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Deconstructing the most sensationalistic recent findings in Human Brain Imaging, Cognitive Neuroscience, and Psychopharmacology

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  • June 14, 2013
  • 05:45 AM
  • 77 views

A New Biomarker for Treatment Response in Major Depression? Not Yet.

by The Neurocritic in The Neurocritic

Is a laboratory test or brain scanning method for diagnosing psychiatric disorders right around the corner? How about a test to choose the best method of treatment? Many labs around the world are working to solve these problems, but we don't yet have such diagnostic procedures (despite what some might claim). A new study by McGrath et al. (2013) might be a step in that direction, but the results are very preliminary and await further validation.The principal investigator of that study is Dr. Helen Mayberg, a leader in neuroimaging studies of major depression. She and her colleagues have pioneered the use of deep brain stimulation (DBS) as a treatment for severe, intractable depression, which was "the culmination of 15 years of research using brain imaging technology," says Dr. Mayberg.Psychotherapy or Drugs?The choice of treatment modality in depression, as in other psychiatric disorders, is by trial and error. If one drug doesn't work, switch to another one. If your insurance covers it, a short course of evidence-based psychotherapy1 might be in order.The whole concept of a DSM-based classification scheme for mental illnesses has come under fire, especially with the release of the new Diagnostic and Statistical Manual. In the real world, psychiatric disorders don't always show such clear boundaries; overlap and co-morbidity are common. The National Institute of Mental Health has endorsed a new approach, the Research Domain Criteria project, that incorporates dimensions of observable behavior along with neurobiological measures. Here's where the new work by McGrath et al. (2013) fits in. Their goal was... To identify a candidate neuroimaging “treatment-specific biomarker” that predicts differential outcome to either medication or psychotherapy.Fewer than 40% of depressed patients remit with their first course of treatment, so this would be an important advance. A more scientific way of choosing among possible treatment options would benefit patients and society at large.The study (registered at clinicaltrials.gov, NCT00367341) enrolled a total of 82 depressed people. The neuroimaging method might surprise some of you: FDG-PET to measure glucose metabolism -- not the popular and trendy resting state fMRI to examine functional connectivity or any sort of fMRI activation study. However, the authors cite an established literature using this technique in studies of antidepressant treatment response.Patients diagnosed with moderate to severe depression (a score of 18 or more on the Hamilton Depression Rating Scale, HDRS) received a PET scan and were randomized to receive 12 weeks of either cognitive behavioral therapy (CBT, n=41) or escitalopram (Lexapro, n=39), an SSRI antidepressant. Sixty-three patients completed this phase and also had a PET scan. The endpoint considered a successful response to treatment was remission (HDRS score of 7 or less), while non-response was a change in HDRS of 30% or less. Partial responders were omitted, leaving the final groups as follows:CBT remission, n=12escitalopram remission, n=11CBT nonresponse, n=9escitalopram nonresponse, n=6Right away we see that the number of patients in each group is very small, particularly for a study designed to identify biomarkers that will generalize to a larger population. Let me repeat that: a successful biomarker must generalize to an independent population. We haven't seen that here, so any conclusions drawn from this paper must be considered very preliminary.How was the biomarker identified? The PET images were co-registered with the corresponding structural MRIs. A whole brain analysis identified regions showing a treatment × outcome interaction (at a significance level of p<.001 uncorrected). Six regions met this uncorrected standard: right anterior insula, right inferior temporal cortex, left amygdala,2 left premotor cortex, right motor cortex, and precuneus (medial superior parietal lobe). Most of these are pretty surprising, but even more surprising is that the rostral anterior cingulate (and subgenual cingulate, BA 25) were not involved:Contrary to past published studies,63 the rostral anterior cingulate did not discriminate the outcome subgroups in either the main effect or interaction analyses. A post hoc examination of responder and nonresponder differences within each treatment arm did reveal a nonsignificant rostral cingulate activity difference, with metabolism in responders greater than nonresponders, but solely in the escitalopram group. While consistent with past reports, this finding did not meet the TSB [treatment-specific biomarker] criteria defined for the current study, ie, a region whose activity can differentiate both good and poor outcomes for both treatments.- click on image for a larger view -... Read more »

McGrath CL, Kelley ME, Holtzheimer PE, Dunlop BW, Craighead WE, Franco AR, Craddock RC, & Mayberg HS. (2013) Toward a Neuroimaging Treatment Selection Biomarker for Major Depressive Disorder. JAMA psychiatry (Chicago, Ill.), 1-9. PMID: 23760393  

  • June 10, 2013
  • 05:37 AM
  • 105 views

How to Measure Female Desire

by The Neurocritic in The Neurocritic

A Sexual Laboratory of One's Own, aka A Clean Well-Lighted Place for SexPsychophysiologic studies of sexual response should be done in a comfortable, well-designed laboratory to minimize subject anxiety and discomfort (Woodard & Diamond, 2009, Fig. 5). How do scientists measure the physiological aspects of sexual arousal in women? A 2009 paper by Woodard and Diamond reviewed 45 years of research using instruments that measure female sexual function. These devices include the vaginal photoplethysmograph (right), vaginal and labial thermistors, pressure/compliance balloons, clitoral electromyography, and the electrovaginogram. For a full list, see Table 1 at the bottom of this post.The authors note that these physiological measures do not correlate very well with subjective ratings of sexual arousal. Furthermore, clinicians who treat women with sexual dysfunctions are of two minds. Some say the distinction between female desire and arousal may be artificial (see DSM-5 changes, p. 13), while others maintain that the merger of female sexual arousal disorder (FSAD) with Hypoactive Sexual Desire Disorder (HSDD) will be disastrous (Clayton et al., 2012).The previous post about Lybrido and Lybridos, the drugs in clinical trials for HSDD, talked briefly about Emotional Brain, the Dutch drug company that is developing them. Putting aside the many objections to the HSDD diagnosis for now, and the fact that the trials pathologize sexual boredom within marriage, the company has conducted some interesting studies1 to assess sexual desire. Foremost among these is the development of an at-home testing environment, or ambulatory lab, to conduct studies of sexual function (Bloemers et al., 2010).Fig. 1 (Bloemers et al., 2010). Schematic overview of the ambulatory measurement setting. (1) Generic laptop, (2) genital probe, (3) wireless sensor system, (4) handheld computer, and (5) secure central database.The participants must be so much more comfortable watching hardcore porn and measuring their own vaginal pulse amplitude and clitoral blood volume in the privacy of their homes, without the prying eyes of hoards of scientists in white lab coats (although some people might be into that).And that's what was found, for the most part (Bloemers et al., 2010):The results of this study support our hypothesis that in healthy controls, clitoral and subjective laboratory measures of sexual arousal show stronger increases to erotic stimuli in the home environment than in the environment of the institutional laboratory. This effect was apparent in response to hardcore stimuli, but not to erotic fantasy. ... To our knowledge, this is the first study that investigates ecological validity of sexual psychophysiological measures by comparing those assessed in the institutional laboratory to those assessed at home with an ambulatory laboratory. Footnote1 Albeit flawed studies, from a cognitive perspective (especially their implementation of an 'Emotional Stroop' task). I am not particularly qualified to comment on other aspects of this research.ReferencesBloemers, J., Gerritsen, J., Bults, R., Koppeschaar, H., Everaerd, W., Olivier, B., & Tuiten, A. (2010). Induction of Sexual Arousal in Women Under Conditions of Institutional and Ambulatory Laboratory Circumstances: A Comparative Study Journal of Sexual Medicine, 7 (3), 1160-1176 DOI: 10.1111/j.1743-6109.2009.01660.xWoodard, T., & Diamond, M. (2009). Physiologic measures of sexual function in women: a review Fertility and Sterility, 92 (1), 19-34 DOI: 10.1016/j.fertnstert.2008.04.041
... Read more »

Bloemers, J., Gerritsen, J., Bults, R., Koppeschaar, H., Everaerd, W., Olivier, B., & Tuiten, A. (2010) Induction of Sexual Arousal in Women Under Conditions of Institutional and Ambulatory Laboratory Circumstances: A Comparative Study. Journal of Sexual Medicine, 7(3), 1160-1176. DOI: 10.1111/j.1743-6109.2009.01660.x  

Woodard, T., & Diamond, M. (2009) Physiologic measures of sexual function in women: a review. Fertility and Sterility, 92(1), 19-34. DOI: 10.1016/j.fertnstert.2008.04.041  

  • May 27, 2013
  • 07:05 AM
  • 140 views

Can Pot Smoking Counter the Negative Metabolic Consequences of Atypical Antipsychotics?

by The Neurocritic in The Neurocritic

DISCLAIMER: This is a hypothetical question and not a medical recommendation. But it might be an idea worth investigating in epidemiological studies.Everyone knows that pot gives you the munchies. So the paradoxical finding that marijuana use is associated with a lower prevalence of obesity and diabetes came as a quite surprise to me. Now, a new study has concluded that pot smokers also have lower fasting insulin levels and smaller waistlines (Penner et al., 2013).I'll let the authors summarize the clinical significance of their study (Penner et al., 2013):Marijuana use is increasingly common, and use of medical marijuana is now legal in 19 states and the District of Colombia.Despite its associations with increased appetite and caloric intake, marijuana use also is associated with lower body mass index and prevalence of diabetes.In a nationally representative survey population, we found current use of marijuana to be associated with lower levels of fasting insulin, lower insulin resistance (homeostasis model assessment of insulin resistance), and smaller waist circumference.More complete descriptions of this article are available at Addiction Inbox and Time Healthland.Marijuana Use and Mental IllnessSome other observations that I will attempt to string together:Cannabis use (and misuse) is higher among individuals with schizophrenia and bipolar disorder (Green et al., 2005; Lev-Ran et al., 2013).I will not address the issue of whether cannabis use is a risk factor for psychosis here.1 In fact, all of my observations will be related to the metabolic effects of marijuana and not to its psychoactive properties and possible detrimental effects on mental health.People with schizophrenia and bipolar disorder are often on atypical antipsychotic drugs, which are notorious for causing significant weight gain that can lead to high cholesterol, hypertension, diabetes and metabolic syndrome. Although cigarette smoking, alcohol use, unhealthy diet, and lack of exercise may contribute to shorter life expectancy in patients with serious mental illnesses (Lawrence et al., 2013), one has to wonder about the effects of atypicals on physical health.2 These drugs can have a very positive effect on mental health, but it comes at a cost.Interestingly, cannabis use is not associated with greater mortality. In fact, the opposite has been reported by Koola et al. (2012), who "observed a lower mortality risk in cannabis-using psychotic disorder patients compared to cannabis non-users despite subjects having similar symptoms and treatments." A total of 762 patients with a psychotic disorder were included in that study. All were on atypical antipsychotics, and 39% used marijuana (although this is often under-reported). The authors speculated on the potential health benefits of cannabis, including its anti-inflammatory effects. However, they didn't mention reductions in obesity and diabetes as possible causes of lower mortality in cannabis users. This association bears further investigation, in my view.Nevertheless, eliminating marijuana to counteract the increase in appetite brought on by atypicals seems like common sense. In fact, this has been proposed as a specific behavioral intervention (Werneke et al., 2013).Those authors assumed that cannabis contributes to the weight gain caused by the prescription medication, which I also assumed (until reading the new papers cited here). But this relationship hasn't really been studied (Werneke et al., 2013):As the endocannabioid system is linked to increased appetite and cannabioid receptor antagonists can induce weight loss [15] cannabis consumption will most likely potentiate antipsychotic-associated weight gain. As the prevalence of cannabis use in people suffering from psychosis is so high, the contribution of cannabis to weight gain in this population is likely to be significant. Surprisingly, this link between cannabis and weight gain remains largely ignored at present. A recent paper in Medical Hypotheses (of all places) takes the opposite stance and proposes cannabis as a weight loss drug (Le Foll et al., 2013):We recently discovered that the prevalence of obesity is paradoxically much lower in cannabis users as compared to non-users and that this difference is not accounted for by tobacco smoking status and is still present after adjusting for variables such as sex and age. Here, we propose that this effect is directly related to exposure to the Δ9-tetrahydrocannabinol (THC) present in cannabis smoke. We therefore propose the seemingly paradoxical hypothesis that THC or a THC/cannabidiol combination drug may produce weight loss and may be a useful therapeutic for the treatment of obesity and its complications.These authors have filed a patent application for 'Use of marihuana and compounds therein for treating obesity' (which they acknowledge in the paper).One of the same authors (Le Foll) has also published on 'Cannabis use and cannabis use disorders among individuals with mental illness' (Lev-Ran et al., 2013), which they found to be particularly high in individuals with Bipolar I disorder (especially in men). Many of these bipolar cannabis users are probably on atypical antipsychotics. This information was not reported in the paper, but it might be available in the National Epidemiologic Survey on Alcohol and Related Conditions (although this is not certain).To be completely clear, I am not advocating the use of marijuana by persons with schizophrenia or bipolar disorder. Rather, I am suggesting that the relationship between atypical antipsychotics and variables such as body mass index, waist circumference, insulin, glucose, and diabetes be compared between groups who do use cannabis vs. those who don't. If there is a benefit in the pot smokers, perhaps there could be a psychiatrically safe, cannabis-derived compound for weight loss in the future. Isn't that more likely than the development of 'third generation' antipsychotics that do not cause substantial weight gain?Footnotes1 Interested readers can consult these articles and posts.2 See also Rising Mortality Rates for People with Serious Mental Illness and Improving the Physical Health of People With Serious Mental Illness.ReferencesGreen B, Young R, Kavanagh D. (2005) Cannabis use and misuse prevalence among people with psychosis. Br J Psychiatry 187:306-13. ... Read more »

Koola, M., McMahon, R., Wehring, H., Liu, F., Mackowick, K., Warren, K., Feldman, S., Shim, J., Love, R., & Kelly, D. (2012) Alcohol and cannabis use and mortality in people with schizophrenia and related psychotic disorders. Journal of Psychiatric Research, 46(8), 987-993. DOI: 10.1016/j.jpsychires.2012.04.019  

Le Foll, B., Trigo, J., Sharkey, K., & Strat, Y. (2013) Cannabis and Δ9-tetrahydrocannabinol (THC) for weight loss?. Medical Hypotheses, 80(5), 564-567. DOI: 10.1016/j.mehy.2013.01.019  

Lev-Ran, S., Le Foll, B., McKenzie, K., George, T., & Rehm, J. (2013) Cannabis use and cannabis use disorders among individuals with mental illness. Comprehensive Psychiatry. DOI: 10.1016/j.comppsych.2012.12.021  

Penner, E., Buettner, H., & Mittleman, M. (2013) The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults. The American Journal of Medicine. DOI: 10.1016/j.amjmed.2013.03.002  

  • May 22, 2013
  • 06:19 AM
  • 74 views

The Mental Health of Lonely Marijuana Users

by The Neurocritic in The Neurocritic

Mr. Lonely 1Does Smoking Pot Offer Relief to the Lonely?  A new paper by the original Tylenol and social pain researchers claims that it does (Deckman et al., 2013). Let's take a closer look.Comfortably Numb: Marijuana Use Reduces Social Pain, Research FindsMarijuana use buffers people from experiencing social pain, according to research published online on May 14 in Social Psychological and Personality Science."Prior work has shown that the analgesic acetaminophen, which acts indirectly through CB1 receptors, reduces the pain of social exclusion," Timothy Deckman of the University of Kentucky and his colleagues wrote in the study. "The current research provides the first evidence that marijuana also dampens the negative emotional consequences of social exclusion on negative emotional outcomes."You could be forgiven if you thought, as I initially did, that the University of Kentucky IRB must hold a liberal view on the administration of controlled substances to undergrads participating in psychology experiments. But that's not what happened here... the data are entirely correlational, based on self-report, and largely problematic (in my view).Marijuana Lowers Self-Worth and Worsens Mental Health in Those Who Are Not LonelyThat's my interpretation of the article, which is SO clunky compared to the fun and breezy query, Can Marijuana Reduce Social Pain? 2The paper begins with the premise that "Social and physical pain share common overlap at linguistic, behavioral, and neural levels" (Deckman et al., 2013). So let's give a pain reliever to reduce the sting of rejection!  A critique of the original work asked why the authors chose Tylenol, as opposed to an NSAID like aspirin, ibuprofen, or naproxen. In the current study they tried to develop a mechanistic account of why acetaminophen might reduce social pain:Prior research has shown that acetaminophen—an analgesic medication that acts indirectly through cannabinoid 1 receptors—reduces the social pain associated with exclusion. Yet, no work has examined if other drugs that act on similar receptors, such as marijuana, also reduce social pain.The problem is that acetaminophen's mechanism of action is surprisingly unclear (Toussaint et al., 2010). One prominent hypothesis claims that Tylenol might exert its analgesic effects through descending serotonergic pathways at the level of the spinal cord. In fact, the paper that Deckman et al. cited in favor of cannabinoid 1 (CB1) receptors describes a very complex pathway that includes indirect involvement of CB1, with actual pain suppression occurring in the spinal cord. 3An even more basic question: if acetaminophen acts through CB1 receptors, then why isn't it a potential drug of abuse, or known by experienced pharmanauts for its psychoactive properties?  The drug experience vault Erowid says:Acetaminophen is a non-salicylate analgesic and antipyretic (pain killer and fever reducer). It is a common over-the-counter pain medication found in hundreds of products around the world. At higher doses it is known to cause liver-damage and has a low therapeutic index (ratio of effective dose to toxic dose), making it dangerous when included in recreationally used pharmaceuticals [e.g., Tylenol with codeine]. It is not known to be psychoactive.On the other hand, we all know that cannabis is psychoactive. The design of the cannabis study included cross-sectional national survey data, a two year longitudinal survey of 400 high school students, and a Mechanical Turk-implemented version of cyberball, an online game to simulate social exclusion. In all cases, participants reported their marijuana use, and this was related to the variables of interest.I'll focus on the national survey data in this post, which comprised Study 1 (Marijuana Use Buffers Lonely People From Lower Self-Worth and Self-Rated Mental Health) and Study 2 (Marijuana Use Predicts Fewer Major Depressive Episodes Among the Lonely).Study 1 used data from the National Comorbidity Survey: Baseline (NCS-1), 1990-1992 (ICPSR 6693), which you can download for yourself. The survey recruited 8,098 individuals from the ages of 15 to 54 living in the U.S., and included over 4,000 variables. Only four variables were chosen for the present study: self-reported loneliness (1= often, 4 = never), marijuana use (0 = none, 1 = daily, 8 = once or twice a year), self-worth (1 = high, 4 = low), and overall mental health (1 = excellent, 5 = poor).Loneliness was used as a proxy for social pain. Contrary to what the headlines suggested, the impact of pot smoking on social pain was not directly examined. Instead, the study assessed the effects of loneliness (high, low), marijuana use (high, low) and their interaction on self-worth and mental health.Loneliness and pot smoking interacted to predict feelings of self-worth [B = 0.03, t(5609) = 2.20, p = .03]. Given the huge number of participants, this level of statistical significance is not very impressive.Fig. 1 (modified from Deckman et al., 2013). Study 1: Marijuana use moderates the relationship between loneliness and self-reported feelings of self-worth. [NOTE: items were reverse-scored for display purposes.]For lonely people, the amount of pot smoked didn't make too much of a difference in their self-worth (see red arrow above).  For socially connected people, greater marijuana use resulted in lower self-worth, although it's not clear this was significant (pairwise statistical tests were not reported).I also question how the High Marijuana Use and Low Marijuana Use groups were determined, because over 5,000 participants did not smoke pot at all in the last 12 months. Does the heavy use group combine those who smoke 6 joints a year with those who smoke daily?... Read more »

Deckman, T., DeWall, C., Way, B., Gilman, R., & Richman, S. (2013) Can Marijuana Reduce Social Pain?. Social Psychological and Personality Science. DOI: 10.1177/1948550613488949  

  • May 15, 2013
  • 04:50 PM
  • 52 views

What RDoC Research Might Look Like

by The Neurocritic in The Neurocritic

The month of May is a violent thingIn the city their hearts start to singWell, some people sing, it sounds like they're screamingI used to doubt it, but now I believe itMonth Of May   ------The Arcade FireToday is Mental Health Month Blog Day, sponsored by the American Psychological Association (APA). It's designed to:...educate the public about mental health, decrease stigma about mental illness, and discuss strategies for making lasting lifestyle and behavior changes that promote overall health and wellness.If the public has been following the recent hullabaloo about how to diagnose mental illnesses, they might be confused about the current and future direction of the field. How did we get here?As most of you know, the American Psychiatric Association (the other APA) is about to release its updated Diagnostic and Statistical Manual of Mental Disorders, the much maligned DSM-5. Weeks before the big launch, however, the National Institute of Mental Health (NIMH) stole the show by announcing that it will be re-orienting its research away from DSM categories:...While DSM has been described as a “Bible” for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been “reliability” – each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. Instead, the Research Domain Criteria (RDoC) framework would become the preferred method for organizing biologically-based research on mental illnesses, with the ultimate goal of constructing a new classification scheme.This caused quite a commotion, leading many to comment on NIMH's shocking repudiation of DSM-5. However, to long-time observers of RDoC's development, this was not a surprise. And the initial lack of clarity on the distinction between the RDoC Dimensional Approach for Research vs. DSM-5 for Diagnosis didn't help matters, nor did the uncertainty about whether NIMH would fund DSM-based research at all.1NIMH issued a press release on May 13 to clarify its position:DSM-5 and RDoC: Shared InterestsThomas R. Insel, M.D., director, NIMHJeffrey A. Lieberman, M.D., president-elect, APANIMH and APA have a shared interest in ensuring that patients and health providers have the best available tools and information today to identify and treat mental health issues, while we continue to invest in improving and advancing mental disorder diagnostics for the future.Today, the APA's Diagnostic and Statistical Manual of Mental Disorders (DSM), along with the International Classification of Diseases (ICD) represents the best information currently available for clinical diagnosis of mental disorders  Patients, families, and insurers can be confident that effective treatments are available and that the DSM is the key resource for delivering the best available care. The NIMH has not changed its position on DSM-5. As NIMH’s Research Domain Criteria (RDoC) project website states, “The diagnostic categories represented in the DSM-IV and the International Classification of Diseases-10 (ICD-10, containing virtually identical disorder codes) remain the contemporary consensus standard for how mental disorders are diagnosed and treated.”Yet, what may be realistically feasible today for practitioners is no longer sufficient for researchers. Looking forward, laying the groundwork for a future diagnostic system that more directly reflects modern brain science will require openness to rethinking traditional categories. It is increasingly evident that mental illness will be best understood as disorders of brain structure and function that implicate specific domains of cognition, emotion, and behavior. This is the focus of the NIMH’s Research Domain Criteria (RDoC) project. RDoC is an attempt to create a new kind of taxonomy for mental disorders by bringing the power of modern research approaches in genetics, neuroscience, and behavioral science to the problem of mental illness.So what is RDoC, and how might it be applied to new research projects? From the DSM perspective of categorical disorders (e.g, schizophrenia, major depression, and obsessive compulsive disorder), RDoC embraces diagnostic messiness. Patients previously excluded from a study due to comorbidities, or because they don't meet full criteria? Misfits from the "Not Otherwise Specified" (NOS) category? Now they're in. Specifically, the instructions for RFA-MH-14-050 state:Priority will be given to applications that have a well-justified plan to include patients from multiple diagnostic groups (including Not Otherwise Specified and forme fruste diagnoses) as appropriate for explicating the dimensions and constructs of interest in the study design. Studies that include patients from a single diagnostic group may also be considered if there is a particularly strong justification for examining constructs of interest within one diagnostic category.  A defensible approach might be to study all patients presenting themselves at a specialty clinic, e.g., mood disorders clinic, anxiety clinic, or psychotic disorders clinic, regardless of whether they meet criteria for a particular DSM diagnosis.One potential pitfall of this approach is the money required to enroll huge numbers of patients. If commonalities in cognitive function or brain circuitry or especially genetic risk factors are to emerge from studying all patients with mood disorder-like symptoms, then sample sizes must be very large to overcome potential noise in the system(s).The applicant would propose to study one or more of the five different domains, or constructs, that have been fleshed out at NIMH Workshops:Negative Valence SystemsPositive Valence SystemsCognitive SystemsSystems for Social ProcessesArousal/Regulatory SystemsThe possible units of analysis run the gamut from genes to circuits to behavior, and the studies should use specific tasks (paradigms) and self-report measures, as shown in the Negative Valence Systems matrix below.Draft Research Domain Criteria Matrix Animal ... Read more »

Vaidyanathan, U., Nelson, L., & Patrick, C. (2011) Clarifying domains of internalizing psychopathology using neurophysiology. Psychological Medicine, 42(03), 447-459. DOI: 10.1017/S0033291711001528  

Dichter, G., Damiano, C., & Allen, J. (2012) Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings. Journal of Neurodevelopmental Disorders, 4(1), 19. DOI: 10.1186/1866-1955-4-19  

  • April 28, 2013
  • 08:22 AM
  • 134 views

Want to remember something? Clenching your fist doesn't help!

by The Neurocritic in The Neurocritic

Image Credits: fist and brain.You might have seen this news story the other day:Want to remember something? Clench your fists!Giving a speech and need to remember what to say? Just clench your right fist while rehearsing. Then, when it's time to give the speech, clench your left fist, and voila, you’ll recall what you rehearsed! That's what a new study found, which was published April 24 online at PLOS ONE. Sounds too easy now, doesn't it? And if you're exclaiming, "that's just too good to be true!" — then you'd be correct.The new study by Propper et al. (2013) has unleashed a torrent of criticism on Twitter, including this starter by @js_simons.What motivated such a study in the first place? I'll try to run through the authors' rationale here, starting with statements from the abstract, which are followed by my commentary.Unilateral hand clenching increases neuronal activity in the frontal lobe of the contralateral hemisphere. It's true that unilateral hand movement is executed via motor cortex activity in the opposite hemisphere, so the right hemisphere controls the left hand and vice versa.Such hand clenching is also associated with increased experiencing of a given hemisphere’s “mode of processing.”This statement is based on EEG studies that have looked at alpha power suppression recorded at scalp electrodes over left and right frontal cortex (Harmon-Jones, 2006). The hypothesis is that left hand contractions "activate" (i.e., suppress alpha waves in) the unhappy right hemisphere, thereby producing negative affect, while right hand contractions activate the happy left hemisphere, which results in positive affect. The affective "modes of processing" aspect of this research isn't directly relevant to the Propper et al. (2013) paper, and further discussion is beyond the scope of this post. I'll just say that attributing EEG activity to a specific cortical region is a dicey proposition, because the spatial resolution of the technique isn't great.1 Together, these findings suggest that unilateral hand clenching can be used to test hypotheses concerning the specializations of the cerebral hemispheres during memory encoding and retrieval.Here the EEG research on emotion is being applied to memory. We investigated this possibility by testing effects of unilateral hand clenching on episodic memory. The hemispheric Encoding/Retrieval Asymmetry (HERA) model proposes left prefrontal regions are associated with encoding, and right prefrontal regions with retrieval, of episodic memories. The Hemispheric Encoding/Retrieval Asymmetry (HERA) model of Tulving et al. (1994) postulates that the left prefrontal cortex encodes information into memory, while the right prefrontal cortex retrieves information from memory. This was back in ye olden days of PET using block designs with 40 seconds of one condition subtracted from 40 seconds of another condition. In other words, poor temporal resolution.The HERA model was revisited and confirmed by its proponents using fMRI data (Habib et al., 2003), but the evidence against it was considerable (Owen, 2003). The general consensus is that HERA has been discredited. In fact, noted memory researcher Dr. Jon Simons posted a comment at the PLOS ONE website explaining why the underlying hypothesis of Propper et al. is problematic (among other issues).It was hypothesized that right hand clenching (left hemisphere activation) pre-encoding, and left hand clenching (right hemisphere activation) pre-recall, would result in superior memory. Here we're expecting to see better memory in the R/L condition than in the control condition. There is no mention that the other fist-clenching conditions would result in worse performance than in the control condition. Results supported the HERA model. Results did NOT support the HERA model, and I'll explain why below (and you can read the PLOS ONE comment).In the experiment, participants studied a list of 36 words, engaged in a filler task, and then recalled as many words as possible. Approximately 10 subjects participated in each of 16 conditions, only five of which are reported in the paper. These involved squeezing a small pink ball in one hand (2 sets of 45 sec) before the encoding and the retrieval phases of the study. The control condition did not involve clenching, but the participants held a small pink ball in each hand.2 The five conditions are shown below, named by the hand used during encoding/retrieval. You'll notice that the number of participants in each group (n) is pretty small. I calculated standard deviations from the standard error values to determine effect sizes using this effect size calculator. 3 Although the authors reported the total number of words written down (correct or not) and the number of correct words in Figs. 1 and 2 respectively, the important result is shown in Fig. 3, which takes into account the false alarms, or incorrectly recalled words. Figure 3 (Propper et al., 2013). Corrected scores as a function of hand clench condition. [NOTE: NENR = None Encoding/None Recall, or control.]The one-way ANOVA for this comparison "did not reach traditional significance" (p=.08), but two of the post hoc comparisons did (uncorrected for multiple comparisons involving 16 groups). The p<.09 bar in the figure is in the wrong pla... Read more »

Propper, R., McGraw, S., Brunyé, T., & Weiss, M. (2013) Getting a Grip on Memory: Unilateral Hand Clenching Alters Episodic Recall. PLoS ONE, 8(4). DOI: 10.1371/journal.pone.0062474  

Tulving E, Kapur S, Craik FI, Moscovitch M, & Houle S. (1994) Hemispheric encoding/retrieval asymmetry in episodic memory: positron emission tomography findings. Proceedings of the National Academy of Sciences of the United States of America, 91(6), 2016-20. PMID: 8134342  

  • April 19, 2013
  • 08:25 PM
  • 94 views

Does Tylenol Exert its Analgesic Effects via the Spinal Cord?

by The Neurocritic in The Neurocritic

What do we (not) know about how paracetamol (acetaminophen) works? (Toussaint et al., 2010). . .From the beginning, the focus of the search for paracetamol’s analgesic mechanism has concentrated on the central nervous system. When administered intraventricularly [i.e., directly into the ventricular system of the brain], acetaminophen produces no significant analgesia (115, 132). This finding lead to attempts to inject acetaminophen into the spinal cord (i.t.), which produced marked dose-related antinociception (132).Yesterday’s post about Tylenol as a cure for mortality salience and existential dread got me a little worked up. The first author’s public endorsement of acetaminophen as a possible treatment for chronic anxiety disorders was too much to handle (along with the less than stellar experimental rigor). Is watching a 4 min clip of a David Lynch film really the same thing as a clinically diagnosed psychiatric disorder (Randles et al., 2013)? Why Tylenol and not other pain relievers? What is the hypothesized mechanism of action? Wouldn’t we already know by now, from epidemiological studies at the very least, if Tylenol was an effective anti-anxiety medication?So I started wondering about acetaminophen's actual mechanism of action. I was quite surprised that it's somewhat mysterious. Randles et al. cited one paper on this:Second, acetaminophen affects a number of brain regions, some of which are not directly related to physical or social distress (Toussaint et al., 2010).This led me to believe there was evidence from human neuroimaging studies. Turns out there isn't, beyond the Dewall et al. (2010) paper, which states:Although the precise mechanisms by which acetaminophen exerts an analgesic effect are still unclear, it is widely accepted that acetaminophen reduces pain through central, rather than peripheral, nervous system mechanisms (Anderson, 2008; H.S. Smith, 2009).I would like to point out that the spinal cord is part of the central nervous system. So if it's really true that acetaminophen exerts its pain-relieving effects through synapses in the spinal cord, then what does this say about providing relief from the angst of social exclusion, mortality salience, and existential dread? That it's based on nociceptive spinal cord neurons in laminae I, II, and V? For a visual illustration of this pathway, I highly recommend viewing the animation, Dissection of DLF blocks analgesia, at Neuroscience Online. One hypothesis is that Tylenol (acetaminophen) may act on descending serotonergic pathways (purple projection) at the level of the spinal cord (red synapses). Figure modified from Neuroscience Online.However, it's not that simple. The review paper by Toussaint et al. (2010) concluded, "No one mechanism has been definitively shown to account for its analgesic activity." For its proposed mechanisms of action, they presented evidence both for and against Cyclooxygenase (EC 1.14.99.1, COX) inhibition, COX-1, COX-2, 'COX-3', peroxidase, nitric oxide synthase, cannabinoid receptors, and of course serotonin:There is substantial evidence that paracetamol’s mechanism of analgesia in some manner involves the descending serotonergical pathway. 5-HT neurons, largely originating in raphe nuclei located in the brain stem (117, 118) send projections down to the spinal cord that synapse on afferent neurons entering the spinal cord. These descending projections exert an inhibitory (analgesic) effect on the incoming pain signal before it is transmited to higher CNS centres.Note that these are not the same serotonergic pathways often implicated in depression. The terminal synapses for the latter are indeed located in the brain and not the spinal cord.Last night, in real life, I followed the Watertown news live via @sethmnookin and @taylordobbs (like many others).This morning I dreamt that my workplace had transformed into an institutional fortress taken over by a gang of murderous criminals. The actual law enforcement authorities were too busy watching television talk shows to do anything about it. The thugs were threatening and torturing and killing people in the building. I managed to escape down a balcony exit and hid out for a while, avoiding detection but fearful that the thugs would find me and kill me. They were unstoppable, and there seemed to be no way out. I informed an old West-style sheriff, who managed to detain a carload of the evildoers. While continuing to hide, I wondered whether I would be able to shoot them all dead with a fully automatic weapon before they shot and killed me.Then an early morning doorbell rang and woke me up. It was an unexpected FedEx delivery. In my barely awake state, I thought it might be a bomb.Why am I telling you all this?? Because I find it very hard to believe that Tylenol, a drug that's relatively ineffective for my own headache pain, could possibly alleviate the anxiety caused by this nightmare. Or by the real life nightmare that's affected so many people in Boston.ReferencesDewall CN, Macdonald G, Webster GD, Masten CL, Baumeister RF, Powell C, Combs D, Schurtz DR, Stillman TF, Tice DM, Eisenberger NI. (2010). Acetaminophen reduces social pain: behavioral and neural evidence. Psychol Sci. 21:931-7. Randles, D., Heine, S., & Santos, N. (2013). The Common Pain of Surrealism and Death: Acetaminophen Reduces Compensatory Affirmation Following Meaning Threats. Psychological Science DOI: 10.1177/0956797612464786... Read more »

Toussaint, K., Yang, X., Zielinski, M., Reigle, K., Sacavage, S., Nagar, S., & Raffa, R. (2010) What do we (not) know about how paracetamol (acetaminophen) works?. Journal of Clinical Pharmacy and Therapeutics, 35(6), 617-638. DOI: 10.1111/j.1365-2710.2009.01143.x  

  • April 18, 2013
  • 09:02 PM
  • 134 views

Existential Dread of Absurd Social Psychology Studies

by The Neurocritic in The Neurocritic

Scene from Rabbits by David Lynch“In a nameless city, deluged by a continuous rain, three rabbits live with a fearful mystery.”The latest "elegant and breathtaking"1 paper in Psychological Science presents a rather muddled view of film aesthetics, continental philosophy, surrealism, mortality salience, and stigmatizing attitudes towards sex work (Randles et al., 2013). Oh, and how Tylenol® brand acetaminophen can ease the existential dread evoked by all of these modern horrors.The authors explained the purpose and implications of their study in the APS press release:According to lead researcher Daniel Randles and colleagues at the University of British Columbia in Canada, the new findings suggest that Tylenol may have more profound psychological effects than previously thought:“Pain extends beyond tissue damage and hurt feelings, and includes the distress and existential angst we feel when we’re uncertain or have just experienced something surreal. Regardless of the kind of pain, taking Tylenol seems to inhibit the brain signal that says something is wrong.”Randles and colleagues knew from previous research that when the richness, order, and meaning in life is threatened — with thoughts of death, for instance — people tend to reassert their basic values as a coping mechanism.The researchers also knew that both physical and social pain — like bumping your head or being ostracized from friends — can be alleviated with acetaminophen. Randles and colleagues speculated that the existentialist suffering we face with thoughts of death might involve similar brain processes. If so, they asked, would it be possible to reduce that suffering with a simple pain medicine?No!!  I think this is a ridiculous assertion that gets away with using language (and dependent measures) that not only lack precision, but also lack an analogical relation to the real phenomenon under discussion. The leaps of logic were so egregious that I don't know where to begin......so let's start with the meaning-maintenance model (MMM) that motivated the work. MMM "posits that any violation of expectations leads to an affective experience that motivates compensatory affirmation" (Randles et al., 2013). Any violation?? So all sorts of psycholinguistics experiments that involve syntactic violations 2 will motivate compensatory affirmation? If that's the case, then David Lynch films will often "motivate compensatory affirmation."But does a David Lynch film “hurt” you?...Lynch’s films have the ability to “disturb, offend or mystify” (Rodley, 2005, p. 245). Insofar as it “hurts” to watch some of Lynch’s films, as it arguably hurts whenever one is assaulted by thoughts and experiences that are at odds with one’s expectations and values, the question arises as to how this uncomfortable feeling is represented in the brain. First, David Lynch is one of my favorite directors, and I have never felt "hurt" by watching one of his films. Second, Randles et al. never, at any point in their experiments, address how Lynch-viewing is represented in the brain.What did the authors actually do? In brief, they asked ~350 young Vancouverites to participate in one of two experiments. In the first study, 121 subjects wrote about death or about dental pain. In the second study, 228 subjects watched a 4 min clip from Rabbits or from The Simpsons. In each case, half of the participants received acetaminophen, half received placebo. Why? What motivated the choice of acetaminophen, as opposed to aspirin, ibuprofen, or naproxen? This was based on a study by Dewall et al. (2010), another problematic paper3 in Psych Sci. There was no mechanistic reason for the original choice.Here's the neuro-rationale for the current study (Randles et al., 2013):The present research is predicated on four key findings in the literature: (a) Both physical and social pain are associated with activation in the dACC [dorsal anterior cingulate cortex]4 (e.g., Eisenberger et al., 2003), (b) the dACC is activated in response to anomalies (e.g., Botvinick et al., 2004), (c) social rejection can produce the same compensatory affirmation as other meaning threats (e.g., Nash et al., 2011), and (d) acetaminophen has been shown to reduce physical and social pain, as well as activation in the dACC (DeWall et al., 2010). These findings led us to predict that acetaminophen may also inhibit compensatory affirmation following meaning threats.The acetaminophen group in Dewall et al. (dose of 2,000 mg a day for 3 weeks) did show less dACC activity in response to cyberball exclusion, but they did not report lower hurt feelings in that situation. The treatment administered by Randles et al. was quite different: a single acute dose of 1,000 mg Tylenol-brand acetaminophen (Rapid Release formula) or 1,000 mg sugar placebo, given 30 min before the critical manipulation.In Exp. 1, writing two paragraphs about what will happen to your body after death was designed to trigger mortality salience, or thoughts about the inevitability of death. This in turn would lead to compensatory affirmation of cultural views. How was this measured? By assessing the severity of punitive attitudes towards women who engage in sex work! This is the worst part of the study, in my opinion.Social judgment surveyFinally, participants read a hypothetical arrest report about a prostitute and were asked to set the amount of the bail (on a scale from $0 to $999). This measure has been used in a number of other meaning-threat studies (Proulx & Heine, 2008; Proulx et al., 2010; Randles et al., 2011; Rosenblatt, Greenberg, Solomon, Pyszczynski, & Lyon, 1989). Participants are expected to increase the bond amount after experiencing a threat, because trading sex for money is both at odds with commonly held cultural views of relationships and against the law. Increasing the bond assessment provides participants n opportunity to affirm their belief that prostitution is wrong. The study took place in Vancouver, Canada. What are the laws on prostitution?In Canada, the buying and selling of sexual services are leg... Read more »

Randles, D., Heine, S., & Santos, N. (2013) The Common Pain of Surrealism and Death: Acetaminophen Reduces Compensatory Affirmation Following Meaning Threats. Psychological Science. DOI: 10.1177/0956797612464786  

  • March 31, 2013
  • 06:56 PM
  • 235 views

Are Cognitive Factors Related to Criminal Reoffending?

by The Neurocritic in The Neurocritic

Image from Graphic SociologyCan Brain Activity Predict Criminal Reoffending?  The previous post discussed a functional MRI study suggesting that the level of error-related activation in the anterior cingulate cortex (ACC) might have value in predicting whether a recently released prisoner will be rearrested within 4 years (Aharoni et al. 2013):The odds that an offender with relatively low anterior cingulate activity would be rearrested were approximately double that of an offender with high activity in this region, holding constant other observed risk factors. These results suggest a potential neurocognitive biomarker for persistent antisocial behavior.However, using ACC activity as a dichotomous variable misclassified 40% of low ACC participants who did not reoffend and 46% of high ACC participants who did commit crimes after release, not exactly the odds you'd want for making parole decisions. Even the senior author was doubtful that an fMRI test would ever be useful for risk assessment purposes on a case by case basis.Since Aharoni and colleagues made their individual subject data available as supplementary material (Download Dataset_S01, XLSX), I was interested in how some of the demographic and performance variables might be related to recidivism, since these are obviously cheaper and easier to collect from incarcerated prisoners than MRI scans.The cognitive task performed during the fMRI experiment required responding to a frequent stimulus presented 84% of the time ("X") and inhibiting responses to a rare stimulus ("K").Fig. S4. (Aharoni et al., 2013). Go/No-Go task.The study compared brain activity on incorrect responses to "K" (commission errors) and correct responses to "X" (hits) in a region of interest in the dorsal ACC, which has been implicated in error processing (Simons, 2010), among many other things. The authors framed the results largely in the context of impulse control, but other explanations are possible (as we'll see later).Are any of the task performance variables related to recidivism? Starting with some very simple-minded t-tests, the rate of commission errors in the group of participants arrested for nonviolent offenses1 (n=40) did not differ significantly from what was seen in those not arrested again (n=56).2Data from (Aharoni et al., 2013). Commission errors in the Go/NoGo task (% incorrect responses on NoGo trials) and omission errors (% missed responses on Go trials) for inmates that went on to commit nonviolent offenses within 4 years after release (Nonviolent) and those that did not (None). The trend for the reoffenders to commit more errors was not significant (p=.09) even without correcting for multiple comparisons.Although there were data from a large control group of nonoffenders (n=102) used to set the ACC ROI, we don't have their behavioral results. I consulted an earlier fMRI paper by Kiehl et al. (2000) that used a very similar Go/NoGo task in 14 control participants. Commission errors occurred on 23.7% of NoGo Trials and omission errors on 3% of Go Trials, which is similar to what was seen in the offenders (overall means of 25.04% and 3.44%, respectively).Reaction times (RTs) did not differ between the two offender groups either, suggesting there wasn't a differential speed-accuracy tradeoff (e.g., if the reoffenders were slower yet making marginally more errors).Data from (Aharoni et al., 2013). RTs in milliseconds for commission errors (incorrect responses on NoGo trials) and hits (correct responses on Go trials) for inmates that went on to commit nonviolent offenses within 4 years after release (Nonviolent) and those that did not (None). There were no group differences.Surprisingly, RTs were slower on commission errors (358 ms) than on hits (346 ms), a small but highly significant difference (p=.0005). This is the opposite of what you'd expect if the errors were due to impulsive responses. If the participants were becoming careless and not fully evaluating the NoGo stimulus, they'd be faster on error trials. This is why I'm not convinced the ACC activations are entirely related to behavioral impulsivity. In EEG studies of error processing, the degree of ACC activity3 is related to the emphasis placed on accuracy (Gehring et al., 1993), so if the reoffenders didn't care as much about accuracy, this could account for their low ACC status. One interesting bit of data for the authors to examine would be RT and accuracy on responses following an error, which indicates the amount of behavioral adjustment after making a mistake. Did the reoffenders show a lower propensity to slow down and become more careful? If so, this might reflect a lack of concern about the consequences of their actions.However, the most puzzling thing to me were scores on Factor 2 of the Psychopathy Checklist-Revised (PCL-R) (Hare, 2003). Factor 2 is thought to reflect impulsivity, stimulation seeking, and irresponsibility (Ermer et al., 2012). The rearrested and not-rearrested groups were significantly different as expected, but in the opposite direction (unless I'm missing something here) — scores were lower in the group that was rearrested, in comparison to those who were not (p=.001).Data from (Aharoni et a... Read more »

Aharoni, E., Vincent, G., Harenski, C., Calhoun, V., Sinnott-Armstrong, W., Gazzaniga, M., & Kiehl, K. (2013) Neuroprediction of future rearrest. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1219302110  

Kiehl, K., Liddle, P., & Hopfinger, J. (2000) Error processing and the rostral anterior cingulate: An event-related fMRI study. Psychophysiology, 37(2), 216-223. DOI: 10.1111/1469-8986.3720216  

  • March 28, 2013
  • 04:13 PM
  • 175 views

Can Brain Activity Predict Criminal Reoffending?

by The Neurocritic in The Neurocritic

Is it possible for a brain scan to predict whether a recently paroled inmate will commit another crime within 4 years? A new study by Aharoni et al. (2013) suggests that the level of activity within the anterior cingulate cortex might provide a clue to whether a given offender will be rearrested.Dress this up a bit and combine with a miniaturized brain-computer interface that continuously uploads EEG activity to the data center at a maximum security prison. There, machine learning algorithms determine with high accuracy whether a given pattern of neural oscillations signals the imminent intent to reoffend that will trigger deep brain stimulation in customized regions of prefrontal cortex, and you have the plot for a 1990s cyberpunk novel.But we're getting way ahead of ourselves here...Dr. Kent Kiehl outside the mobile scanner his group uses to look at the brains of inmates at New Mexico prisons. Credit: Nature News.The actual study in question used functional MRI to scan the brains of 96 male inmates at two New Mexico state correctional facilities while they performed a cognitive task (Aharoni et al., 2013). The task required responding to a frequent stimulus presented 84% of the time ("X") and inhibiting responses to the rare stimulus ("K").Fig. S4. (Aharoni et al., 2013). Go/No-Go task.The major comparison examined brain activity on incorrect responses to "K" (commission errors) vs. correct responses to "X" (hits). This contrast was restricted to a region of interest (ROI) in the dorsal anterior cingulate cortex (dACC), which has been associated with a wide array of cognitive and emotional control functions (Posner et al., 2007).Results from a separate group of 102 age-matched control participants (mean = 33.9 yrs) from Hartford, CT1 determined the a priori ROI, with the peak voxel located at coordinates x = −3, y = 24, z = 33 in the center of a 14 mm sphere. One control ROI was chosen in a more ventral and anterior region of medial prefrontal cortex (mPFC) at 0, 51, −6.The most strongly activated voxel in the offender group for the error vs. hit contrast was remarkably close to the one determined from the independent sample and fell well within the a priori ROI (see blue crosshairs in figure below).Fig. 2 (modified from Aharoni et al., 2013). (B) Mean hemodynamic response change in offender sample (n = 96) during commission errors vs. correct hits from sagittal (Upper Left), coronal (Right), and axial (Lower Left) orientations. Peak activation located at x = 3, y = 24, z = 33 within the anterior cingulate cortex region of interest (P < 0.00001, FWE).The dACC has been strongly implicated in error processing (Simons, 2010), and that was no different in the offenders as a group. Other regions significantly activated by commission errors included bilateral inferior frontal cortex/insula, fusiform gyrus, and cerebellum but these were not discussed.Of greatest interest is whether this dACC activity can predict recidivism. For this the authors did a survival analysis:First, a Kaplan–Meier survival function was computed to describe the proportion of participants surviving any felony rearrest over the 4-y follow-up period, ignoring the influence of any particular risk factor (Fig. S1). Cox proportional hazards regression was then used to examine (i) the zero-order effects of ACC activity on months to rearrest for any crime, (ii) the shared and unique influence of the ACC and other potential risk factors on months to rearrest for any crime, (iii) for nonviolent crimes, and (iv) the shared and unique influence of the medial prefrontal cortex (mPFC) control region and other potential risk factors on months to rearrest for any crime. ...... A significant association was found whereby, for every one unit increase in ACC activity, there was a 1.39 (i.e., 1/exp[B]) decrease in the probability of rearrest....Meaning that the participants with greater ACC activity were less likely to reoffend. The mPFC  ROI did not show this association. Then a median split divided the offender sample into high ACC and low ACC groups (survival function shown below).Fig. 1 (Aharoni et al., 2013). Cox survival function showing proportional rearrest survival rates of high (solid green) vs. low (dashed red) ACC response groups for any crime over a 4-y period. Results of this median split analysis were equivalent to that of the parametric model: bootstrapped B = 0.96; SE = 0.40; P < 0.01; 95% CI, 0.29–1.84. The mean survival times to rearrest for the low and high ACC activity groups were 25.27 (2.80) mo and 32.42 (2.73) mo, respectively. The overall probabilities of rearrest were 60% for the low ACC group and 46% for the high ACC group.So for all felonies (both violent and nonviolent), a substantial percentage of participants were likely to be rearrested within 4 years. The ACC classification scheme would wrongly condemn the 40% of low ACC parolees who did not reoffend, and would miss the 46% of high ACC parolees who did commit crimes after release. When you look at it that way, it's not all that impressive and completely inadmissable as evidence for decision-making purposes. For nonviolent felonies only, the probability of rearrest for high ACC offenders was 31%, compared to 52% for low ACC offenders.A number of other variables were considered in the regression models (and singly as predictors), including age at release, drug and alcohol use, scores on the Psychopathy Checkli... Read more »

Aharoni, E., Vincent, G., Harenski, C., Calhoun, V., Sinnott-Armstrong, W., Gazzaniga, M., & Kiehl, K. (2013) Neuroprediction of future rearrest. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1219302110  

  • March 15, 2013
  • 05:16 AM
  • 317 views

How Neuroscientists Scan the Media

by The Neurocritic in The Neurocritic

In case you missed it, I had a guest post this week in Nature's SpotOn NYC series on Communication and the Brain (#BeBraiNY), held in conjunction with Brain Awareness Week. The theme concerned the challenges of engaging the public's interest in cognitive sciences, and communicating the knowns (and unknowns) of brain disorders:In the current funding climate of budget cuts and sequestration, there’s a wide latitude between overselling the immediate clinical implications of "imaging every spike from every neuron" in the worm C. elegans (as in the proposed Brain Activity Map Project) and ignoring science communication entirely, leaving it up to the university press office.Who occupies the middle ground between the industry cheerleader and the disinterested academic? Science bloggers, for one. Scientist bloggers comprise a growing segment of the science communication world.Many of us have been critical of how traditional media channels can distort the actual scientific results and mislead the public. With the mainstreaming of neurocriticism, I felt this topic had been discussed extensively in recent months, so I moved on to the responsibilities we face in presenting accurate information. Some examples were drawn from my posts on unusual neurological disorders, including Prosopometamorphopsia (a condition where faces look distorted on one side) and Othello Syndrome (delusional jealousy). Both posts can turn up on the first page of a Google search, so I do feel an obligation to be factual and informative.Another example was a critique of public brain scanning on Celebrity Rehab with Dr. Drew. Although I wrote that post (and a follow-up) in 2010, readers were finding them now because former program participants Mindy McCready and Dennis Rodman were in the news, for very different reasons. My guest post concludes with:Scientist bloggers serve an important function in the continuum of science communication. We should take our responsibility for presenting high quality, ethical information very seriously, to help stem the ongoing flood of neurocrackpottery.Amidst the SpotOn NYC series extolling the virtues of science blogging came a new paper suggesting that science blogs are inferior sources of information relative to traditional media (Allgaier et al., in press):Scientists may understand that neuroscience stories in legacy media channels are likely to be of higher quality than similar narratives found in blogs. Stories in social channels are often crafted on the fly, without the help of experienced editors who can point out holes in the narrative or who can insist on rewriting and revision. Blog posts also tend to be shorter narratives, bereft of the kind of complexity and nuance possible only in long-form journalism.Obviously, there's a lot of high quality "long-form" journalism (which is never defined in the paper), but a huge number of high quality, complex and nuanced blog posts can be found as well. The passage above sparked quite the discussion on social media. Here's one initiated by respected journalist, blogger, and science writer Carl Zimmer:Blogs versus journalism in neuroscience--IT LIVES!I found passages like the one I just quoted [the one above] to be puzzling on many levels. Science blogs pretty much came into existence as a way for scientists themselves to critique bad coverage in traditional media. And, ten years later, that remains a powerful tradition.The paper presents a romantic, uncritical view of the press. Speaking as a journalist, I can say this is a view we can ill-afford.What's more, neuroscience blog posts are very often deep, nuanced, and more accurate than "churnalism" driven by glib press releases.If neuroscientists are indeed avoiding blogs for this reason (no data provided in the paper that this is true), then they are sadly misguided.Eight others joined in the discussion, which is worth reading.  One of the participants was Dominique Brossard, an author on the article in question.In brief, Allgaier et al. (in press) randomly contacted 1,248 "productive" neuroscientists who had published at least 8 articles in the preceding 2-year period. The survey participation rate was 21.3% in the US and 32.6% in Germany.The scientists responded to questions about three dimensions of public media channels, both traditional and online: (1) their personal use of these channels to “follow news and information about scientific issues”; (2) their assessment of the impact of scientific information in these channels on public opinion about science; and (3) their assessment of the impact of such information on “science-related decisions made by policymakers.” The respondents answered the questions with respect to a comprehensive list of traditional print or broadcast media, online analogs of those media channels, blogs, and content in social networks. Respondents were primarily male (78%) and over 40 (79%). Is this a typical sampling of neuroscientists? Obviously not, since it is gender-imbalanced1 and excludes most grad students and the average post-doc. The results in this group of participants suggested a preference for old media:The results of our survey indicate that the respondents in both countries remained heavily reliant on journalistic narratives, in both traditional and online forms, for information about scientific issues. Only a modest number of the surveyed neuroscientists reported that they use blogs or social networks to monitor such issues.Fig. 1a (modified from Allgaier et al., in press). Media use (in percentages) among neuroscientists in the United States and Germany. For the exact wording of the questions, detailed data, and significance information, consult supplemental table S1, available online at http://dx.doi.org/10.1525/bio.2013.63.4.8  [not online as of this writing].The over 40 crowd was more reliant on newspapers and valued online articles less than the younger set, who used social media more often as a source of popular science news. Women were less reliant on newspapers and printed pop sci magazines for science issue information than men.Do we really know if the participants consider blogs and social media to be inferior sources of information for the reasons quoted above? We do not. The authors were speculating, as they were in this paragraph (which elicited howls in the ... Read more »

Joachim Allgaier, Sharon Dunwoody, Dominique Brossard, Yin-Yueh Lo, & Hans Peter Peters. (2013) Journalism and Social Media as Means of Observing the Contexts of Science. BioScience. info:/10.1525/bio.2013.63.4.8

  • March 12, 2013
  • 02:28 AM
  • 263 views

What Is This Thing Called Neuroscience?

by The Neurocritic in The Neurocritic

"It depends upon what the meaning of the word 'is' is." -President Bill Clinton, August 17, 1998image: Brain electrodes, by laimagendelmundoDr. Vaughan Bell at Mind Hacks wrote a terrific post on The history of the birth of neuroculture as a follow-up to his Observer piece on Folk Neuroscience. That article explained how neuro talk has invaded many aspects of everyday discourse. In the new post he briefly covers the history of modern neuroscience, a necessary prelude to contemporary neuroculture:Neuroscience itself is actually quite new. Although the brain, behaviour and the nervous system have been studied for millennia the concept of a dedicated ‘neuroscience’ that attempts to understand the link between the brain, mind and behaviour only emerged in the 1960s and the term itself was only coined in 1962. Since then several powerful social currents propelled this nascent science into the collective imagination.To me, those dates seem quite recent in relation to brain research that has been conducted for centuries. Was there no neuroscience research prior to the 60s? My general perception is that ‘neuroscience’ research has been around a lot longer than that, even if it wasn't called by that precise name. It might have been called psychobiology (Yerkes, 1921), neurobiology (Brodmann, 1909),1 neurophysiology (1938) or neurochemistry (Lewis, 1948), but the types of questions asked and the experiments performed appear to be in line with much of what passes as a dedicated neuroscience in modern times. Here's Dr. Nolan D.C. Lewis speaking at the 96th Annual Session of the American Medical Association, Atlantic City, NJ, June 13, 1947 (Lewis, 1948):The actual nature of the thought processes is annoyingly elusive. What is the nature of thought? It is probably a manifestation of energy, but one can ask many questions about this. ... Do small areas of intact brain produce thoughts? Does the brain produce the mind independently or is it an instrument used by some other somatic processes or agents in the body? Does the brain itself think or is it a transmission center utilized by some other force? Is the mind the product of cerebral matter or is it dependent on something else which governs it? Can matter think? Either matter can produce mind or it cannot. Is mind a unique form of matter different from any other known forms of matter? While these questions and problems are probably not solvable by means of present technics, they are challenging, approachable and must eventually become elucidated if we are to get to the core of mental disorders.2What's in a name?I became curious enough to investigate whether the term ‘neuroscience’ was actually coined in 1962. @AliceProverbio confirmed that "Francis Schmitt used the term Neuroscience for the first time in 1962 to name his Neuroscience reserch group [at] MIT".  I found the paper in the Journal of the History of Neurosciences that clearly recognizes the role of Schmitt, but it also opined that the word might have been invented earlier (Adelman, 2010):...the word might have been coined by Ralph Gerard in the early 1950s...Does it really matter when the word itself was first used? No, not for Vaughan's history of the birth neuroculture. I'm not going to get to the bottom of who should get credit, either. But I do find it interesting to see how the word is used in various historical contexts.Not to be outdone by MIT, Harrison (2000) reviews the contributions and recollections of Five Scientists at Johns Hopkins in the Modern Evolution of Neuroscience, including those of pioneering neurophysiologist Professor Vernon Mountcastle:‘In the 1940’s, and on, this place [Johns Hopkins University] was red hot for the development of Neuroscience’.Noted historian of neuroscience Professor Stanley Finger, in his review on Women and the History of the Neurosciences, named several famous women neuroscientists of the 19th century (Finger, 2002):3 Women have been underrepresented in the early years of the neurosciences, much as they have been in other scientific endeavors. Nevertheless, the names of many important women contributors stand out if one begins in the latter part of the 19th century...Two women, who worked in part with their husbands but also achieved greatness on their own as the 19th century drew to a close and the 20th century began, are Augusta Marie (Dejerine-) Klumpke (1859-1927), who was married to Joseph Jules Dejerine (1849-1917), and Cécile Mugnier Vogt (1875-1962), who was married to Oskar Vogt (1870-1950)....Three other famous women neuroscientists from the later period are Christine Ladd-Franklin (1847-1930), Maria MichailovnaManasseina (also known as Marie de Manacéine, (1843-1903), and Margaret Floy Washburn (1871-1939). But in describing the vision of Professor Francis O. Schmitt in founding the Neurosciences Research Program at MIT, Adelman (2010) gets the last word on ‘neuroscience’:Ideally, Schmitt and his colleagues thought, the various physical, biological, and neural sciences could be brought together to attack a single goal, and what a goal — the ultimate one of all science and philosophy — how does the mind/brain work! Every field with some involvement in mind-brain studies would be included, from the molecular and subcellular areas of cell biology to the higher reaches of psychology and psychiatry. Such areas as cognitive psychology might not be able to contribute much to neurobiology; parallel fibers and psychophysical parallelism have little in common. But this field could pose major questions about higher brain function and the mechanisms of thinking, with molecular genetics perhaps providing answers about mechanisms operating at subcellular levels of the nervous system. Ha, ha! So much for the modern convergence of brain and behavioral sciences...Footnotes1 Dr. Korbinian Brodmann worked as an Assistant in the Neurobiological Laboratory of the University of Berlin.2 It goes without saying that modern techniques have opened up new avenues of study. And that ethical standards for the proper conduct of human and animal research (e.g., The Purring Center in Cats) have improved... Read more »

Adelman, G. (2010) The Neurosciences Research Program at MIT and the Beginning of the Modern Field of Neuroscience. Journal of the History of the Neurosciences, 19(1), 15-23. DOI: 10.1080/09647040902720651  

LEWIS, N. (1948) SUGGESTIVE RESEARCH LEADS IN CONTEMPORARY NEUROCHEMISTRY. JAMA: The Journal of the American Medical Association, 136(13), 866. DOI: 10.1001/jama.1948.02890300016005  

  • February 27, 2013
  • 10:47 PM
  • 252 views

Can a Slow-Growing Brain Tumor Cause a Gambling Problem?

by The Neurocritic in The Neurocritic

Maureen O’Connor, former mayor of San Diego and heir to her late husband Robert O. Peterson’s Jack-in-the-Box fortune, won over $1 billion playing video poker over the course of 9 years (2000-2009), according to U-T San Diego. However, she lost an even greater amount during that time, resulting in a net gambling debt of $13 million. To cover some of these losses, she transferred $2 million from her husband's nonprofit foundation to her personal bank account. She was recently charged with misappropriation of funds in federal court.In 2011, O'Connor had surgery to remove a large brain tumor:The tumor was in an area of the brain that involves "logic, reasoning and judgment," said O'Connor's attorney, Eugene Iredale. Is It Possible That Maureen O’Connor’s Gambling Problem Was Caused by the Brain Tumor?Can a tumor cause irrational economic decision-making (Koenigs & Tranel, 2007) and insensitivity to future consequences (Bechara et al., 1994)? In cases of orbitofrontal meningiomas, the answer is yes.T1 + contrast MRI scan shows a large olfactory groove meningioma affecting the medial orbitofrontal cortex.  Image source:  Radiopedia.While I cannot speak to Ms. O'Connor's specific case, there are a number of reports in the neurological literature of patients who do incur large gambling debts during the time a slow-growing, non-fatal tumor impinges upon the frontal lobes. Specifically, a meningioma (a relatively common and “benign” non-infiltrating tumor in the meninges, or membranes that cover the brain) in the region of the orbitofrontal cortex (OFC) can grow to be the size of an orange over decades before it is discovered (Tomasello et al., 2011).1Eslinger and Damasio (1985) reported the case study of patient EVR, who had surgery to remove a large meningioma affecting medial OFC bilaterally. Although EVR showed intact cognitive function through standardized neuropsychological testing, he made a series of unwise decisions that led to very negative consequences in his life. His business went bankrupt after he took on an unsavory business partner. He drifted from job to job, often being fired for his unreliability. He got divorced, remarried against the advice of others, and then divorced again shortly thereafter. Bechara et al. (1994) developed what came to be known as the Iowa Gambling Task (IGT) to assess the decision-making capacity of patients like EVR. In the task, participants are shown 4 decks of cards (real or virtual) from which they are allowed to draw in a series of gambles. They are told they can win money, but might also win and lose money, and will be informed of the consequences of their choice only after picking a card from one of the decks. Unbenownst to the subjects initially, Decks A and B pay out $100 but also incur larger penalties on an unpredictable schedule ("disadvantageous decks" resulting in a net loss) while Decks C and D only pay $50 but result in smaller penalties ("advantageous decks" resulting in a net gain). In the long run, patients with lesions in medial OFC (aka ventromedial prefrontal cortex, or VMPFC) preferred the higher immediate payoff than the safer decks, while controls showed the opposite pattern.In other words, EVR (and 6 other patients like him) chose from the disadvantageous decks significantly more often than control participants, who appeared to better learn the good and bad nature of the decks. Although the IGT is not without its critics in terms of the cognitive and affective processes necessary for optimal task performance, other studies suggest that VMPFC is indeed important for future-oriented thinking (Fellows & Farah, 2005).2 O'Connor's Plea BargainIn court, Ms. O'Connor pleaded not guilty to money laundering under the terms of a deferred prosecution, according to U-T San Diego. As part of the deal, she has two years to pay back funds "borrowed" from the nonprofit foundation, and she must attend treatment for gambling addiction:The resolution of the case takes into account her poor health but also requires O’Connor to acknowledge she misappropriated the money and obligates her to pay it back and any tax penalties, [Assistant U.S Attorney Philip Halpern] said.She also has to get psychiatric treatment for gambling addiction. [Defense attorney] Iredale said that O’Connor’s doctors have said it’s possible her brain tumor pressed on centers of the brain that affect judgment and reasoning, and could explain in part her gambling addiction.Prosecutors dispute that. “We believe the gambling preceded her medical condition,” Halpern said.ABC 10 News reported:If she does not obey all laws, she could face 10 years in prison.All parties agreed that O'Connor's medical condition render it highly improbable -- if not impossible -- that she could be brought to trial."We think largely as a result of the brain tumor, she had engaged in a period of compulsive gambling in which she systematically gambled away an inheritance that was left to her of several million dollars," said Iredale.CBS News aired an interview with the former mayor. O'Connor said that video poker was "...like electronic heroin. You know, the more you did, the more you needed and the more it wasn't satisfied."As mayor she was always in control. Her gambling was out of control."I thought I could beat that machine," she said. "And when it got worse, I didn't know I had the silent grenade in my head that could go off at any time."The "silent grenade" was a golf ball-sized tumor doctors removed from her brain. They discovered it two years ago when she started hallucinating. She says she believes the slow-growing tumor contributed to her gambling addiction. "It's not an excuse for my gambling, but I think that was, yes, a part of it. You lose your sense of control," she said. How slow-growing?Prosecuting attorney Halpern was skeptical of the tumor explanation, saying "she began her gambling run in 2001 -- a decade earlier. It would have to be a pretty slow-growin... Read more »

Bechara A, Damasio AR, Damasio H, & Anderson SW. (1994) Insensitivity to future consequences following damage to human prefrontal cortex. Cognition, 50(1-3), 7-15. PMID: 8039375  

Koenigs, M., & Tranel, D. (2007) Irrational Economic Decision-Making after Ventromedial Prefrontal Damage: Evidence from the Ultimatum Game. Journal of Neuroscience, 27(4), 951-956. DOI: 10.1523/JNEUROSCI.4606-06.2007  

Tomasello, F., Angileri, F., Grasso, G., Granata, F., De Ponte, F., & Alafaci, C. (2011) Giant Olfactory Groove Meningiomas: Extent of Frontal Lobes Damage and Long-Term Outcome After the Pterional Approach. World Neurosurgery, 76(3-4), 311-317. DOI: 10.1016/j.wneu.2011.03.021  

  • February 10, 2013
  • 03:53 AM
  • 281 views

The Neuroanatomical Correlates of Self-Sabotage

by The Neurocritic in The Neurocritic

Self-Sabotage, by jesse.millanI should be preparing for a Very Important Presentation at an upcoming meeting. But I'm not. I'm sitting at home on a Saturday night, blogging about self-sabotage."Self Sabotage is when we say we want something and then go about making sure it doesn't happen."-AlyceI do have a lot of clever ideas and useful data that are relevant for the meeting in question, I just haven't been able to start preparing my presentation yet. Am I afraid of failing? Angry at the complete lack of incentive structures at my workplace (which is organized and run in such a laughably inept manner as to be totally demotivating)? Psychology of Self-HandicappingWhat is behind the act of setting yourself up for failure, for unconsciously compiling a list of excuses for why you didn't perform at your best? What motivates this behavior?It's an act of self-preservation, actually, to have external reasons for why you didn't achieve what you set out to accomplish. That way, you're not a complete and total failure as a person. It protects your fragile self-esteem, but this comes at a price.Zuckerman and Tsai (2005) found the long-term costs of this strategy include a loss of perceived self-competence, negative mood, increased substance use, and a decline in motivation. Self-handicapping can be an effective strategy in the short-term, but eventually you'll suffer the consequences and end up a failure anyway.Anatomy of Self-HandicappingA group of Japanese researchers (Takeuchi et al., 2013) wanted to determine the neuroanatomical correlates of self-handicapping behavior, to see what sets this population apart from others. They used voxel-based morphometry (VBM) to quantify individual differences in brain anatomy across a large group of healthy students (94 men and 91 women). The participants were administered a Japanese version of the self-handicapping scale, along with assessments of self-esteem and depressive mood. The scale included questions like these (PDF):When I do something wrong, my first impulse is to blame circumstances.I always try to do my best, no matter what.I tend to put things off until the last moment.I would do a lot better if I tried harder.Regional gray matter volumes (rGMV) were quantified in a whole-brain analysis and related to scores on the self-handicapping scale with age, sex, total brain volume, intelligence, self-esteem, and depression as covariates.The major finding is that self-handicapping was positively correlated with rGMV in a portion of the subgenual cingulate gyrus (sgCG), or Brodmann area 25. This general area has been dubbed the "sad cingulate" by some, because it's the region targeted by deep brain stimulation for severe intractible depression by Helen Mayberg, Andres Lozano and colleagues (e.g., Riva-Posse et al. 2012).1 Fig. 1a (adapted Takeuchi et al., 2013). Anatomical correlates of self-handicapping tendency. The region of correlation is overlaid on a single subject T1 image rGMV in sgCG was correlated with individual self-handicapping tendency. Results are shown with P < 0.05 after correction for multiple comparisons at voxel-level FWE at the whole brain level.The extent of this correlation did not differ between males and females (see fig below). No other regions showed positive or negative correlations with self-handicapping scores. It might seem a little implausible that the size of such a circumscribed area is the only one that correlated with the tendency for self-sabotage, but there you go.Fig. 1b (adapted Takeuchi et al., 2013). Scatter plot of the relationship between the self-handicapping scale score and rGMV values at the peak voxel (x, y, z = −5, 11, −16). The blue line represents the regression line for males, while the red line represents that for females. A counterintuitive aspect of this result stands in contrast with previous studies of depressed individuals, who show smaller rGMV in sgCG (Drevets et al., 2008). In the present study, higher self-handicapping was correlated positively with depression symptoms and negatively with self-esteem. But remember, this was a non-clinical population of 21 yr old students, not treatment-resistant patients with severe depression. In fact, it would be interesting to follow this population longitudinally, to see if continued use of self-handicapping tactics eventually wears down mood and sgCG volumes to pathologically low levels.After a lifetime of self-sabotage, the fill-in-the-blank answer to..."When I do something wrong, my first impulse is to _____"...might change from "blame circumstances" to "blame myself for being such a miserable failure." When there's no self-esteem left, why try harder? What's the point?Footnote1 However, the sgCG region in the present study seems inferior and posterior to the DBS target (Riva-Posse et al. 2012).ReferencesDrevets WC, Savitz J, Trimble M. (2008). The subgenual anterior cingulate cortex in mood disorders. CNS Spectr. 13:663-81. Riva-Posse P, Holtzheimer PE, Garlow SJ, Mayberg HS. Practical Considerations in the Development and Refinement of Subcallosal Cingulate White Matter Deep Brain Stimulation for Treatment Resistant Depression. World Neurosurg. 2012 Dec 12. [Epub ahead of print]Hikaru Takeuchi, Yasuyuki Taki, Rui Nouchi, Hiroshi Hashizume, Atsushi ... Read more »

Hikaru Takeuchi, Yasuyuki Taki, Rui Nouchi, Hiroshi Hashizume, Atsushi Sekiguchi, Yuka Kotozaki, Seishu Nakagawa, Carlos Makoto Miyauchi, Yuko Sassa, Ryuta Kawashima. (2013) Anatomical correlates of self-handicapping tendency. Cortex. info:/

  • January 30, 2013
  • 01:12 AM
  • 289 views

Dr. David H. Barlow and Aversion Therapy for Gays

by The Neurocritic in The Neurocritic

Should a professional society honor a highly accomplished investigator who conducted studies in the past that would now be considered unethical? Distinguished professor and clinical psychologist Dr. David H. Barlow was recognized for his achievements by the Association for Psychological Science (APS) last year as the recipient of the 2012 James McKeen Cattell Fellow Award:David H. Barlow has made enormous theoretical and empirical contributions in many areas of clinical psychology. He is best known for his efforts to develop psychological treatments for anxiety disorders. His early work on the treatment of agoraphobia laid the groundwork for exposure-based treatments that are today regarded as the gold standard. As we learned more about the relationship of agoraphobic avoidance to the occurrence of panic attacks, Barlow led the way in the development of treatments for the remediation of panic symptoms.Much of Barlow’s research is based on the notion that anxiety is a disorder of emotion. He holds this to be the case regardless of the specific emotional disorder, and this has led him in the later years of his career toward the development and testing of a unified protocol for the transdiagnostic treatment of such disorders....What you might not have known is that such disorders have included homosexuality and transsexualism. Barlow advocated and practiced aversion and conversion therapies to "cure" gay and transgendered people of their "deviant" sexuality.While I do not wish to detract from Dr. Barlow's many positive accomplishments, I feel it is important to expose the questionable practices of the past and to hold people accountable for their actions. I looked far and wide to find a mea culpa from Dr. Barlow, much like Dr. Robert Spitzer's public apology for his published work on reparative therapy as a "cure" for homosexuality (Spitzer, 2003).1 But I did not find such a statement anywhere. Should we question the judgment of APS in honoring Dr. Barlow with the Cattell Award? 2 Are they tacitly condoning exorcism in transsexuals (Barlow et al., 1977) and aversion therapy in gay men (Barlow et al., 1969; Hayes et al., 1983)? At the very least, APS did not publicly acknowledge or condemn these former practices, which remain secretly buried in the past.I contacted two divergent experts to ask their opinions. Psychologist Dr. John Grohol, who founded the mental health networking and education site Psych Central, turned the question around:"Should we honor professionals who may have made questionable judgments in their early career? I would ask a question in return -- Should we forever withhold such honors for the poor judgments one makes in one's early career?"On the other hand, Professor Lynn Conway, the pioneering computer scientist, electrical engineer, and transgender activist, was surprised about the award. She felt an appropriate course of action is..."... to expose these old miscreants and get their misdeeds on the record. That way they'll all have to run for cover in the years ahead..." Let's examine some of these practices below so you can decide for yourself.Exorcism for Transsexualism?As some of you might have gathered, I came across this paper during my exorcism research.  Barlow and colleagues (1977) didn't actually perform the exorcism themselves, but observed the resulting change in behavior "fortuitously" and used it as an example of how atypical gender identity could be modified, if not prevented all together:Although the prevention of transsexualism is the ideal, work in this area has been fraught with ethical problems... The authors reported the detailed case history of "John", a 21 year old patient who had a clear identity as female and wished to transition. Before doing so, John was persuaded to visit a Fundamentalist Christian doctor, who performed an exorcism:The physician administered a total physical exam and said that he could live quite well as a woman, but the real problem was possession by evil spirits. After some discussion of this, John reported a session which lasted 2-3 hr and involved exhortations and prayers over John by the physician and laying on a hands on John's head and shoulders. During this period, John reported fainting several times and arising to the continuing of the prayers and exhortations, resulting in the exorcism of 22 evil spirits which the physician called by name as they left his body.  ... The physician noted ... that he showed John that his life was a fake and that Jesus could redeem him and that a standard prescription of Scripture readings caused the spirit of the woman in John to disappear.Immediately after the session John announced he was a man, discarded his female clothes (hiding his breasts as best he could), and went to the barber shop to have his long hair cut into his current short, masculine style...Rather than condemn the outlandish and unethical behavior of this physician, and counsel John (who had identified as Judy) on her previously excellent adjustment as female and readiness for surgery, they considered this a successful change in gender identity. An even more questionable event was a visit to a faith healer. After the laying on of hands, John reported that his breasts (size 36B) had disappeared immediately. Personally, I think a psychiatric assessment would have been in order.Very worth reading in regard to this paper is the text on Rogue Theories of Transsexualism written by Professor Conway. She says that "By seeing a collection of such theories side-by-side, we grasp the strangeness of them all."Aversion Therapy to Cure Sexual Deviance Even more outrageous were the papers on aversion therapy. As a prelude to the actual practices described by Barlow et al. (1969), I will use American Horror Story: Asylum as a near-exemplar.The year is 1964. Lana Winters is a reporter investigating the unethical practices at Briarcliff Manor, a mental institution for the criminally insane. She's caught snooping around and is committed against her will to keep her quiet, with the ostensible reason being that she is gay. She is forced to have shock treatment. Sympathetic psychiatrist Dr. Oliver Thredson tries to persuade her to undergo aversion therapy, which is presented as more "humane." She eventually agrees because she thinks it'll get released her from Briarcliff once Thredson pronounces her "cured."Under the direction of Dr. Thredson, Winters views a slide show of erotic pictures of women. She has an iv drip going into her left arm. She starts to get physically ill while viewing the slides and then throws up into a metal bucket.... Read more »

Barlow DH, Abel GG, & Blanchard EB. (1977) Gender identity change in a transsexual: an exorcism. Archives of sexual behavior, 6(5), 387-95. PMID: 921523  

Barlow DH, Agras WS, & Leitenberg H. (1972) The contribution of therapeutic instruction of covert sensitization. Behaviour research and therapy, 10(4), 411-5. PMID: 4637499  

Barlow DH, Leitenberg H, & Agras WS. (1969) Experimental control of sexual deviation through manipulation of the noxious scene in covert sensitization. Journal of abnormal psychology, 74(5), 597-601. PMID: 5349402  

Hayes SC, Brownell KD, & Barlow DH. (1983) Heterosocial-skills training and covert sensitization. Effects on social skills and sexual arousal in sexual deviants. Behaviour research and therapy, 21(4), 383-92. PMID: 6138027  

  • January 23, 2013
  • 02:09 PM
  • 179 views

Is CTE Detectable in Living NFL Players?

by The Neurocritic in The Neurocritic

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease seen most often in athletes with repeated concussions.1 The condition has drawn extensive media attention due to the number of cases reported among retired NFL players. The disease can only be diagnosed at autopsy, because the brain tissue has to be stained for characteristic protein abnormalities which cannot be visualized in a living human.Until now, that is, according to a new study by Gary Small and colleagues at UCLA (Small et al., 2013). Positron emission tomography (PET) and the molecular imaging probe FDDNP 2 were use to visualize levels of the protein tau, which forms neurofibrillary tangles in Alzheimer's disease and other tauopathies. Or what is presumed to be tau.Elevated levels of FDDNP were observed in in the brains of 5 former NFL players relative to those of 5 control participants. The players were referred for testing because of symptoms of mild cognitive impairment. These five participants in the study (out of 19 potential volunteers) had a mean age of 59 yrs; MMSE scores of 28 vs. 30 in controls; and higher depression scores than controls, but no clinically significant depression in most.The authors admit this is a very preliminary study that needs to be replicated and validated in larger samples. Yet they are optimistic they have a discovered a means of imaging CTE pathology in the brains of living patients. But I would like to cast some doubt on this notion for two reasons:(1) FDDNP is supposedly a tracer for both tau and amyloid beta (which forms plaques in Alzheimer's and other dementia), but some experts think it's neither. Studies have shown that it binds to a variety of misfolded proteins. For example, it selectively labels prion plaques in Creutzfeldt–Jakob disease (Bresjanac et al., 2003).At any rate, FDDNP does not appear to be specific for CTE pathology.(2) The distribution of FDDNP binding in the brains of the retired players does not appear to be the same as CTE tau pathology that has been observed at autopsy (McKee et al., 2012). Last month the Boston University group found evidence of CTE in the brains of in 68 male subjects, most of whom played contact sports. McKee et al. identified a series of four stages of CTE, with progressive worsening of clinical symptoms and neuropathology. My guess is that the participants in the Small et al. study, if they do indeed have CTE, might be at stage I or perhaps stage II, but this is hard to tell given the very limited clinical and cognitive data on these patients (they had "a history of cognitive or mood symptoms").The FDDNP results showed elevated signals in the players in a number of subcortical regions (including caudate, putamen, thalamus, subthalamus, midbrain, and amygdala), but nowhere in the cerebral cortex. On the other hand, stage I CTE tau pathology in post mortem brains is found in limited discrete locations: mild pathology in the cerebral cortex and minimal pathology in the amygdala and hippocampus (McKee et al., 2012). In stage II, pathology within the cortex spreads, and pathology in the medial temporal lobe (amygdala and hippocampus) is still mild. Maybe there's a bias for subcortical labelling with FDDNP PET, versus cortical pTDP-43 immunoreactivity in post-mortem tissue. 3  That's possible, but Small and colleagues have previously reported extensive neocortical FDDND signal in mild cognitive impairment (Small et al., 2012).I'm not an expert, and I could certainly be wrong about all of this. Development of in vivo imaging probes for neurodegenerative diseases is a very active area of research. The new hyperphosphorylated-tau radioligand [F-18]-T807 could be more specific for imaging tauopathies (Chien et al., 2012). Scientific developments like these will be especially crucial once any type of treatment for CTE comes along. - Original link to study via Deadspin and Nature editor Noah Gray.Footnotes1 More background information, taken from my earlier post on Blast Wave Injury and Chronic Traumatic Encephalopathy: What's the Connection? A defining pathological feature is tauopathy - abnormal accumulations of the tau protein seen in other dementias (e.g., Alzheimer's disease). Aggregations of hyperphosphorylated tau into neurofibrillary tangles (NFTs) are a defining feature, as in frontotemporal lobar degeneration and amyotrophic lateral sclerosis -- yet CTE is distinct from both of these (McKee et al., 2009). CTE results in cognitive and behavioral changes including memory impairments, poor impulse control, alterations in mood, suicidal behavior, disorientation, and ultimately dementia.2 Co-authors Small and Barrio are among the inventors of the FDDNP approach. They have received royalties and may receive royalties on future sales.3 Noah Gray raised this point.ReferencesBresjanac M, Smid LM, Vovko TD, Petric A, Barrio JR, Popovic M. (2003). Molecular-imaging probe 2-(1-[6-[(2-fluoroethyl)(methyl)amino]-2-naphthyl]ethylidene) malononitrile labels prion plaques in vitro. J Neurosci. 23(22):8029-33.Chien DT, Bahri S, Szardenings AK, Walsh JC, Mu F, Su MY, Shankle WR, Elizarov A, Kolb HC. Early Clinical PET Imaging Results with the Novel PHF-Tau Radioligand[F-18]-T807. J Alzheimers Dis. 2012 Dec 12. [Epub ahead of print]McKee, A., Stein, ... Read more »

McKee, A., Stein, T., Nowinski, C., Stern, R., Daneshvar, D., Alvarez, V., Lee, H., Hall, G., Wojtowicz, S., Baugh, C.... (2012) The spectrum of disease in chronic traumatic encephalopathy. Brain. DOI: 10.1093/brain/aws307  

Gary W. Small, Vladimir Kepe, Prabha Siddarth, Linda M. Ercoli, David A. Merrill, Natacha Donoghue, Susan Y. Bookheimer, Jacqueline Martinez, Bennet Omalu, Julian Bailes, Jorge R. Barrio. (2013) PET Scanning of Brain Tau in Retired National Football League Players: Preliminary Findings. Am J Geriatr Psychiatry. info:/

  • January 20, 2013
  • 04:15 AM
  • 238 views

Possession Trance Disorder in DSM-5

by The Neurocritic in The Neurocritic

American Horror Story: Asylum takes place in 1964 at Briarcliff Manor, a terrifying mental institution for the criminally insane. The show uses every over-the-top stereotype in the book — straightjackets, isolation cells, shock treatment, the chronic masturbator, the nymphomaniac, the sadistic nun, the evil mad doctor, unethical experimentation, wrongful commitment, alien abduction, demonic possession, you name it — yet it still manages to be scary and stylish and suspenseful.The episode about a poor soul possessed by the devil naturally includes an exorcism by Catholic priests. The afflicted boy becomes ugly and deformed by the demon, who spews out lewd words and exerts its supernatural telekinetic powers by throwing objects (and priests) across the room.Regarding exorcism, the Catholic Encyclopedia says:Exorcism is (1) the act of driving out, or warding off, demons, or evil spirits, from persons, places, or things, which are believed to be possessed or infested by them, or are liable to become victims or instruments of their malice; (2) the means employed for this purpose, especially the solemn and authoritative adjuration of the demon, in the name of God, or any of the higher power in which he is subject. Religious belief in the existence of demons is a sincere part of the Catholic faith, so demonic possession can be a particularly frightening Hollywood trope for devout Catholics (and former Catholics). Walking out of the theater into the dark parking lot and entering your empty apartment after a midnight showing of The Exorcist can be creepy for the believer and the agnostic alike. Even if Satan isn't lurking in your shower, a serial killer like "Bloody Face" could be under your bed. Indoctrination into a belief system where devils are real can haunt a young child into adulthood.In contrast, the rationalist perspective presents historical and medically-based views of possession phenomena in terms of epilepsy, schizophrenia, and possession trance disorder (PTD), a possible variant of dissociative identity disorder. Nothing evil or supernatural takes over the identity of the person with PTD. Nonetheless, exorcisms performed on mentally ill people continue to this day.For example, Tajima-Pozo and colleagues (2011) reported on the case of a 28 yr old woman in Spain who had been diagnosed with paranoid schizophrenia. Over the course of 5 yrs she had been treated with the antipsychotic drugs clozapine, risperidone, ziprasidone and onlanzapine, without complete remission. She was an inpatient on a psychosis ward, and yet some diabolical priests managed to get in and convince her that she was possessed by demons. Some of the priests had knowledge of the patient's psychiatric history and should have known better. But they performed multiple exorcisms anyway, which disrupted her clinical treatment.1 In DSM-IV, spirit possession falls under the category of Dissociative Disorder Not Otherwise Specified, with more specific research criteria (but not an official diagnosis) fitting Dissociative Trance Disorder (possession trance): This category [DDNOS] is included for disorders in which the predominant feature is a dissociative symptom (i.e., a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment) that does not meet the criteria for any specific dissociative disorder.. . .Dissociative trance disorder: single or episodic disturbances in the state of consciousness, identity, or memory that are indigenous to particular locations and cultures. Dissociative trance involves narrowing of awareness of immediate surroundings or stereotyped behaviors or movements that are experienced as being beyond one's control. Possession trance involves replacement of the customary sense of personal identity by a new identity, attributed to the influence of a spirit, power, deity, or other person and associated with stereotyped involuntary movements or amnesia, and is perhaps the most common dissociative disorder in Asia. Examples include amok (Indonesia), bebainan (Indonesia), latah (Malaysia), pibloktoq (Arctic), ataque de nervios (Latin America), and possession (India). The dissociative or trance disorder is not a normal part of a broadly accepted collective cultural or religious practice.  Note the culture-specific aspect of the disorder, which shows substantial heterogeneity in its expression. Dr. Romeo Vitelli at the blog Providentia has written about some of these phenomena. For instance, Amok is an aggressive trance-like state in Malay culture, whereas Pibloktoq is an acute dissociative reaction in the Inuit tradition, caused by evil spirits possessing the living. In two previous posts here at The Neurocritic, we also learned about cen in Uganda, ghosts that replace the identity of the afflicted individual.  Dissociative Disorders in DSM-5Will there be changes for Dissociative Trance Disorder (DTD) in DSM-5? The new (and already reviled) psychiatric manual makes its debut in May 2013.2  A 2011 paper by Spiegel et al. described some of the proposed changes to the dissociative disorders. The Pathological Possession Trance (PPT) component of DTD is claimed to be be similar to dissociative identity disord... Read more »

Tajima-Pozo, K., Zambrano-Enriquez, D., de Anta, L., Moron, M., Carrasco, J., Lopez-Ibor, J., & Diaz-Marsa, M. (2011) Practicing exorcism in schizophrenia. Case Reports, 2011(feb15 1). DOI: 10.1136/bcr.10.2009.2350  

Duijl, M., Kleijn, W., & Jong, J. (2012) Are symptoms of spirit possessed patients covered by the DSM-IV or DSM-5 criteria for possession trance disorder? A mixed-method explorative study in Uganda. Social Psychiatry and Psychiatric Epidemiology. DOI: 10.1007/s00127-012-0635-1  

Spiegel, D., Loewenstein, R., Lewis-Fernández, R., Sar, V., Simeon, D., Vermetten, E., Cardeña, E., & Dell, P. (2011) Dissociative disorders in DSM-5. Depression and Anxiety, 28(9), 824-852. DOI: 10.1002/da.20874  

  • January 12, 2013
  • 04:50 PM
  • 219 views

Fisher-Price Synesthesia

by The Neurocritic in The Neurocritic

Synesthesia is a rare perceptual phenomenon in which the stimulation of one sensory modality, or exposure to one type of stimulus, leads to a sensory (or cognitive) experience in a different, non-stimulated modality. For instance, some synesthetes have colored hearing while others might taste shapes.GRAPHEME-COLOR SYNESTHESIA is the condition in which individual printed letters are perceived in a specific, constant color. This occurs involuntarily and in the absence of colored font. It is the most common and widely-studied of all types of synesthesia (Mattingley, 2009). Many studies have suggested that the phenomenon is not due to associative learning, i.e. exposure to colored letters or blocks as a child (Rich et al., 2005). One neurological explanation is that it's due to greater white matter connectivity between the inferior temporal lobe regions that process letters and colors (Rouw & Scholte, 2007). 1Learned SynesthesiaHowever, a new study has identified 11 synesthetes whose grapheme-color mappings appear to be based on the Fisher Price plastic letter set made between 1972-1990 (Witthoft & Winawer, 2013). 2 Letter-color mapping data were obtained from the participants using either The Synesthesia Battery Web site (synesthete.org) or in-house software. This required that the subjects use a color picker to identify the hue of 26 upper case letters and 10 numerals three times each (presented in random order). They did this in two separate sessions, and then the consistency within and across sessions was evaluated. The participants also completed a speeded Stroop-like task, where they had to identify whether the color font was congruent (A) or incongruent (A) relative to their synesthetic mapping.Lo and behold, the resultant mappings were "startlingly similar" to the colors used in the Fisher Price toys from their childhoods! And 10 of the 11 participants reported owning the colorful plastic magnetic letters. In the figure below, the subjects are arranged left to right according to the number of matches with the Fisher Price set. S11 showed the fewest matches (n=14), yet the probability of obtaining 14 or more matches in 26 chances was estimated to be less than 1 in 1 billion...Fig. 2 (modified from Witthoft & Winawer, 2013). Letter-color matching data from the 11 subjects. The diagram shows the color selected for each letter, averaged across three trials for each subject. The left-most column indicates the colors of the Fisher-Price refrigerator magnets used by all but 1 of the subjects as children.Thus, the results provided clear evidence of a learned contribution to color-grapheme synesthesia, at least in this group of participants. But they don't negate a more purely perceptual version of the phenomenon in other synesthetes. The two synesthesiae can peacefully coexist:Whereas some researchers have focused on genetic and perceptual aspects of synesthesia, our results indicate that a complete explanation of synesthesia must also incorporate a central role for learning and memory. We argue that these two positions can be reconciled by thinking of synesthesia as the automatic retrieval of highly specific mnemonic associations, in which perceptual contents are brought to mind in a manner akin to mental imagery or the perceptual-reinstatement effects found in memory studies. Nonetheless, for some color-grapheme synesthetes, it's always a Red Letter A...Footnotes1 However, a newer study says it's more complicated than that (Hupé et al., 2012). These authors found that synesthetic letter experience did not activate color area V4, and that grapheme-color synesthetes did not show greater connectivity in the inferior temporal cortex:At the end, careful reading of the relevant literature casts some doubt on the textbook story that synesthetes activate “color area V4” when viewing achromatic graphemes (but experiencing color) and on structural brain differences reported between synesthetes versus nonsynesthetes.2  Interestingly, Witthoft and Winawer cited a 19th century study that proposed the same thing (Calkins, 1893).References Mattingley JB. (2009). Attention, automaticity, and awareness in synesthesia. Ann NY Acad Sci. 1156:141-67.Rich AN, Bradshaw JL, Mattingley JB. (2005). A systematic, large-scale study of synaesthesia: Implications for the role of early experience in lexical-colour associations. Cognition 98:53-84.Rouw R, Scholte HS (2007). Increased structural connectivity in grapheme-color synesthesia. Nature Neuroscience 10:792-797.Witthoft, N., & Winawer, J. (2013). Learning, Memory, and Synesthesia Psychological Science DOI: 10.1177/0956797612452573It's a Red Letter A...... Read more »

Witthoft, N., & Winawer, J. (2013) Learning, Memory, and Synesthesia. Psychological Science. DOI: 10.1177/0956797612452573  

  • January 5, 2013
  • 10:06 PM
  • 248 views

Spirit Possession as a Trauma-Related Disorder in Uganda

by The Neurocritic in The Neurocritic

The Lord's Resistance Army (LRA) has waged a long and brutal campaign to overthrow the government of Uganda. Rape and torture are commonly used tactics. Children are kidnapped and forced to serve as soldiers — children and youth comprise almost 90% of the LRA, according to the UN. These child soldiers experience incredibly high rates of trauma exposure, post-traumatic stress, and depression.A recent study examined the culturally-specific psychological syndrome of spirit possession in this population (Neuner et al., 2012). Although spirit possession is common in many cultures, the phenomenon investigated here is a local variant called cen, where "the ghost of a deceased person visits the affected and replaces his or her identity." It is particularly prevalent in former child soldiers who have killed others. Although some forms of spirit possession are considered relatively benign in Northern Uganda, cen is seen as harmful.It is important here to consider the complex role of religion and magical belief in motivating and sustaining the LRA (Jackson, 2010), along with socioeconomic and political grievances. The Acholi ethnic group has been depicted as marginalized victims of the Ugandan government by the LRA leader, Joseph Kony. Religion is used as a further means of control (Jackson, 2010):The quasi-religious aspects of Kony’s internal cosmology take this sense of victimhood and expand it, through a magpie-like propensity to adopt elements from other belief systems into which he has come into contact. The result is a hotch-potch of beliefs that are used to reinforce the idea that the Acholi are victims and Kony the mystic who can stop protect them. Violence, in this world-view, is conveniently seen as a means of ‘cleansing’ – an evil that is necessary to purify the Acholi so that they can be saved...Furthermore, the Neuner et al., (2012) paper notes that Kony......justified his claim to power by spirit possession and said to have supernatural abilities.1 It is reasonable to assume that this propaganda, which drew on widespread local beliefs, has been a fertile ground for the development of harmful forms of spirit possession in the local population, in particular former child soldiers. With this background in mind, the authors conducted a survey of 1,113 individuals between the ages of 12 and 25 yrs to determine the rates of spirit possession, trauma exposure, and psychological distress. The actual interviewers were members of vivo, an organization that provides psychosocial support to children in Northern Uganda. During a pilot study, the five-item Cen Spirit Possession Scale was developed (shown below).-- click on image for a larger view --Notably, a high level of spirit possession (four or more characteristics) was observed in 14.3% of those who were abducted, but only 3.7% of the participants who were not abducted. Girls were more likely to experience cen than boys. In addition, spirit possession was associated with extreme poverty, greater trauma exposure, sexual trauma, and being forced to kill. Most of the youths were treated via traditional means:Among those who had ever sought help for spirit possession, 15.2% had carried out the nyono tonggweno ritual (stepping on the egg in a cleansing ceremony), 7.9% mato oput (reconciliation ritual after killing), 7.9% lwoko pik wang (washing away the tears), 31.5% other traditional interventions, mainly taking traditional herbs, and 70.2% sought help at a church or from a priest. Cen led to worse outcomes compared to those without spirit possession, including higher suicide risk, lower functioning, greater perceived discrimination, and higher incidence of PTSD (44.5% vs. 9.8%).2 The authors conclude:Although cen was not limited to former child soldiers, they reported higher rates of spirit possession, which may be related to the fact that they were more intensely exposed to the LRA belief system.At the same time it has to be emphasized that spirit possession is usually not perceived as psychopathology within the local culture. Although our data is consistent with the association of cen with impaired mental health, a reduction of this phenomenon to mere psychopathology is inappropriate. The clinical perspective taken in this survey must be complemented by sociological, historical and anthropological studies investigating the cultural and social interpretation of this phenomenon.Given the cultural specificity of cen, it might be interesting to consider how Western psychiatry views cases of spirit possession.3 In DSM-IV, this syndrome would be classified as Dissociative Disorder Not Otherwise Specified, with more specific research criteria (but not official diagnosis) fitting Dissociative Trance Disorder (possession trance). Has this changed in DSM-5? We'll take a look in the next post.Footnotes1 The New York Times has a fascinating document that details Kony's religious beliefs. He was "possessed" by quite a large number of spirits...2 See also Remembering and Forgetting in Traumatized Ugandan Refugees.3 The film industry presents its own flamboyantly supernatural depiction of demon possession for entertainment, as we all know.ReferencesJackson P (2010). Politics, Religion and the Lord’s Resistance Army in Northern Uganda. Religions and Development, Working Paper 43. University of Birmingham.Neuner, F., Pfeiffer, A., Schauer-Kaiser, E., Odenwald, M., Elbert, T., & Ertl, V. (2012). Haunted by ghosts: Prevalence, predictors and outcomes of spirit possession experiences among former child soldiers and war-affected civilians in Northern Uganda. Social Science & Medicine, 75 (3), 548-554 DOI: 10.1016/j.socscimed.2012.03.028Grace, Milly, Lucy… Child Soldiers (trailer)... Read more »

Neuner, F., Pfeiffer, A., Schauer-Kaiser, E., Odenwald, M., Elbert, T., & Ertl, V. (2012) Haunted by ghosts: Prevalence, predictors and outcomes of spirit possession experiences among former child soldiers and war-affected civilians in Northern Uganda. Social Science , 75(3), 548-554. DOI: 10.1016/j.socscimed.2012.03.028  

  • December 30, 2012
  • 09:15 PM
  • 425 views

More Music, More Empathy

by The Neurocritic in The Neurocritic

Fig. 1 (Molnar-Szakacs & Overy, 2006). Model of the possible involvement of the human mirror neuron system in representing meaning and affective responses to music. ... The shared recruitment of this neural mechanism in both the sender and the perceiver of the musical message allows for co-representation and sharing of the musical experience. Music notes from ‘The Lady Sings the Blues’ by Billie Holiday and Herbie Nichols.The previous post examined the relationship between music and empathy, including the emotional connection that can occur between musician and audience. My thoughts on the issue were originally inspired by a quote in the book Rat Girl, a memoir by musician Kristin Hersh:...We'd play what the audience felt and feel it at the same time and they'd feel it reflected back to them in sound and we'd all care about each other's stories and clouds of feeling and ... good luck with that I think miserably through my stage fright, trudging past the knitters, hippies, junkies, drunks, painters and psychos.-Kristin Hersh, Rat Girl, p. 43Molnar-Szakacs and Overy (2006) suggested that these profound human experiences are mediated by activity in the supercharged mirror neuron system (Fig. 1).2 Although the box and arrow model is lacking in explanatory value, the hypothesis raised two questions: (1) Are musicians more empathetic? and (2) Do they engage the mirror neuron system to a greater extent than those without musical training?Are Musicians More Empathetic?Self-absorbed rock star stereotype aside, it would be difficult to determine causality if this were the case. Do more empathetic people choose to take up music (à la the tortured artist), or does musical training make one more empathetic? The best way to address question #1 is to look at those undergoing musical training. One such study reported that a 9 month-long program of musical group interaction (MGI) increased emotional empathy in 8-11 year old children (Rabinowitch et al., 2012). The MGI program consisted of musical "games" that seemed [to me, at least] designed to increase empathy, rather than musical prowess: entrainment games to be as rhythmically coordinated as possible, imitation games to repeat the musical phrases or gestures of the previous participant, and other games that called on the constructs of shared intentionality and intersubjectivity.Along with a passive control group that received no training, an active control group engaged in a verbal storytelling and drama version of group interaction that didn't involve music, singing, or gesture. It's notable that 33% of all children did not play a musical instrument (which included singing), so the study didn't really ask whether musical training per se can make you more empathetic. Nonetheless, there was a p=.054 level interaction of time (pre- vs. post-training) and group (MGI vs. both controls, who did not differ) on the self-report measure of empathy [which might have resulted from a higher pre-training empathy in controls, along with less improvement].Fig. 3 (Rabinowitch et al., 2012). Index of Empathy scores.However, the MGI and control groups improved to an equivalent extent on an emotional face matching task, also designed to measure emotional empathy. While it's probably beneficial for children to engage in these group activities, we do not yet have a positive answer to question #1.Do Musicians Show More Mirror Neuron Activity?This question has a trivial element to it: of course a trained violinist will have a greater understanding of the movements and sounds involved in Beethoven's Violin Concerto in D major, so you'd expect differences in brain activity somewhere to reflect this. There are at least two studies potentially relevant to question #2 (Chapin et al., 2010; Babiloni et al., 2012). In neither case, however, do we need to invoke the existence of the mirror neuron system.In the first, BOLD signal changes in response to two different versions of the same musical piece (Chopin's Etude in E major) were compared in an fMRI study (Chapin et al., 2010). One version was an expressive piano performance with dynamic stimulus fluctuations, and the other was a synthesized "mechanical" version. In addition, the participants had varying levels of musical training: 7 were experienced (mean 9.2 yrs training) and 7 inexperienced (0.7 yrs training), with 7 more thrown out for various reasons. These are very small groups by modern fMRI standards.3Participants rated their emotional arousal and emotional valence while listening to the pieces before and after scanning, but not during the fMRI experiment. The combined arousal and valence ratings were not consistently correlated across the two time points, so making inferences about what the participants were feeling during the experiment is dicey.The fMRI results showed different activation patterns according to the main effects of performance type and musical experience (shown below). Mirror neuron-ish areas (inferior parietal lobule, inferior frontal gyrus but too anterior) showed greater activation for the expressive piece in both groups (A), but these regions didn't differ as a function of musical experience (B).Fig. 4 (Chapin et al., 2010). fMRI ANOVA results. Brain activations (F-maps) showing a significant main effect of a) performance type (F (1,24) > 7.19, corrected p < .02), SCG = subcallosal gyrus, PHG = parahippocampal gyrus, vACC = ventral anterior cingulate, FPC = frontopolor cortex, DMPFC = dorsal medial prefrontal cortex; and b) main effect of musical experience, BG = basal ganglia, vStri = ventral striatum.But there was an interaction between performance type and musical training, with experienced participants showing greater activation for the expressive piece in the too-anterior-for-mirror neurons IFG and the inferior parietal lobe. Importantly, activation in the mirror neuron-ish areas related to tempo changes in the expressive piece did not differ according to musical training:An unexpected finding of this study was that, for all participants, the tempo fluctuations of the expressive performance correlated with dynamic activation changes in brain regions that are consistent with the human mirror neuron system, including bilateral BA 44/45, superior temporal sulcus, ventral PMC, and inferior parietal cortex, along with other motor-related areas and with insula.Thus, ... Read more »

Babiloni, C., Buffo, P., Vecchio, F., Marzano, N., Del Percio, C., Spada, D., Rossi, S., Bruni, I., Rossini, P., & Perani, D. (2012) Brains “in concert”: Frontal oscillatory alpha rhythms and empathy in professional musicians. NeuroImage, 60(1), 105-116. DOI: 10.1016/j.neuroimage.2011.12.008  

Chapin, H., Jantzen, K., Scott Kelso, J., Steinberg, F., & Large, E. (2010) Dynamic Emotional and Neural Responses to Music Depend on Performance Expression and Listener Experience. PLoS ONE, 5(12). DOI: 10.1371/journal.pone.0013812  

Rabinowitch, T., Cross, I., & Burnard, P. (2012) Long-term musical group interaction has a positive influence on empathy in children. Psychology of Music. DOI: 10.1177/0305735612440609  

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