59 AM
326 views

More Depressed Than Average?

by Neuroskeptic in Neuroskeptic

Whether we think of ourselves as "depressed" or "anxious" depends on what we think about other people's emotional lives, rather than our own, according to an important paper just published: Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom SeverityThe work appears in the obscure Journal of Behavioural Decision Making, which is downright criminal. It deserves to be in the British Journal of Psychiatry ... and it's not often I think that about a paper.In the first experiment, the authors quizzed people how many days per month they felt “depressed, sad, blue, tearful” or had “excessive anxiety about a number of events or activities.” They then asked them a series of questions designed to work out how they thought other people would answer than question. So they could work out where each individual thought they ranked within the general population, in terms of depression or anxiety symptoms.Take a look. The top panel shows someone who felt depressed on 5 days a month, but believed this put him in the most depressed 70% of people. The second person felt depressed twice as often, but she thought she was below average. They found that perceived rank was strongly correlated with whether people thought they "had depression" or "had anxiety" - much more strongly than actual frequency of symptoms. "Having depression" meant "being more depressed than other people".That's just a correlation and doesn't prove causation, but in the second experiment, they randomly assigned people to get different versions of a survey which manipulated perceived rank, and they confirmed that rank was indeed associated with how "disabling" they felt a given level of symptoms would be.Now, this is just common sense, in a way. Of course whether you think of yourself as abnormal will depend on what you think of as normal - that's what "abnormal" means. We understand ourselves in the context of other people.But this common sense is maybe not so common nowadays; you can read a hundred papers about the chemistry, genetics or causes of "depression" without a consideration of what "depression" (i.e. "abnormal" as opposed to "normal" mood) is.The implications are big. Here's my main concern. Right now a lot of people think that promoting the idea that mental illness is very common is a good idea. Their stated goal is that by 'normalizing' mental illness, we'll destigmatize it. This will both help the mentally ill to cope, and encourage people to talk about their own mental health and get help.All very nice. I've accused such campaigns of being based on dodgy stats, but this paper suggests that such campaigns could end up having exactly the opposite effect from that intended - they could lead to under-diagnosis, and increased stigma.Suppose being depressed or anxious becomes seen as more 'normal'. According to these data, this will make people who are depressed or anxious less likely to seek help, for any given level of symptoms. Change people's perceptions of other people, and you'll change how they see themselves.Worse, normalizing distress could - paradoxically - make those who do seek help seem more abnormal. Think about it: if depression and anxiety are normal, surely only an abnormal person would need special help to deal with them. It's a small step from this to the idea that mental illness is mere personal weakness, laziness, attention-seeking, or scrounging. 'What's your problem? Everyone feels down or worried sometimes... most of us just deal with it.' If everyone is mentally ill, then no-one is really mentally ill... so the "mentally ill" must have something else wrong with them. Not very nice.I'm not sure if this has happened, or will ever happen, but it's something to think about.Melrose, K., Brown, G., and Wood, A. (2012). Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom Severity Journal of Behavioral Decision Making DOI: 10.1002/bdm.1754... Read more »

Melrose, K., Brown, G., & Wood, A. (2012) Am I Abnormal? Relative Rank and Social Norm Effects in Judgments of Anxiety and Depression Symptom Severity. Journal of Behavioral Decision Making. DOI: 10.1002/bdm.1754

May 2, 2012
01:32 PM
392 views

Spurious Positive Mapping of the Brain?

by Neuroskeptic in Neuroskeptic

Many fMRI studies could be giving false-positive results according to an important new paper from Anders Eklund and colleagues: Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets.The authors examined the SPM8 software package, probably the most popular tool for analyzing neuroimaging data.Their approach was beautifully simple. They wanted to check how often conventional analysis of fMRI would "find" a signal when there wasn't really anything happening. So they took data from nearly 1,500 people who were scanned when they were just resting, and saw what would happen if you looked for "task related" activations in those scans, even though there was in fact no task. It's a very clever use of the resting state data.Eklund et al ran the analysis many thousands of times, under various different conditions. This is the key finding:This shows the proportion of analyses which produced significant "activations" associated with various different "tasks". In theory, the false positive rate should be way down at the bottom at 5% in each case. That's the error rate they told SPM8 to provide. As you can see, it was often much higher. Oh dear.The error rate depended on two main things. Most important was the task design. Block designs were much worse than event-related designs (see the labels at the bottom: B1,2,3,4 are block, E1,2,3,4 are event.) The longer the blocks, the more errors. B4, the most error-ridden design of all, corresponds to 30 second blocks.That's bad news because that's a very common design.Secondly, the repeat time (TR) mattered, especially for block designs. The TR is how long it takes to scan the whole brain once. The longer the TR, the better, the data showed: 1 second TRs are really dodgy. Luckily, they are rarely used. 2 seconds is OK for most event-related designs, but block designs really suffer. 3 seconds is even better.Because most fMRI studies today use 2-3 second TRs, this is somewhat reassuring, but for block design B4 the error rate was still up to 30% even with TR=3. Oh dear, oh dear.So what went wrong? It's complicated, and you should read the paper, but in a nutshell the problem is that fMRI data analysis assumes that there are only two sources of data: the real brain activation signal, and white noise. The key assumption is that it's white noise, which essentially means that it is random at any moment in time: knowing about what the noise did in the past tells you nothing about what it will do in the future. "Random" noise that's actually correlated with itself over time is not white noise.Now noise in the brain is certainly not white, for various reasons, including the effects of breathing and heart rate (which of course are cyclical, not random.) All fMRI analysis packages try to correct for this - but Eklund et al have shown that SPM8's approach doesn't manage to do that, at least for many designs.What about rival fMRI software like FSL or BrainVoyager? We don't know. They use different approaches to noise modelling, which might mean they do better, but maybe not.And the really big question: does this mean we can't trust published SPM8 results? Does SPM stand for Spurious Positive Mapping? Well, that's also not clear. All of Eklund et al's analyses were based on single subject data. But most fMRI studies pool the results from more like 20 or 30 subjects. Averaging over many subjects might make the false positives cancel out, but we don't yet know if that would solve the problem or only lessen it.Eklund, A., Andersson, M., Josephson, C., Johannesson, M., and Knutsson, H. (2012). Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets NeuroImage DOI: 10.1016/j.neuroimage.2012.03.093... Read more »

Eklund, A., Andersson, M., Josephson, C., Johannesson, M., & Knutsson, H. (2012) Does parametric fMRI analysis with SPM yield valid results?—An empirical study of 1484 rest datasets. NeuroImage. DOI: 10.1016/j.neuroimage.2012.03.093

April 27, 2012
02:02 PM
287 views

Who Invented Autism?

by Neuroskeptic in Neuroskeptic

The concept of "autism" is widely believed to have been first proposed by Leo Kanner in his 1943 article, Autistic Disturbances Of Affective Contact.But did Kanner steal the idea? That's the question raised in a provocative paper by Nick Chown: ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald. The piece stems from a debate between Chown and Irish autism expert Michael Fitzgerald, who first made the accusation in a book chapter.On the evidence presented, I don't think there's good reason to believe that Kanner did "steal" autism, and Chown doesn't seem convinced either. But there's an interesting story here anyway.Fitzgerald says that in 1938, Hans Asperger - of Asperger's Syndrome fame - gave a series of lectures in Vienna. These were published in a Vienna journal called Wiener Klinischen Wochenzeitschrift as an article called "Das psychisch abnorme kind" ("The mentally abnormal child").In this article, Asperger put forward the concept of autism. The term was coined by Eugen Bleuler in 1911 in reference to symptoms seen in 'schizophrenia' (he came up with that word too), but that was nothing to do with children.In 1943, Kanner published his landmark paper, in which he did not mention Asperger. Asperger published his first major description of 'autistic psychopathy' in 1944. The big question, then, is - had Kanner read or heard of Asperger's ideas before 1943?Asperger was working in Austria while Kanner, although Austrian-born, was in the USA. WW2 would have made it impossible for them to have communicated directly - however, word of Asperger's ideas could have reached Kanner via one of the many European doctors who fled to America, over that period.There is however no direct evidence that this happened. Fitzgerald makes much of the fact that Kanner opened his 1943 paper by saying "Since 1938, there have come to our attention a number of children..." This could be a reference to Asperger's 1938 work - but Kanner said it referred to his first "diagnosis" of autism, Donald T.This leaves us with a fluke: two Austrian-born psychiatrists independently discovered the syndrome we now call childhood autism, decided to borrow Bleuler's term "autism" for it, made their first observations in 1938 and first published properly in 1943-1944.Personally, I think that while that is a remarkable coincidence, such things are not uncommon in science. I see no reason to think that Kanner plagiarized Asperger, although it remains possible. If someone were to discover a copy of Asperger's 1938 article tucked away in one of Kanner's old notebooks, then I'd change my mind, but not before...Chown, N. (2012). ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald Journal of Autism and Developmental Disorders DOI: 10.1007/s10803-012-1529-5... Read more »

Chown, N. (2012) ‘History and First Descriptions’ of Autism: A response to Michael Fitzgerald. Journal of Autism and Developmental Disorders. DOI: 10.1007/s10803-012-1529-5

April 24, 2012
02:03 PM
283 views

Bias in Studies of Antidepressants In Autism

by Neuroskeptic in Neuroskeptic

There's little evidence that antidepressants are useful in reducing repetitive behaviors in autism - but there is evidence of bias in the published literature. That's according to Carrasco, Volkmar and Bloch in an important report just out in Pediatrics: Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication BiasThey looked at all of the published trials examining whether antidepressant drugs (mostly SSRIs, like Prozac) were better than placebo in reducing repetetive behaviours in children or adults with an autism spectrum disorder (ASD).A meta-analysis showed that there was a statistically significant benefit of the drugs overall, but it was marginal, with a small effect size d=0.22, and it was driven mainly by two old, very small studies that found big benefits. One of them only had 12 subjects. By far the largest study, King et al (2009) with 149 people, showed zero effect.This plot shows all of the studies, with the red line being no benefit of drug vs placebo. The further to the right of the line, the bigger the benefit, but the grey horizontal lines show the uncertainty. As you can see, two small, messy studies found big effects, the others didn't.Worse yet, although there were 5 published studies, the authors also found that there had been 5 studies that had been completed, but never published. Carrasco, Volkmar and Bloch wrote to the people in charge of those studies and asked for data; only one out of 5 replied. The data showed no benefit.We don't know what the other 4 unpublished studies found, but the way science works means they probably came out negative. If we assume that they did, then even the small benefit seen in the published studies disappears.This paper, incidentally, is great example of why trial registration is a great thing. Without mandatory pre-registration on clinicaltrials.gov, no-one would know about the 6 unpublished trials at all. It would have been even better if the researchers had been forced to make public the results, as well as the existence, of the unpublished trials; but it's a lot better than nothing.Finally, the authors of this paper stress that this doesn't mean antidepressants don't help at all in autism - just that they probably don't help with repetitive behaviors.Carrasco, M., Volkmar, F., and Bloch, M. (2012). Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication Bias Pediatrics, 129 (5) DOI: 10.1542/peds.2011-3285... Read more »

Carrasco, M., Volkmar, F., & Bloch, M. (2012) Pharmacologic Treatment of Repetitive Behaviors in Autism Spectrum Disorders: Evidence of Publication Bias. Pediatrics, 129(5). DOI: 10.1542/peds.2011-3285

April 23, 2012
02:03 PM
274 views

Are Psychologists All Mad?

by Neuroskeptic in Neuroskeptic

A fun little study from 2008 looked at rates of self-reported mental illness in mental health professionals: Psychologists' And Social Workers' Self-Descriptions Using DSM-IV PsychopathologyThe authors did an anonymous survey of clinical psychologists and social workers in Israel. They found thatThe sample of 128 professionals included 63 psychologists and 65 social workers. The presence of Axis I traits (i.e. mental illness) was reported by 81.2%, the three most frequent traits being mood, obsessive-compulsive disorder, and eating disorder. Axis II traits (personality disorders) were reported by 73.4% of subjects, the three most frequent conditions being narcissistic, avoidant, and obsessive-compulsive personality traits.Take a look:There were few differences between the two professions although for what it's worth, social workers were more likely to report psychosis and substance abuse problems, while clinical psychologists were more narcisstic, with a full 40% of them admitting to having narcisstic traits. On that note the authors (perhaps unwisely) comment:While speculative, it may be suggested that narcissistic traits include some important factors in motivating individuals to choose to enter the mental health care profession. In a psychotherapeutic relationship, the ability to influence and understand another person's psyche may include features of "narcissistic gratification".Ouch!The problem with all this, though, is that it's not clear what reporting "DSM-IV psychopathology" means; people rated their symptoms on a 5 point scale where 1 = "no evidence of the disorder" and 5 is "greatest severity". Most of the reported symptoms were low in severity, but we don't know what "low" is relative to.If you said that your narcissism was rated "2" out of 5, you might just mean that you have some narcissistic traits sometimes. That's how I'd interpret the question, anyway.But in that case, what exactly are you saying? Not much. You're not saying you're very narcissistic. You're not saying you're more narcissistic than average: you might well think that most other people would also score a "2", or even higher. You're not actually saying "I am narcissistic" at all, just admitting that you're not wholly un-narcissistic... and who of us can really say that?The same goes for all the questions. I think this study would have been much more interesting if they'd just asked people whether, in their clinical judgement, they meet criteria for the disorder. Or whether, if they had to assess a patient who was just like them, what would they diagnose them with? Because criteria are what professionals use on their patients, not 5 point scales.Nachshoni, T., Abramovitch, Y., Lerner, V., Assael-Amir, M., Kotler, M., and Strous, R. (2008). Psychologists' And Social Workers' Self-Descriptions Using DSM-IV Psychopathology Psychological Reports, 103 (1), 173-188 DOI: 10.2466/pr0.103.1.173-188... Read more »

Nachshoni, T., Abramovitch, Y., Lerner, V., Assael-Amir, M., Kotler, M., & Strous, R. (2008) Psychologists' And Social Workers' Self-Descriptions Using Dsm-Iv Psychopathology . Psychological Reports, 103(1), 173-188. DOI: 10.2466/pr0.103.1.173-188

April 19, 2012
01:43 PM
268 views

Facial Expressions of Emotion Still Culturally Universal

by Neuroskeptic in Neuroskeptic

Do people from different cultures express emotions differently?A new paper says yes: Facial expressions of emotion are not culturally universal. But as far as I can see the data show that at least some of them very much are universal.First some background. The authors, Rachael Jack and colleagues of Glasgow, have published before on this theme. Back in 2009 I blogged about one of their previous papers, which showed that East Asians were less accurate than Westerners at categorizing certain emotions.But although there were cultural differences in ability to classify some emotions, East Asians still did much better than just guessing. To me, this said that there are fundamental universal emotional expressions, albeit culture can subtly modify them.That's my verdict on this study as well.The authors adopted a new (and very clever) method this time. Rather than just showing people photos of actors posing expressions, and asking subjects to label them with an emotion, they generated virtual faces using a 3D modelling software, and made the faces display "expressions", with their 41 virtual facial muscle groups.Subjects (either white Westerners, or recent East Asian immigrants) saw 4,800 random assortments and had to label each one; the authors could therefore work back to calculate their "mental model" of that emotion based on the set of facial movements that best fit, individually (it reminds me of this method).What happened? The Westerners mental models clustered into the classic 6 "basic emotions" of happy, sad, disgust, fear, anger, and surprise. The Asians however didn't; although they were pretty much the same on happy and sad, they were less clear about the other 4.But how much less? Take a look:Cluster analysis and dissimilarity matrices of the Caucasian and Asian models of facial expressions. In each panel, vertical color coded bars show the k means (k = 6) cluster membership of each model. Each 41-dimensional model (n = 180 per culture) corresponds to the emotion category labelled above (30 models per emotion). The underlying grayscale dissimilarity matrices represent the Euclidean distances between each pair of models, used as inputs to k-means clustering. Note that, in the Caucasian group, the lighter squares along the diagonal indicate higher model similarity within each of the six emotion categories compared with the East Asian models. Correspondingly, k-means cluster analysis shows that the Western Caucasian models form six emotionally homogenous clusters... In contrast, the Asian models show considerable model dissimilarity within each emotion category and overlap between categories.This shows that yes, Asians "confused" some emotions more than Westerners but the basic emotional distinctions seemed to be intact, with Happy and Sad especially solid.And look at these examples of the "mental model" for one subject of each group: yes they're different, but not very.These are fine results, and I think there are real questions over whether the Ekman 6 emotions model really captures the essence of human emotions (especially negative ones.)But, especially in the context of previous work from the same authors, I don't think these data really justify the paper's title ("Facial expressions of emotion are not culturally universal"), or the statement thatOur data directly show that across cultures, emotions are expressed using culture-specific facial signals. Although some basic facial expressions such as fear and disgust originally served as an adaptive function... facial expression signals have since evolved and diversified to serve the primary role of emotion communication during social interaction. As a result, these once biologically hardwired and universal signals have been molded by the diverse social ideologies and practices of the cultural groups who use them for social communication.Overall, (ahem) I'm happy to admit that these data show some surprising cultural differences, but I'm afraid that the authors' overblown rhetoric makes me disgusted, sad and angry.Jack, R., Garrod, O., Yu, H., Caldara, R., & Schyns, P. (2012). Facial expressions of emotion are not culturally universal Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1200155109... Read more »

Jack, R., Garrod, O., Yu, H., Caldara, R., & Schyns, P. (2012) Facial expressions of emotion are not culturally universal. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1200155109

April 18, 2012
06:16 PM
286 views

Preventing Psychosis?

by Neuroskeptic in Neuroskeptic

Can we prevent psychosis? In a major study just published, Early detection and intervention evaluation for people at risk of psychosis, 288 young British adults who were deemed to be 'at risk of psychosis' were randomized to get cognitive therapy (CT) or a control condition. The hope was that it could prevent transition to serious psychotic illness.The primary outcome measure was how many of them later went on to get diagnosed with full-blown psychosis. 2 years later, 7% of the CT group and 9% of the controls had, so that's no significant benefit of treatment. CT slightly reduced the level of mild psychotic-like symptoms, but not how much distress they caused.So, in other words, no we can't prevent psychosis, not with CT alone at any rate. But there's lots more interesting stuff here... Now a transition rate of some 8% over 2 years is lower than in previous studies and might suggest that the concept of the 'psychosis risk syndrome' or 'at-risk mental state' (under consideration for inclusion in DSM-5) is a bit dodgy. The venerable Prof. Allen Frances thinks so. But he misses the fact that the rate was 18% when you also count the people who went psychotic during the baseline assessments (to be fair to Frances, the authors buried that bombshell quite deep in the Discussion).Still, that's still 82% false positives. Is that too high?We can't tell, from a study like this. As in any disease screening program, we need to know the relative costs and benefits of true and false 'hits', as well as the percentages of them.Here's some food for thought on that note. One of the key tenets of the CT model of psychosis is that 'psychotic' symptoms are a more or less normal response to stress, and that psychosis is maintained by a cycle of thoughts and feelings in which these experiences are themselves a source of concern, because they're felt to be abnormal, pathological, or otherwise threatening, thus leading to more stress, and more symptoms, and hence more concern... and so on. CT aims to break that cycle.Check it out (image from here, coauthored by Graham Dunn, senior author of the present work.)If you accept that, then it seems that literally the worst possible thing you could say to someone in the 'at risk mental state' is "Watch out! You're at risk of going psychotic!" According to CT, exactly that line of thinking is the root of the whole problem.The authors of this paper indeed write that "Key ingredients of the approach [include] a focus on normalising psychotic-like experience". But who deemed them abnormal in the first place? The patient, all by themselves... or some well-meaning professional? It's not clear.We are told that the patients were "seeking help for symptoms", but why? Of their own accord, or after someone else raised concerns? 45 people were referred to the study but excluded because they said that they didn't want help. So there was at least some degree of professional 'railroading', driven by the idea that people with such symptoms ought to seek help If you accept the CT account of psychosis, then I'd say you ought to think very seriously about whether this whole thing isn't equivalent to giving everyone an X-ray to detect cancers. The X-rays might end up causing more tumours than they find.I wonder if the authors of this study considered this.Anyway. Keith Laws of LawsNeuroBlog has a good post about the study and the rather overexcited way it's been received in the press (even, er, the BMJ...)Despite the authors not being able to make any claims about CT positively affecting transition rates... and the lack of any medication analysis (in fact all patients were unmedicated as an entry requirement) they conclude: "On the basis of low transition rates, high responsiveness to simple interventions such as monitoring, a specific effect of cognitive therapy on the severity of psychotic symptoms, and the toxicity associated with antipsychotic drugs, we would suggest that antipsychotics are not delivered as a first line treatment to people meeting the criteria for being in an at risk mental state" So the article in the UK Guardian entitled Drugs not best option for people at risk of psychosis, study warns is not simply misunderstanding by a journalist, but what looks like author spinning.... The BMJ press release itself is headlined Cognitive therapy helps reduce severity of distress among psychotic patients - even though the paper (and the press release itself!) clearly states: "Cognitive therapy did not significantly affect distress related to these psychotic experiences...nor levels of depression, social anxiety, or satisfaction with life..."Morrison, A., French, P., Stewart, S., Birchwood, M., Fowler, D., Gumley, A., Jones, P., Bentall, R., Lewis, S., Murray, G., Patterson, P., Brunet, K., Conroy, J., Parker, S., Reilly, T., Byrne, R., Davies, L., and Dunn, G. (2012). Early detection and inte... Read more »

Morrison, A., French, P., Stewart, S., Birchwood, M., Fowler, D., Gumley, A., Jones, P., Bentall, R., Lewis, S., Murray, G.... (2012) Early detection and intervention evaluation for people at risk of psychosis: multisite randomised controlled trial. BMJ, 344(apr05 1). DOI: 10.1136/bmj.e2233

April 15, 2012
05:33 AM
357 views

How A Stroke Changed Katherine Sherwood's Art

by Neuroskeptic in Neuroskeptic

In 1997, American artist Katherine Sherwood was 44 when she suffered a major stroke. She writes about her experience and how it changed her work in a fascinating article just out, How a Cerebral Hemorrhage Altered My ArtAll of the images below are examples of her work, taken from the paper.Sherwood writes that she had long been interested in the brain. She incorporated neuroscience themes into her work even before the stroke. Here's a 1990 piece: Then, out of the blue, her life was changed:The next May I experienced a cerebral hemorrhage affecting the parietal lobe of the dominant hemisphere [i.e. the left side of the brain, which controls the right side of the body]. I lost my ability to walk, talk, read, and think as my right side became paralyzed within the course of 2 min. It happened during a graduate student’s critique... I do not recall saying this but one of my colleagues reported that the last thing I said was “Oh no, not again.” I was referring to the death of my father at age 33 from an aneurysm. This was when my life caught up to my art...Six months later after my brain had absorbed my spilled blood I had a cerebral angiogram. Relieved that it was over and the possible second stroke had not occurred, I sat up on the gurney and looked at the computer screen in the corner of the room. The images of the arterial system of my brain both stunned and reminded me of the Southern Song Dynasty Chinese landscape paintings that I had deeply admired. I immediately said without thinking, “I need those images.” The room broke out in laughter which I still do not understand. I repeated, “No, I am an artist and I really need those images.”Sherwood never regained the use of her right hand. She had previously relied on her right hand to pain with, and she was forced to learn to use her left, and this led to changes in her style.To compensate for the loss of fine dexterity from using her off hand, she started to paint on larger canvasses, using different materials and a "freer" approach.As a neuroscientist, the main question at the back of my mind reading this was, did damage to her left parietal lobe have a "direct" effect on her mind and personality which altered her artistic process, beyond making her use her left hand etc? Sherwood writes that she's just not sure: [some writers] proposed that my new success came from changes in my brain, particularly in the disruption of “the interpreter.” My artist friends vehemently disagreed with this assessment, preferring to believe it had something to do with the 20-years of painting I had done before my cerebral hemorrhage and my ample time to paint while I was recovering. I leave it up to mystery, a category that drives my doctors crazy. Link: On a slightly different note see the Neurocritic's Suffering For Art Is Still Suffering Sherwood, K. (2012). How a Cerebral Hemorrhage Altered My Art Frontiers in Human Neuroscience, 6 DOI: 10.3389/fnhum.2012.00055... Read more »

Sherwood, K. (2012) How a Cerebral Hemorrhage Altered My Art. Frontiers in Human Neuroscience. DOI: 10.3389/fnhum.2012.00055

April 11, 2012
02:39 PM
344 views

Psychology vs Astrology

by Neuroskeptic in Neuroskeptic

Are personality tests any more accurate than astrology?A lovely study I just came across examined this question: Science Versus the Stars. The researchers took 52 college students and got them to complete a standard NEO personality questionnaire. They also had to state the date, time and place of their birth.Three weeks later, the participants were then given two personality summaries - one based on the personality tests, and one on their astrological chart generated with a computer program.The trick was that everyone also got a pair of bogus summaries, one of each kind. These were simply someone else's results, picked at random from the other 51 volunteers. They weren't told which were the fakes and which were real - they had to work it out, based on which one matched them best.The results showed that the subjects were no better than guessing when trying to tell which of the two astrology charts was theirs. They were able to pick their own personality scores better than chance, although only 80% of them got it right, and guesswork gets you to 50% - so this is not all that impressive. Psychology beat astrology, but hardly by a landslide.This study is a modern update of Shawn Carlson's classic 1985 Nature paper, A double-blind test of astrology. In Carlson's experiment, though, people weren't even able to accurately pick out their own personality scores.When asked to say which of the four reports was the best match overall match to their personality, 55% of the participants picked their own real personality one - but no fewer than 35% preferred one of the astrology charts, and 10% went for someone else's personality scores. Hmm.The authors say the present results represent less of an endorsement of psychological measures than a further indictment of astrology. but I think it's interesting that even under very favorable conditions (only one fake personality test), people were well short of perfect accuracy at spotting their own psychological scores - which they had themselves produced by filling out a questionnaire, just weeks before. Whether that tells us more about the NEO test, the participants' memory, or the fact that all the students at Conneticut College are pretty much the same, I'll leave it for you to judge...Wyman, A., and Vyse, S. (2008). Science Versus the Stars: A Double-Blind Test of the Validity of the NEO Five-Factor Inventory and Computer-Generated Astrological Natal Charts The Journal of General Psychology, 135 (3), 287-300 DOI: 10.3200/GENP.135.3.287-300... Read more »

Wyman, A., & Vyse, S. (2008) Science Versus the Stars: A Double-Blind Test of the Validity of the NEO Five-Factor Inventory and Computer-Generated Astrological Natal Charts. The Journal of General Psychology, 135(3), 287-300. DOI: 10.3200/GENP.135.3.287-300

April 11, 2012
02:11 AM
298 views

Homosexuals Are Smart?

by Neuroskeptic in Neuroskeptic

Evolutionary psychologist Satoshi Kanazawa has never been far from controversy. When he's not having his blog cancelled for saying black women are unattractive, he's arguing that some nations just aren't smart enough to be monogamous.Given which, his latest work, saying that gay people are smarter on average, is probably his most politically correct paper in years, strange as that may sound.In three large population surveys (USA's AddHealth and GSS, UK's NCDS), Kanazawa found a small positive correlation between estimated IQ and self-reported homosexual behaviour or identity. Now I'm not sure what to make of this. He controlled for confounds such as race, religion and political orientation (and those correlations are interesting in themselves), but you can never measure and correct for everything in a study like this.Kanazawa interprets all this in terms of the Savanna hypothesis, essentially the idea that intelligence allows us to transcend our evolutionary programming (according to which we ought to all be straight, amongst many other things) -The Savanna-IQ Interaction Hypothesis (Kanazawa, 2010a), implies that the human brain’s difﬁculty with evolutionarily novel stimuli may interact with general intelligence, such that more intelligent individuals have less difﬁculty with [evolutionarily novel] stimuli than less intelligent individuals...Evolutionarily novel entities that more intelligent individuals are better able to comprehend and deal with may include ideas and lifestyles that form the basis of their preferences and values; it would be difﬁcult for individuals to prefer or value something that they cannot truly comprehend...However, it could be that in America and the UK today, smarter people tend to end up in the kind of social circles where being gay is (for whatever reason) more acceptable.The main problem with this is that the effects are very small. For example, in the AddHealth study, IQ in childhood was correlated with later adult sexual identity with a coefficent of 0.013... but the association of homosexuality with political attitude (liberalism) of 0.613, 60 times as high.The Savanna hypothesis is all very well, but does it predict such small effects? Isn't there a point where very weak evidence in favor of a theory actually becomes evidence against it...? Kanazawa, S. (2012). Intelligence and Homosexuality Journal of Biosocial Science, 1-29 DOI: 10.1017/S0021932011000769... Read more »

KANAZAWA, S. (2012) INTELLIGENCE AND HOMOSEXUALITY. Journal of Biosocial Science, 1-29. DOI: 10.1017/S0021932011000769

April 8, 2012
04:49 AM
276 views

Bigender - Boy Today, Girl Tomorrow?

by Neuroskeptic in Neuroskeptic

An interesting report in (believe it or not) Medical Hypotheses - Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex. Bigender individuals report alternating between male, female, and (sometimes) mixed gender states. Case and Ramachandran - that's V.S. Ramachandran of phantom limb fame - write:Under the transgender umbrella, a distinct subset of "Bigender" individuals report blending or alternating gender states. It came to our attention that many (perhaps most) bigender individuals experience involuntary alternation between male and female states, or between male, female, and additional androgynous or othergendered identities ("Multigender")...But almost no-one's studied the bigender phenomenon - A survey of the transgender community by the San FranciscoDepartment of Public Health found that about 3% of genetic malesand 8% of genetically female transgendered individuals identifiedas bigender. To our knowledge, however, no scientific literature has attempted to explain or even describe bigenderism; a search ofPsychInfo and PubMed databases returned zero results... the study of this condition could proveilluminating to scientific understanding of gender, body representation,and the nature of self.No scholarly paper would be complete without some elaborate new jargon, of course -For the purposes of our research we are calling this condition "alternating gender incongruity" (AGI). We seek to establish AGI as a nosological entity based in an understanding of dynamic brain representations of gender and sex.So they designed a survey (details in the paper) and sent it to members of a bigender internet forum. The forum had 600 members, although many were lurkers; they got a total of 39 replies. So it's a highly self-selected sample, then, but that's inevitable I think. Here's what they had to say -Of the 32 alternating bigender respondents included [some were excluded for diagnoses of DID etc], 11 were anatomically female (identified as female at birth)... One respondent identified as intersex, but only for reasons of androgynous facial appearance...10/32 respondents agreed that their gender switches were "predictable." The period of gender switches was highly variable, ranging from multiple times per day to several times per year. A majority (23/32) of respondents, however, reported that their gender switched at least weekly [with 14 saying it switched at least once per day]. What are the switches like? Some respondents are quoted -"I still have the same values and beliefs, but a change in gender is really a change in the filter through which I interact with the world and through which it interacts with me.""My voice usually ends up being higher than other times, I’ll be more emotional, my views on things like politics tend not to change, but how I react to certain things does. Like if I’m in male mode and I see someone crying I’ll think more along the lines of, 'Man up...' while if I’m in girl mode I’ll think more along the lines of ‘Oh sweety!’"This being Ramachandran, the paper also touches on left handedness, brain hemispheres, phantom genitals and more, but it's fair to say that all this is pretty speculative -In myth, art, and tradition throughout the world the left side of the body (and hand) – and therefore the right hemisphere – is regarded as more "feminine" – intuitive and artistic. One wonders therefore whether gender alternation may reflect alternation of control of the two hemispheres. Such alternation is seen to a limited extent even in normal individuals but may be exaggerated (and more directly involve the gender aspect) in AGI...Personally, what I find most interesting about this is the question of what would have happened to 'bigender' people before the term 'bigender' came along; it seems to be newer, and certainly less widely used, than 'transgender'/'transsexual'.Would they have been identified as transgender? Maybe... but maybe not. Would they have had any label at all?Case, L., and Ramachandran, V. (2012). Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex Medical Hypotheses, 78 (5), 626-631 DOI: 10.1016/j.mehy.2012.01.041... Read more »

Case, L., & Ramachandran, V. (2012) Alternating gender incongruity: A new neuropsychiatric syndrome providing insight into the dynamic plasticity of brain-sex. Medical Hypotheses, 78(5), 626-631. DOI: 10.1016/j.mehy.2012.01.041

April 6, 2012
05:15 AM
281 views

Neurostimulation - The Genius Machine?

by Neuroskeptic in Neuroskeptic

Do you wish you were smarter? Are you often baffled by puzzles?According to Australian neuroscientists Chi and Snyder, all you need is a bit of electric assistance: Brain stimulation enables the solution of an inherently difficult problem.In their study, 22 volunteers were faced with the 9 dots problem, a notoriously difficult puzzle. The goal here is to draw exactly four straight lines connecting all nine of these dots, without retracing any line, or lifting your pen from the page.Can you do it? If not, don't worry; not many people can. None of Chi and Snyder's 22 subjects did it in the 3 minutes before the stimulation was turned on.But 5 of the 11 volunteers later managed to do it, after 5 minutes of transcranial direct current stimulation (tDCS), a simple form of neurostimulation in which a weak electric current is passed through the head via electrodes attached to either side. The "L− R+" current was designed to boost the right temporal lobe while inhibiting the left, on the hypothesis that the right side of the brain helps us "think outside the box" (literally.)None of the 11 volunteers in the placebo control group succeeded. They were given tDCS but after 30 seconds, it was gradually turned off; this is intended to produce the same tingling sensations as real tDCS, but without affecting the brain. That's statistically significant (p=0.018, one tail ﬁsher’s exact test), although the numbers are small.The authors also refer to other unpublished data:We would like to emphasize the robustness of our finding. The finding that tDCS enabled more than 40% of participants to solve the ‘unsolvable’ nine-dot problem is consistent with our pilot study (see Section 2), which shows that whereas no one solved the nine-dot problem in the sham stimulation condition, 3 out of 7 participants in the L−R+ stimulation condition did so after stimulation. It is also strongly supported by subsequent studies where we, for curiosity, included the nine-dot problem at the end of an unrelated experiment. In fact, of all the data we have ever collected by 2 different experimenters over eight months, we found that 0 out of 29 participants in the sham stimulation condition solved the nine-dots problem, whereas 14 out of 33 participants (naïve to the problem) in the L−R+ stimulation condition did so. The probability that by chance 14 out of 33 participants solved the problem is less than 1 in a billion, according to analysis using binominal distribution (assuming that the expected solution rate without stimulation is 5%).Hmm. When these guys published similar tDCS results with a different puzzle last year, not everyone was convinced. Critics said that 'Thinking caps' are pseudoscience masquerading as neuroscience:Chi and Snyder's participants solved maths puzzles that the researchers claim required "insight", yet crucially the subjects did not perform any other tasks to show that only puzzles requiring "insight" were influenced by the brain stimulation... Rather than encouraging novel thinking, maybe brain stimulation made participants less cautious in reaching a decision, or maybe it helped them recall a similar problem seen a few minutes earlier, or maybe it made them temporarily less distractable (or even dulled their hearing), or maybe it boosted general alertness.The point is that without appropriate experimental controls, the results are virtually meaningless...Personally I don't think this is all that concerning because the 9 dots problem is really hard and I find it implausible that general alertness would help much; in this study, Chi and Snyder did give people a mental arithmetic task as well to try to control for such non-specific effects. Everyone did it three times - before,... Read more »

Chi, R., & Snyder, A. (2012) Brain stimulation enables the solution of an inherently difficult problem. Neuroscience Letters. DOI: 10.1016/j.neulet.2012.03.012

April 4, 2012
06:03 PM
315 views

Co-Vary Or Die

by Neuroskeptic in Neuroskeptic

I've just come across a striking example of why correcting for confounding variables in statistics might not sound exciting, but can be a matter of life and death.Imagine you're a doctor or researcher working with HIV/AIDS. You're taking a sample of blood from a HIV+ patient when you slip and, to your horror, jab yourself with a bloodied needle.What do you do?In a 1997 study, researchers Cardo et al studied hundreds of cases of this kind of accidental HIV exposure ("needlestick injuries") in medical and scientific workers. They wanted to find differences between the people who contracted the virus, and the ones who didn't.One factor they considered was post-exposure prophylaxis - taking HIV drugs as soon as possible after a suspected exposure. Now these drugs were still pretty new in 1997, and it wasn't clear how well they prevented infection, as opposed to just delaying symptoms. Many people with needlestick injuries were offered a course of drugs - but did they work?Cardo et al's raw data found no significant benefitBy univariate analysis, there was no significant difference between case patients and controls in the use of zidovudine [AZT, the first HIV drug] after exposure.But it turned out that this was due to confounding variables. When they corrected for other factors...Infected case patients were significantly less likely to have taken zidovudine than uninfected controls (odds ratio 0.19, P=0.003). This is a classic example of confounding, since the adjusted odds ratio differed from the crude odds ratio (0.7) because zidovudine use was more likely among both case patients and controls after exposure characterized by one or more of the four risk factors in the model.So while people who took zidovudine were just as likely to catch HIV than ones who didn't, they were also more severely exposed to the virus i.e. by being exposed to a greater quantity of blood, or a deeper wound. People were more likely to decide to take it after severe exposures. Zidovudine actually dramatically reduced the risk.Post-exposure prophylaxis has since become standard procedure and it has undoubtedly saved many lives since. Without statistical correction, it might have taken longer for people to see the benefits.In summary, I guess what I'm saying is, remember to correct for confounds - or die.Cardo DM, Culver DH, Ciesielski CA, Srivastava PU, Marcus R, Abiteboul D, Heptonstall J, Ippolito G, Lot F, McKibben PS, and Bell DM (1997). A case-control study of HIV seroconversion in health care workers after percutaneous exposure. Centers for Disease Control and Prevention Needlestick Surveillance Group. The New England journal of medicine, 337 (21), 1485-90 PMID: 9366579... Read more »

Cardo DM, Culver DH, Ciesielski CA, Srivastava PU, Marcus R, Abiteboul D, Heptonstall J, Ippolito G, Lot F, McKibben PS.... (1997) A case-control study of HIV seroconversion in health care workers after percutaneous exposure. Centers for Disease Control and Prevention Needlestick Surveillance Group. The New England journal of medicine, 337(21), 1485-90. PMID: 9366579

March 31, 2012
11:57 AM
291 views

DSM-V: A Little Mix Up

by Neuroskeptic in Neuroskeptic

Proposals in the upcoming DSM-V psychiatric manual for diagnosing "mixed" mood states may be muddled, according to a new paper.The mixed state - the name alluding to a mix between depression and mania - has traditionally been viewed (more or less) as combining the dysphoria of depression with the energy of mania. Anger, agitation, restlessness and so forth. I've been depressed and I know only too well the difference between that "active" depression and the "inactive" kind; if I had to choose, I'd always go for the latter, because at least you're in less danger of doing or saying something you later regret.However, in the proposals for DSM-V, "mixed" episodes as such will be abolished. Instead, a depressive episode will have "mixed features" if it is associated with at least 3 of 7 symptoms normally seen in (hypo)mania. But - and here's the key novelty - those 7 are only the "good" symptoms of mania. Not things like anger, irritability, insomnia or 'aimless' hyperactivity.What will this mean? In a new paper, psychiatrists Perlis, Cusin, and Fava tried to find out. The large STAR*D antidepressant trial recruited people with depression, but it gave everyone the Psychiatric Diagnosis Screening Questionnaire (PDSQ), amongst many other measures. This helpfully included six items on "mania symptoms", which correspond pretty closely to the DSM-V proposed "mixed" features.Perlis et al found that depressed patients who reported experiencing these "mixed" items had a better response to antidepressant treatment. The more mixed symptoms, the more likely they were to get better on the common SSRI citalopram, even adjusting for other variables.That's the exact opposite of what you'd expect from a measure of "mixed states", as these are thought to be less responsive to antidepressants - maybe even caused by them. There was no placebo group, so it's unclear why they got better, but either way, it's unexpected; the authors declare themselves "surprised". Hmm. What a mystery...Or maybe not. These manic symptoms are all things that you're not when you're depressed. The 6 items actually make a good summary of what depression (even agitated depression, except maybe #6) isn't. So, one interpretation of these results is that people who endorsed these items just weren't depressed, at some point in the 6 months prior to doing the PDSQ. Assuming they were depressed at other points that means their mood was variable over time.People whose depression is variable might well be more likely to recover than the ones whose depression was unrelenting.Now Perlis et al do consider this -further models were fit incorporating the IDS-C30 pleasure and reactivity items; results were essentially unchanged indicating that they are unlikely to be confounded by mood variability per se...But this assumes that the IDS-C30 questionnaire is a good measure of mood variability in this sample. Maybe it's not, and these data are telling us so. I'd have said that's more likely than the idea that these people were actually both cheerful and depressed at the same time, which seems like a contradiction in terms.Maybe I'm wrong, and these people did feel that, but the problem is, we can't tell, because no-one actually sat down and asked these people what was going on, or heard their account of what they meant by ticking both the "depressed" and "manic" boxes.Did they experience a strange mixed emotional state in which they simultaneously depressed and happy? Did their mood see-saw from one day to the next? Or weekly, monthly? Were they depressed in the day and happier in the evening? Were they depressed, then back to normal, leading them to see the normal as a 'high', by comparison with the lows? Were they depressed when sober and happy when drunk? Vice versa? Are they experiencing normal ups and downs and interpreting them as 'mood swings' because they've become convinced, for whatever reason, that they have a mood disorder? Did they just have a poor command of English and weren't really trying to say what the highly-educated investigators assume they were?Who knows? No-one, because no-one asked. Rely on questionnaire 'measures' (as if emotions can be measured) as a replacement for understanding, and you'll end up where this paper does - with a 'result' that's impossible to understand.Don't seek, and ye shan't find.It's not great news for the DSM-V proposals, either way, although defenders could point out that there are differences between those proposals and the PDSQ measure so the DSM-V might do better. Perlis, R., Cusin, C., and Fava, M. (2012). Proposed DSM-5 mixed features are associated with greater likelihood of remission in out-patients with major depressive disorder Psychological Medicine, 1-7 DOI: 10.1017/S0033291712000281... Read more »

Perlis, R., Cusin, C., & Fava, M. (2012) Proposed DSM-5 mixed features are associated with greater likelihood of remission in out-patients with major depressive disorder. Psychological Medicine, 1-7. DOI: 10.1017/S0033291712000281

March 29, 2012
02:45 PM
225 views

3D fMRI Promises Deeper Neuroscience

by Neuroskeptic in Neuroskeptic

A new approach to fMRI scanning offers a three-dimensional look at brain activation.fMRI is already a 3D technique, of course, but in the case of the cerebral cortex - which is what the great majority of neuroscientists are most interested in - the 3D data are effectively just 2D images folded up in space. The cortex can be thought of a big sheet crumpled up into the shape of a brain, and it's possible to use software to 'unfold' the cortex into a 2D map for the purposes of fMRI data visualization. It's more informative because it shows you which areas are closest to each other.But the cortex isn't really a sheet. It's more like six sheets stacked up - the cortex is formed of six layers, each with distinct cell types, connections, and functions. The difference between Layer III and Layer V of a particular cortical area is, in some ways, as important as the difference between two adjacent areas, but fMRI can't distinguish them because they're too close together. Until now. In a new paper, Minnesota neuroscientists Olman et al say that they've given fMRI a third dimension - Layer-specific FMRI reflects different neuronal computations at different depths in human v1. They used a powerful 7 Tesla MRI scanner and a T2-weighted 3D GRASE pulse sequence that provides extremely high spatial resolution (0.7 mm - whereas 3 mm is the fMRI standard). The trade-off was that they were only able to scan a small chunk of the brain, namely the primary visual cortex. However, this is a good place to start, because it has a very well-understood layering system.Does it work?Probably, although the data they present are a little messy. By showing volunteers various kinds of pictures, they tried to find evidence of layer-specific visual cortex activation. However, most of the stimuli they used activated all layers equally. In my view the best evidence for layer-specific results was this, from two people -Showing that the upper layers of the cortex were more activated by colourful stimuli that activate "P cells" compared to rapidly changing stimuli that act on "M cells".We'll need more data to be sure that this technique works, but if it does, it promises some awesome science in the future. Still, it's not all good news for us neuroscientists. We'll have to relearn all the facts about cortical layers that most of us studied in Neuroscience 101 and then promptly forgot about.Someone remind me, is Layer I or VI the top one...?Olman CA, Harel N, Feinberg DA, He S, Zhang P, Ugurbil K, and Yacoub E (2012). Layer-specific FMRI reflects different neuronal computations at different depths in human v1. PloS one, 7 (3) PMID: 22448223... Read more »

Olman CA, Harel N, Feinberg DA, He S, Zhang P, Ugurbil K, & Yacoub E. (2012) Layer-specific FMRI reflects different neuronal computations at different depths in human v1. PloS one, 7(3). PMID: 22448223

March 27, 2012
01:53 PM
323 views

Broken Hearts and Broken Livers

by Neuroskeptic in Neuroskeptic

In a new paper, Beyond the Blues, German psychologists Postert et al discuss how the Hmong people of South East Asia talk about sadness - or rather, how they don't, because they don't really have a word for it.Based on anthropological fieldwork in a number of Hmong communities in Laos, the focus of this article is on the Hmong term tu siab, literally "broken liver". This is usually translated as "sadness" in the dictionaries, but the authors say that, although it is certainly the closest thing the Hmong have to a word meaning sadness, it is not the same because:The instance of becoming ‘sad’ in Western contexts is that ‘something bad happened’... This may involve disappointment in personal relationships, but also other afflictions beyond the social realm. At the core of the emotional experience of ‘sadness’ are basic violations of values deeply embedded in Western conceptions of the individual. The afflicted individual feels resigned, passive, out of control...In Hmong language, the concept of ‘broken liver’ has a strong emphasis on kin relations. It pertains very often to social situations of isolation and neglect from one’s kin including consanguines, patrilineal ancestors, or affines or their unmarried daughters in cases of romantic love. Persons with a ‘broken liver’ may have been voluntarily offended, excluded, or separated from these persons by bad fortune...One of the highest Hmong values, a person’s vital social integration, is at stake here. However, a state of ‘broken liver’ is usually far from resignation. Contrary to the assumed passivity of a ‘sad’ individual, a ‘broken liver’ is an affective marker highly mobilising social relations and interdependencies ... having a member in one’s group whose liver is ‘broken’ appeals to the collective commitment of all relatives...[like the English "guilt" and "shame", but unlike "sadness"] ‘broken liver’ demonstrates characteristics of a socio-moral emotion in everyday pragmatics of Laotian Hmong villages. It is typically evoked in a – conscious or unconscious – transgression of an important sociocultural rule. When a man is assumed not to accord to basic principles of social reciprocity by keeping substantial gains from an opium sale for himself, close relatives may develop signs of a ‘broken liver’ signalling their disapproval...In short, the argument is that the Hmong "broken liver" differs from our "sadness" in being an active response rather than a passive reaction, a social statement rather than an individual feeling, in having a moral dimension, and so on.But isn't that much like our "broken heart"?"Breaking someone's heart" is a moral issue. It's not good to be a heartbreaker. If someone broke your friend's heart, you'd be angry. It's a specifically social emotion in the sense that it generally results from betrayal, abandonment, or disrepect. It's true that while the Hmong's "liverbreak" seems to extend to all close relationships, "heartbreak" often has a romantic connotation; but we do talk about "breaking your mother's or father's heart", so even that's not an absolute rule.Consider this recently broken heart. Doesn't Tulisa's heartbreak fit the tu siab bill? If so, then the main difference between Hmong and English terminology is that they only have a concept of 'heartbreak', and lack a general concept of 'sadness'. That's quite interesting, but I'm not sure how much to read into it. English doesn't have a word for 'déjà vu'; we had to borrow it from the French, but surely that doesn't mean that no English people ever felt it until the French explained it to them.I'm no expert but judging by this paper, Hmong emotion terminology is really very similar to ours. The big difference is that the Hmong (in common with other East Asian cultures) link emotions to the liver, which to Westerners sounds silly, but it's no more silly than our talk about emotions being in the heart. They're both just metaphors.Replace "liver" with "heart", and the following Hmong terms (listed in the paper) look very familar -zoo siab ‘pleased, happy’ (lit. ‘good liver’)siab npau ‘angry’ (lit. ‘liver boiling’)chob siab ‘inwardly offended’ (lit. ‘pierced liver’) etc.Don't those all make sense? We talk about being "hearty" or "heartened", "taking heart" or having our "hearts lifted" when we're happy or confident; our "blood boils" when we're angry; we talk about feeling "cut", "stung", "pierced" by criticism or insults, and we suffer "heart-rending" traumas.This is certainly a very interesting paper, but it didn't leave me feeling that the Hmong's emotional life is all that different to ours.Postert, C., Dannlowski, U., Müller, J., and Konrad, C. (2012). Beyond the Blues: Towards a Cross-Cultural Phenomenology of Depressed Mood Psychopathology, 45 (3), 185-192 DOI: 10.1159/000330944... Read more »

Postert, C., Dannlowski, U., Müller, J., & Konrad, C. (2012) Beyond the Blues: Towards a Cross-Cultural Phenomenology of Depressed Mood. Psychopathology, 45(3), 185-192. DOI: 10.1159/000330944

March 23, 2012
03:33 AM
315 views

The Mystery of Trephination

by Neuroskeptic in Neuroskeptic

Why did ancient peoples cut holes in their heads?The Woman of Pritschoena who died around 4,500 years ago in what's now Saxony-Anhalt, Germany. Her skeleton was discovered in 1913 by a local archaeologist. Thanks to being buried in a gravel pit, her remains are exceptionally well preserved.The Woman's skull is a fine example of trephination - the practice of deliberately cutting holes in the skull. The Woman was trephined twice, as you can see in the images above taken from a paper just out. In both cases, the skull around the hole shows clear evidence of healing, which shows that the Woman must have survived the procedures.Trephination is a historical mystery. Stone-age peoples around the world were fond of doing it - trephinations have been found on skulls from Europe, the Americas and Asia. The authors of this paper say that there are records of at least 800 trephined skulls.In some parts of Europe, it seems that the survival rate for the operation was over 90%. It was a delicate procedure, with stone tools used to carefully scrape away and remove the bone without damaging the tissue underneath. But no-one knows why they did it. Some argue that it may have been used as a treatment for epilepsy or mental illness, but it's impossible to really know what it was meant to achieve.Alfieri, A., Strauss, C., Meller, H., Stoll-Tucker, B., Tacik, P., and Brandt, S. (2012). The Woman of Pritschoena: An Example of the German Neolithic Neurosurgery in Saxony-Anhalt Journal of the History of the Neurosciences, 21 (2), 139-146 DOI: 10.1080/0964704X.2011.575117... Read more »

Alfieri, A., Strauss, C., Meller, H., Stoll-Tucker, B., Tacik, P., & Brandt, S. (2012) The Woman of Pritschoena: An Example of the German Neolithic Neurosurgery in Saxony-Anhalt. Journal of the History of the Neurosciences, 21(2), 139-146. DOI: 10.1080/0964704X.2011.575117

March 21, 2012
03:45 AM
346 views

Brain Scanning - Just the Tip of the Iceberg?

by Neuroskeptic in Neuroskeptic

Neuroimaging studies may be giving us a misleading picture of the brain, according to two big papers just out.By big, I don't just mean important. Both studies made use of a much larger set of data than is usual in neuroimaging studies. Thyreau et al scanned 1,326 people. For comparison, a lot of fMRI studies have more like n=13. Gonzalez-Castillo et al, on the other hand, only had 3 people - but each one was scanned while performing the same task 500 times over.Both studies found that pretty much the whole brain "lit up" when people are doing simple tasks. In one case it was seeing videos of people's faces, in the other it was deciding whether stimuli on the screen were letters or numbers.With all that data, the authors could detect effects too small to be noticed in most fMRI experiments, and it turned out that pretty much everywhere was activated. The signal was stronger in some areas than others, but it wasn't limited to particular "blobs".So conventional fMRI experiments may just be showing us the tip of the iceberg of brain activity. In a small study, only the strongest activations pass the statistical threshold to show up as blobs, but that doesn't mean the rest of the brain is inactive. It just means it's less active. The idea that only small parts of the brain are 'involved' in any particular task may be a statistical artefact.In fact, I wonder if the whole idea of treating statistically significant blobs as different from nearly-significant areas is itself a form of the error of interacting effects?As if that wasn't enough, Gonzalez-Castillo further show that there are lots of activations in the brain - even to very simple stimuli - that might go undetected in conventional studies, because they don't follow the time-course predicted by the usual models.Have a look -This shows the average neural activation from various regions of the brain during a letter-number task. The two areas I've highlighted in red are the primary visual cortex, and they do follow the expected 'boxcar' pattern - the brain is active when the stimuli are on the screen, inactive when they're not. But you can see that all kinds of other brain areas are also responding to the stimuli - just in different ways.For example, the left primary motor cortex was activated during the task. That area controls the right hand, and that makes sense, as people responded by pressing buttons with the right hand. But interestingly, the same area on the other side of the brain was deactivated at exactly the same time, even though people weren't doing anything with their left hand.These papers illustrate the fact that conventional fMRI is a blunt instrument that often only tells us about the most straightforward events that happen in the brain. A bit like how we only hear the shouts and screams from through our neighbor's walls, not their normal conversations, which aren't loud enough to reach our ears.That's the bad news, but every blob has a silver lining. fMRI is clearly more powerful than most neuroscientists have realized, and this holds out hope for cracking some of the trickiest questions. As Gonzalez-Castillo et al put itThis result helps narrow the gap between thousands of fMRI manuscripts showing limited activation in response to tasks and cognition theories that defend that cognition—understood as the process of “conﬁguring the way in which sensory information becomes linked to adaptive responses and meaningful experiences”—can only result from the distributed collaboration of primary sensory, upstream and downstream unimodal, heteromodal, paralimbic, and limbic regions... [we were able to] switch from a regime where activity detection relates primary to sensory processing to a more sensitive regime, where activity detection includes also cognitive processes with subtler BOLD signatures.Thyreau, B., Schwartz, Y., Thirion, B., Frouin, V., Loth, E., Vollstädt-Klein, S., Paus, T., Artiges, E., Conrod, P., Schumann, G., Whelan, R., and Poline, J. (2012). Very large fMRI study using the IMAGEN database: Sensitivity–specificity and population effect modeling in relation to the underlying anatomy NeuroImage DOI: 10.1016/j.neuroimage.2012.02.083Gonzalez-Castillo, J., Saad, Z., Handwerker, D., Inati, S., Brenowitz, N., and Bandettini, P. (2012). Whole-brain, time-locked activation with simple tasks revealed using massive averaging and model-free analysis Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1121049109... Read more »

Gonzalez-Castillo, J., Saad, Z., Handwerker, D., Inati, S., Brenowitz, N., & Bandettini, P. (2012) Whole-brain, time-locked activation with simple tasks revealed using massive averaging and model-free analysis. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1121049109

Thyreau, B., Schwartz, Y., Thirion, B., Frouin, V., Loth, E., Vollstädt-Klein, S., Paus, T., Artiges, E., Conrod, P., Schumann, G.... (2012) Very large fMRI study using the IMAGEN database: Sensitivity–specificity and population effect modeling in relation to the underlying anatomy. NeuroImage. DOI: 10.1016/j.neuroimage.2012.02.083

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