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The Dark Side of Diagnosis by Brain Scan

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Daniel Amen: Pioneer or profiteer?: Psychiatrist Daniel Amen uses brain scans to diagnose mental illness. Most peers say that’s bonkers.


Right on the heels of a Molecular Psychiatry paper that asked, "Why has it taken so long for biological psychiatry to develop clinical tests and what to do about it?" (Kapur et al., 2012) comes this provocatively titled article in the Washington Post about neurohuckster Dr. Daniel Amen and his miraculous SPECT scans:
Daniel Amen is the most popular psychiatrist in America. To most researchers and scientists, that’s a very bad thing.

By , Published: August 9.

NEWPORT BEACH, Calif. — Daniel Amen is, by almost any measure, the most popular psychiatrist in America.

. . .

He has arisen, like a modern-day American myth, from the fields northeast of San Francisco, where he ran a small-town clinic, to become the creator, chairman and CEO of the Amen Clinics, an empire that includes a string of psychiatric practices, a line of nutritional supplements, book publishing, DVD sales, and television and speaking engagements.

. . .

Amen’s career is very troubling, for one of two things must be true.

One, Daniel Gregory Amen, born in 1954 in Encino, Calif., son of Lebanese immigrants, is 20 years ahead of virtually the entire psychiatric field (he says about three dozen other clinics use SPECT scans, but few as profusely as he does), and the establishment has failed to recognize a historic breakthrough.

Or, two, the man has grown fabulously wealthy — he lives in a $4.8 million mansion overlooking the Pacific Ocean — by selling patients a high-priced service that has little scientific validity, yet no regulatory body has made a move to stop him.

SPECT (single photon emission computed tomography) is a relatively inexpensive cousin of PET scanning (positron emission tomography) with lower spatial resolution.1 There is no peer reviewed literature that establishes SPECT as a reliable method of diagnosing psychiatric disorders.

Amen is well-known to regular PBS viewers, because his informercial "Change Your Brain, Change Your Life" [and others] is on regular rotation during fund raisers.2 In a critical Salon.com piece by Robert Burton, one neuroimaging expert was quoted as saying:
"SPECT scans are not sufficiently sensitive or specific to be useful in the diagnosis of A.D.," neurologist Michael Greicius , who runs the Stanford University memory clinic, and has a special interest in the use of functional brain imaging in the diagnosis of A.D., tells me. "The PBS airing of Amen's program provides a stamp of scientific validity to work which has no scientific validity."

In his Washington Post article, author Neely Tucker assembled an impressive list of naysayers:
No major research institution takes his SPECT work seriously, none regards him as “the number one neuroscience guy,” and his revelations, which he presents to rapt audiences as dispatches from the front ranks of science, make the top tier of scientists roll their eyes or get very angry.

“In my opinion, what he’s doing is the modern equivalent of phrenology,” says Jeffrey Lieberman, APA president-elect, author of the textbook “Psychiatry” and chairman of Psychiatry at Columbia University College of Physicians and Surgeons. (Phrenology was the pseudoscience, popular in the early 19th century, that said the mind was determined by the shape of the skull, particularly its bumps.) “The claims he makes are not supported by reliable science, and one has to be skeptical about his motivation.”

“I think you have a vulnerable patient population that doesn’t know any better,” says M. Elizabeth Oates, chair of the Commission on Nuclear Medicine, Board of Chancellors at the American College of Radiology, and chair of the department of radiology at the University of Kentucky.

“A sham,” says Martha J. Farah, director of the Center for Neuroscience & Society at the University of Pennsylvania, summing up her thoughts on one of Amen’s most recent scientific papers.

“I guess we’re all amateurs except for him,” says Helen Mayberg, a psychiatry, neurology and radiology professor at Emory School of Medicine and one of the most respected researchers into depression and brain scanning. “He’s making claims that are outrageous and not supported by any research.”

“I can’t imagine clinical decisions being guided by an imaging test,” says Steven E. Hyman, former director of the National Institute of Mental Health and current director of the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard.

But wait! Didn't The Neurocritic just write a post that expressed some degree of optimism about the prospect of a "stratified psychiatry" of phenotypic or genotypic subtypes at some unspecified future date?

But beware! This is not the same thing as using a SPECT scan to devise a treatment plan. In his NIMH Director's Blog, Dr. Thomas Insel singles out Amen and warns, Brain Scans – Not Quite Ready for Prime Time.


Where Are the Clinical Tests for Psychiatric Disorders?

In their paper, Kapur, Phillips, and Insel (2012) were careful to distinguish their projections for the future from diagnostic tests:3
The prospects of ‘diagnostic tests’ for DSM entities remain distant for reasons articulated above, and it seems unlikely that we will replace the 300-disorder taxonomy of the DSM-5 with an alternative biologically based classification system anytime soon. Therefore the real opportunity for psychiatry is to use the emerging advances in genetics, molecular biology, imaging and cognitive science to supplement, rather than replace, the symptom-driven diagnosis.

Dr. Amen is not so circumspect, in fact he's rather bullish:
He says he has taught himself — by scanning 45,000 people a total of 70,000 times — to apply SPECT, alongside clinical evaluations, as a diagnostic tool in 90 percent of his patients.

The brain activity he says he sees in these scans — areas of high and low activity — allows him to target those areas with specific treatments and medication, he says. A full initial session, including two scans, costs about $3,500.

Amen says this method has helped him identify new subtypes of anxiety, depression and attention deficit disorder, categories far more specific than even the forthcoming fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, the benchmark of the field.

This is heady stuff — using brain imaging to find biomarkers for mental illnesses has been the great hope of psychiatry for at least two decades...


And what are those treatments and medications? Exercise, healthy diet, supplements from his product line [e.g., Serotonin Mood Support], and prescription refills in some cases.




"Due to overwhelming popularity we are now offering the Brain on Joy Bar by the case (18 bars)."


Am I blue, Dr. Amen?

The SPECT scans often seem to be used as either a scare tactic or a form of reassurance:

Amen’s first scan patient, back in the early 1990s, was Sandy.

She was 40, had ADD and had tried to kill herself the night before their initial meeting. In his telling — it is his Genesis story, and he has told it many times — the resulting scan showed a precipitous drop in activity in her prefrontal cortex, the brain’s decision-making center, when she tried to concentrate.

When he showed her the scan, she wept. “You mean it’s not my fault?”

Realizing it was a “biological, not moral” problem, she accepted the diagnosis, took her medications and was greatly helped.

“I thought, ‘Whoa. Pictures matter. You get great compliance,’ ” Amen says.
Another patient said, “The results [of the scan] were a little disconcerting, but I’m glad to have it.”

And here's Amen's colleague Earl Henslin: “If at all possible, I’m motivating my patients to get that scan at the first session. They see that scan and they’re willing to take responsibility.”


A Picture Is Worth a Thousand Dollars

That's the title of a 2009 editorial by Dr. Martha Farah in the Journal of Cognitive Neuroscience. She argues that cognitive neuroscientists have a responsibility to speak out when clinical [and legal] applications of brain imaging are being misrepresented by for-profit companies such as the Amen Clinics:
Tens of thousands of individuals, many of them children, have been exposed to the radiation of two SPECT scans and paid thousands of dollars out of pocket (because insurers will not pay) against the advice of many experts... The Amen Clinics are now marketing their services outside the medical arena, advising couples with marital problems and even “prescreening” couples.

People are swayed by colorful brain images, whether they're in the classroom, the courtroom, or the clinic. Or on reality TV. SPECT scans should not be used for diagnostic or entertainment purposes; there's no scientific evidence for the former and the latter is unethical.


Further Reading

This Is the Presidential Candidates' Brains On...

On Amen's Dec. 2007 editorial in the Los Angeles Times advocating SPECT scans for presidential candidates.

Celebrity Neurostigma
On celebrity SPECT scans from celebrity patients in the reality show Celebrity Rehab with Dr. Drew. Also a lesson in medical ethics. Special guest appearance by Dr. Amen.

Dennis Rodman-Mindy McCready Mind Meld
On the startling similarities in the SPECT scans of Celebrity Rehab participants Dennis Rodman and Mindy McCready.


Footnotes

1In case you're interested in learning more about how the method works, this review chapter(by the Committee on the Mathematics and Physics of Emerging Dynamic Biomedical Imaging, National Research Council) is one place to start.

2In fact, I can tell when there's a PBS fundraiser because the number of visitors from a search of daniel amen quack increases.

3 However, new research applies machine learning algorithms to neuroimaging data in an attempt to classify patients with neurological and psychiatric disorders (Orrù et al., 2012).


References

Farah MJ. (2009). A picture is worth a thousand dollars. J Cogn Neurosci. 21:623-4.

Kapur S, Phillips AG, & Insel TR (2012). Why has it taken so long for biological psychiatry to develop clinical tests and what to do about it?Molecular psychiatry PMID: 22869033

Orrù G, Pettersson-Yeo W, Marquand AF, Sartori G, Mechelli A. (2012). Using Support Vector Machine to identify imaging biomarkers of neurological and psychiatric disease: a critical review. Neurosci Biobehav Rev. 36:1140-52.

WaPo link via @vaughanbell.


Predicting Brain Age from 231 Neuroanatomical Measures

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Is your child's brain on track to reach normal developmental milestones? A paper in Current Biology reports on a new, composite neuroanatomical metric of maturity that predicts 92% of the variance in brain age (Brown et al., 2012). Structural MRI scans were obtained from 885 healthy children and young adults ranging from 3 to 20 years of age. A set of 231 different measurements, or biomarkers, were used to determine the age that provided the best "fit" for each subject. The model made the most accurate predictions at the youngest ages, and the margin of error was 1.03 years across all ages.



Figure 3 (Brown et al., 2012). Multimodal Quantitative Anatomical Prediction of Age. For 885 individuals, estimated brain age is plotted as a function of actual chronological age. Colors correspond to different sites and scanners. Symbol size represents subject sex (larger = female, smaller = male). A spline-fit curve (solid line) with 5% and 95% prediction intervals (dashed lines) is also shown.



The 231 measures were chosen because they are "known or suspected to change over the ages" (Brown et al., 2012):
This collection of variables was derived from T1-, T2-, and diffusion-weighted imaging and included quantitative measures of brain morphology, signal intensity, and water diffusivity within different tissue types, reflecting anatomical structural organization. Specifically, we measured cortical thickness and area, volumes of segmented subcortical structures, normalized signal intensities, and measures of diffusion magnitude and directionality within cerebral, cerebellar, and white matter fiber tract regions of interest.

The data from each of these imaging modalities alone could explain 81-83% of the variance, and that number rose to 92% when the T1-, T2-, and diffusion-weighted images were combined. The relative contribution from each type of measure changed with age, as shown below.

Figure 4 (adapted fromBrown et al., 2012). Age-Varying Contributions of Different Imaging Measures to the Prediction of Age. The relative contributions of separate morphological, diffusivity, and signal intensity measures within different brain structures are plotted as a function of age. Colors correspond to measure and structure type (T1 cortical area; T1 cortical thickness; T1 subcortical volumes; diffusion (FA/ADC) within white matter tracts; diffusion (FA/ADC) within subcortical ROIs; T2 signal intensity within white matter tracts; T2 signal intensity within subcortical ROIs). Contributions are computed as units of the proportion of total explained variance.


The data were from the Pediatric Imaging, Neurocognition, and Genetics (PING) Study database (http://ping.chd.ucsd.edu), which is open access.
The primary goal of PING has been to create a data resource of highly standardized and carefully curated MRI data, whole genome SNP genotyping data, and developmental and neuropsychological assessments for a large cohort of developing children aged 3 to 20 years. The scientific aim of the project is, by openly sharing these data, to amplify the power and productivity of investigations of healthy and disordered development in children and to increase understanding of the origins of variation in neurobehavioral phenotypes.

Does it sound like the PING investigators are creating a normative database for possible diagnostic purposes in the future?
Perhaps further development of techniques to quantify the complex multidimensional nature of typical brain maturation can also help to improve the early identification of individuals with abnormal developmental trajectories. Our findings suggest that a multimodal neuroanatomical imaging assessment may hold promise for making an objective, quantitative contribution to our clinical evaluations of brain development.

Why yes it does. We already know this promise is not right around the corner (Where Are the Clinical Tests for Psychiatric Disorders?), and we know about the possible hazards of premature commercial ventures that make bold claims not supported by solid scientific evidence (The Dark Side of Diagnosis by Brain Scan). Returning to the first sentence of this post ["Is your child's brain on track to reach normal developmental milestones?"], you can see I was already anticipating franchised scanning facilities in strip malls ready to give worried parents the verdict on their child's neurodevelopment. Kind of like genetic testing outfits that make silly claims:
...unscrupulous businesses like My Gene Profile (which offers the "Inborn Talent Genetic Test" for the low low price of $1,397) have capitalized on the public's desire for simple explanations. Now you can find out whether your child has the Split Personality Gene! The Propensity for Teenage Romance Gene! The Self Detoxifying Gene!
The article in Biopolitical Times is highly recommended, especially since the mygeneprofile.com url seems to be defunct.1





To conclude with some important points about the Current Biology paper, the predictive accuracy of 92% is very impressive. The authors suggest there is a "latent brain phenotype that is tightly linked to chronological age." But they also issue a caveat about psychological maturity, which cannot be inferred from their measurements:
Brain scans, though informative about anatomical and physiological states, cannot be used to make inferences about an individual’s psychological maturity. Rather, these results speak only to the degree to which typically developing children differ among each other in their fundamental structural brain properties.


Footnote

1Biopolitical Times also mentioned the "sprawling website" that sells the "Inborn Talent Genetic Test", which you can still view via the Wayback Machine. [NOTE: EVERYONE wants their child to be the next Tiger Woods!]


Reference

Brown, T., and 21 others. (2012). Neuroanatomical Assessment of Biological Maturity. Current Biology. DOI: 10.1016/j.cub.2012.07.002

The Art of Delicate Sadness

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Sad Noh masks(from Fig. 1 of Osaka et al., 2012).


Noh is a traditional style of Japanese theater where the actors wear masks to convey facial expressions. Many of the masks are known for their ambiguity:
As it is often difficult to tell the actual feelings expressed in a noh mask, it is said to be made with a “neutral” expression. The mask carver tries to instill a variety of emotions in the mask.

It is up to the performer to imbue the mask with emotion. One of the techniques used in this task is to slightly tilt the mask up or down. With terasu (tilting upwards) the mask appears to be slightly smiling or laughing and the expression lightens somewhat. While kumorasu (tilting downwards), produces a slight frown and can express sadness or crying. Basically, by using minute movements, the performer is able to express very fully.

Three pictures of the same nō 'hawk mask' showing how the expression changes with a tilting of the head. The mask was afixed to a wall with constant lighting and only the camera moved.


Professor Michael Lyons has an excellent site explaining The Noh Mask Effect: A Facial Expression Illusion, which you really should see for yourself.


Delicate Sadness

A recent neuroimaging study by Osaka et al., (2012) set out to examine how the amygdala (a limbic structure important for emotion) would respond while participants viewed masks portraying "delicate sadness" -- "a Noh mask that is elegant and artistically polished, and designed to express sadness." To choose the most appropriate stimuli, a separate group of subjects rated a set of 70 masks on a scale of 1 (not at all sad) to 7 (highly sad). The six most "highly sad" masks were selected for comparison to six "neutral" masks. But as we already learned, the neutral masks can be ambiguous.

The amygdala (LeDoux, 2007) is predominantly known for its role in fear conditioning, but it is also activated by other emotions (e.g., Kober et al., 2008). Therefore, the comparison of viewing sad vs. "neutral" masks in the present study could yield minimal differences in the amygdala.

And that is what happened (in my estimation). However, the authors presented their results in a more positive light: a region of interest (ROI) in the right amygdala showed activation in the sad vs. neutral contrast at p<.05 (uncorrected). The ROI in the left amygdala, as well as bilateral "reward-related" ROIs in the nucleus accumbens, caudate nucleus, and putamen did not reach that level of significance. They concluded that:
...viewing Noh masks with expressions of elegant sadness effectively stimulates the right amygdala of the limbic system. Thus, the sadness evoked by such masks seems to be processed by the limbic system in a way similar to the way in which it processes negative emotions such as fear and disgust. Understanding the neurological processing of these facial expressions could effectively contribute to an appreciation of Noh performances in an artistic way.

But I'm not so sure the present finding illuminates the aesthetic and emotional experience of Noh theater. I think we need to understand more about how the brain processes basic emotions before we make neuroaesthetic claims.

I originally thought the study was interesting from the perspective of emotional ambiguity, where even the static images of those elegantly carved masks could capture multiple expressions simultaneously. A recent über meta-analysis of neuroimaging studies of emotion did not find support for the "locationist approach" where "discrete emotion categories can be consistently and specifically localized to distinct brain regions" (Lindquist et al., 2012). Hence, looking at amygdala and striatal regions in isolation will miss important aspects of emotional and aesthetic experiences engendered by viewing traditional Japanese Noh masks.


References

Kober H, Barrett LF, Joseph J, Bliss-Moreau E, Lindquist K, Wager TD. (2008). Functional grouping and cortical-subcortical interactions in emotion: a meta-analysis of neuroimaging studies. Neuroimage 42:998-1031.

LeDoux J. (2007). The amygdala. Current Biology 17: R868-R874.

Lindquist KA, Wager TD, Kober H, Bliss-Moreau E, Barrett LF. (2012). The brain basis of emotion: a meta-analytic review. Behav Brain Sci. 35:121-43.

Osaka N, Minamoto T, Yaoi K, & Osaka M (2012). Neural correlates of delicate sadness: an fMRI study based on the neuroaesthetics of Noh masks. Neuroreport, 23 (1), 26-9 PMID: 22113213

Complainers Kill Neurons! How to save yourself from this menace.

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"That pain you feel listening to complainers? It's real enough to peel away neurons from your brain and render it pretty much useless, reports Inc."

[That pain you feel reading ridiculous made-up articles about the brain? It's real enough to peel away neurons from your brain and render it pretty much useless, reports The Neurocritic.]

That's the worst piece of fiction I've read about the brain in quite some time. So I thought I'd complain about it. Read at your own risk!

Complainers Damage Neurons in the Brain

Entrepreneur Trevor Blake offers tips to save yourself

By Neal Colgrass, Newser Staff
Posted Aug 25, 2012 4:56 PM CDT


(Newser) – That pain you feel listening to complainers? It's real enough to peel away neurons from your brain and render it pretty much useless, reports Inc. "The brain works more like a muscle than we thought," says Trevor Blake, an entrepreneur who wrote Three Simple Steps: A Map to Success in Business and Life. "So if you're pinned in a corner for too long listening to someone being negative, you're more likely to behave that way as well."

The Neurocomplainer

Where to begin? With the distortion of scientific results beyond recognition in order to sell books? The use of such hyperbolic language? Or perhaps reliance on a business magazine as a primary source for neuroscience news. Oh but it gets worse...

But he offers tips for coping:

  • Get Away. Complainers are like chain-smokers who emit dangerous second-hand smoke, so simply move away from them.
  • Ask for a Fix. If you're cornered, suggest that the complainer find a solution. But most will just walk off because they "don't want a solution; they just want you to join in the indignity of the whole thing," says Blake.
  • Protect Yourself. When they just won't stop, delve into your bag of mental self-defense tricks. Imagining a protective, giant bell jar or invisibility cloak might work—or, like Blake, you could see yourself on a far-away island. "I could smile at them and nod in all the right places and meanwhile take myself for a walk on my private beach."
[Save me from Mr. Blake!]


Negative people are toxic, so let's abandon them. It doesn't matter if they're depressed about the foreclosure of their home or upset about being downsized due to corporate malfeasance or venting after being the target of yet another racist / sexist / homophobic insult or angry that their insurance company won't cover that critical medical procedure after all. Instead, ask them to fix the structural inequalities in society and then just move away from them.

[How to protect yourself from my complaining sarcastic blog posts: "Imagining a protective, giant bell jar or invisibility cloak might work."]



Surely the original Inc. article can't be that absurd! I'll let you be the judge...
Listening to Complainers Is Bad for Your Brain

. . .

Even worse, being exposed to too much complaining can actually make you dumb. Research shows that exposure to 30 minutes or more of negativity--including viewing such material on TV--actually peels away neurons in the brain's hippocampus.1 "That's the part of your brain you need for problem solving," he says. "Basically, it turns your brain to mush."
[30 seconds of exposure to Mr. Blake's book will basically turn your brain to mush.]


Speaking of Three Simple Steps (which -- in an amazing coincidence -- was published on August 23, 2012), there's something wrong with this picture...


While this item is available from other marketplace sellers on this page, it is not currently offered by Amazon.com because customers have told us there may be something wrong with our inventory of the item, the way we are shipping it, or the way it's described here.

Newser link via @TheNeuroScience.

Footnote

1 The hippocampus is critical for memory, not problem solving.




Feminist Dopamine, Conscious Vaginas, and the Goddess Array

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Does the Vagina Have a Consciousness?

Naomi Wolf, the famous feminist author and activist, asks that precise question in her new book, Vagina: A New Biography. At first glance, it strikes me as an uneasy balance of sex confessional, self-help, pop neuroscience, and new age goddessyoni worship.1
Could a profound connection between a woman’s brain and her experience of her vagina affect her greater sense of creativity—even her consciousness? In her provocative and important new book, ... bestselling author of The Beauty Myth Naomi Wolf argues that this connection is not only real—and long-overlooked—but that it is fundamental to a woman’s sense of self.

Spurred by the experience of an unexpected medical crisis – an injured pelvic nerve that temporarily affected her own physical sensation – Wolf set out to uncover why and how the brain and vagina are really best understood as “one system.” Understanding the brain-vagina connection, she learned, is not merely a key to more transformative sex for women – it is a key to female self-actualization, and thus to female power, creativity and confidence.

This unlikely combination of pseudoscientific and mystical elements provides a little something for everyone to hate. Among neuroscientists, howlers such as "dopamine is the ultimate feminist chemical in the female brain", oxytocin "is women's emotional superpower" and the vagina is "not only coextensive with the female brain but also is part of the female soul" have been making the rounds of social media.

I almost feel sorry for Ms. Wolf because it's like shooting fish in a barrel. Dopamine is not a feminist neurotransmitter, unless snails and insects have been secretly reading Betty Friedan and listening to Bikini Kill.



Chapter 4 of Vagina is on Dopamine, Opioids, and Oxytocin. Other than the excerpt and review in the Guardian, only three pages of the chapter were available online. But here's one choice quote:
Those of us who are not scientists often forget that brain chemicals are vehicles for very profound human truths.

I thought brain chemicals were vehicles that bind to receptors and trigger signal transduction molecules. Even the most reductionistic neuroscientists among us realize we are worlds away from understanding how oxytocin might explain morality (Paul Zak notwithstanding).

But feminist biology apparently tells us that the vagina is the delivery system for profound female truths:
By the same token, a female self's experience of freedom, and its impulse to seek more freedom, and to do so from a basis of self-love -- the feminist quest and the feminist sensibility -- are all strengthened in women by preorgasmic dopamine, and by the effect of orgasm on the brain. ... So in this way, the vagina is the delivery system for the states of mind we call confidence, liberation, self-realization, and even mysticism in women.

So women who aren't having orgasms cannot be confident liberated feminists?? Sure makes you wonder about Wolf's scientific sources...
An illustrated chart (see insert) compiled by dopamine researcher Marnia Robinson shows how dopamine affects human behavior in relationships and social settings.

When I hear "dopamine researcher", I think of experts like Nora Volkow, Kent Berridge, Wolfram Schultz, and Barry Everitt. I couldn't find any peer reviewed journal articles authored by Robinson. Instead, she has a blog at Psychology Today that promotes her book. Robinson's work is part of the neurorelationship self-help cottage industry, along with books and blogs like Rewire Your Brain for Love and Neuroscience and Relationships. Any knowledge of the brain is completely unnecessary for take-home messages that include the benefits of mindfulness meditation and tips for attaining goals.

Is Wolf at fault here? Was it her responsibility to contact actual experts (or even know who they are)? I can't say who else she might have consulted, having only read a small sampling. In Chapter 2, she cited a serious 1996 paper by Meston and Gorzalka on Differential effects of sympathetic activation on sexual arousal in sexually dysfunctional and functional women. But then she says:
The autonomic nervous system prepares the way for the neural impulses that will travel from vagina, clitoris, and labia to the brain, and this fascinating system regulates a woman's responses to the relaxation and stimulation provided by "the Goddess Array," the set of behaviors a lover uses to arouse his or her partner.

The Goddess and the autonomic nervous system -- together at last or odd bedfellows? In the end (or rather, the beginning), Vagina is part autobiography, and Wolf certainly exposes herself and her orgasms, which in my mind makes her even more vulnerable to personal attacks. I'll stick to the neuroscience for now, and await the sequel.

Forthcoming from Ecco: Penis: A New Biography by Jesse Bering.2


Footnotes

1However, I must declare that I haven't read the entire book, so some of these statements may not be entirely fair.

2Wait, or has he already published that?



The Electroencephalogram Cocktail Party

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In 2005, filmmaker Joyce Draganosky made a short entitled The Science of Love, where...
...the battle between reason and emotion takes center stage. A professor, who believes she has found a way of determining scientifically whether someone is in love, clashes with her department chair, a woman who thinks love and attraction are far too complex to be mapped according to the certainties of science.

The clip above highlights a hilarious event designed to determine the neural correlates of love. How does it work?
"Well, the goal is to identify the part of the brain that controls lust, and to show that it is different from the part of the brain that controls love. In order to do this we had to simulate as natural an environment as possible while still being able to measure neural activity. So I have created the Electroencephalogram Cocktail Party. An EEG Mixer!!"


Draganosky received an Alfred P. Sloan Foundation grant for The Science of Love. She spent a year researching the film, attending presentations and conducting interviews in the laboratory of Dr. Joy Hirsh at Columbia. "I actually audio-taped the interviews because I wanted to get all the scientist-speak perfectly right so that I could write accurate dialogue." We can certainly forgive the confusion of fMRI and EEG results for artistic sake (and comic effect) here. The lead character Syd seems to be modeled after Dr. Helen Fisher, even down to the combination of evolutionary anthropology with brain imaging.1


The Real EEG Mixer

Now, an actual study by Gevins and colleagues (2012) recorded EEG while 10 members of his lab attended a cocktail party furnished with food and alcohol:
The cocktail party was unscripted, other than withholding drinking for the first 10 minutes to record a pre-drinking baseline. The partiers intermingled, chatted, ate sushi and hors d'oeuvres and drank vodka martinis or vodka and cranberry cocktails according to their personal inclinations. They also measured BACs [breath alcohol content], took photos and checked up on the automated data collection.



The goal here was not to evaluate the effectiveness of EEG Speed Dating or to explicate a lofty ScienceofLove, but instead to examine the effects of alcohol on the spectral properties, or frequency composition, of EEG in a naturalistic setting. Although the technique of "hyperscanning"3 has been used in fMRI studies, the advantages of EEG recording in this context should be obvious.4

The participants served as both subjects and experimenters:
Teams placed headsets simultaneously on groups of participants; total set up time was about a half hour. Data from each EEG headset was transmitted during the party via Bluetooth protocol to its own dedicated notebook computer. The data were time synchronized across computers by a start signal sent via local Ethernet from one computer to all other recording computers.

They measured breath alcohol contents, took photos and checked the data collection.5



Using data obtained from two prior experiments (collected from separate groups of subjects in a more typical recording environment), multivariate divergence analyses searched for the subset of variables6 that best discriminated between the EEGs of brains on alcohol vs. brains on placebo. These equations were applied to the pre- and post-alcohol EEGs of the partygoers. Although 40% of the ambulatory cocktail party data were lost due to artifacts, the remaining data showed 80% sensitivity in recognizing alcohol and 80% specificity in recognizing no-alcohol. While mandatory Wearable Wireless EEG Fashion Accessories will not be replacing breathalyzers at sobriety stops any time soon, this was certainly a fun pilot study (especially for the participants)!


Footnotes

1Recycling Alert: this paragraph contains portions of my original 2006 review of the entire 18 minute short (combined with additional information). It's only two sentences, but I need to be forthcoming in anticipation of my future blogging gigs at Wired and the New Yorker.

2It looks like Neuroskeptic has already posted coverage of this study: Cocktail-Party Neuroscience.

3The hyperscanning technique was developed by Read Montague and co-workers (Montague et al., 2002). Typically, hyperscanning involves two subjects who interact with each other while playing a "trust" game. Their brains are scanned simultaneously (in adjoining or distant magnets). Specially developed software coordinates the experiments across sites.

4You can't walk around, eat, drink, and directly interact with others while lying in a scanner.

5 Who's real and who's fictional??

6 Technical details:
The individual frequency component powers were then averaged into 3 standard bands, theta (4–7 Hz), alpha (8–13 Hz) and beta (13–18 Hz) determined in prior studies to be sensitive to alcohol's effect on the EEG. The 3 banded powers and their standard deviations constituted a total set of 6 variables for each of the 7 electrode sites.
This is a very low number of variables; compare to a recent structural MRI study that used 231 neuroanatomical variables to predict brain age.


Reference

Gevins A, Chan CS, & Sam-Vargas L (2012). Towards measuring brain function on groups of people in the real world. PloS one, 7 (9) PMID: 22957099

Journomarketing of Neurobollocks

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Are you one of the few Anglophones who haven't yet heard about the frightening new fields of neuromarketing and neuroeconomics? Or that pop neuroscience is popular? Well thank god we have Steven Poole to set us straight!
Your brain on pseudoscience: the rise of popular neurobollocks

The “neuroscience” shelves in bookshops are groaning. But are the works of authors such as Malcolm Gladwell and Jonah Lehrer just self-help books dressed up in a lab coat?

By Steven Poole
Published 06 September 2012

An intellectual pestilence is upon us. Shop shelves groan with books purporting to explain, through snazzy brain-imaging studies, not only how thoughts and emotions function, but how politics and religion work, and what the correct answers are to age-old philosophical controversies. The dazzling real achievements of brain research are routinely pressed into service for questions they were never designed to answer. This is the plague of neuroscientism – aka neurobabble, neurobollocks, or neurotrash – and it’s everywhere.

It may be "everywhere" but it's been around for a while. But you wouldn't guess from reading Poole, who acts as if he's discovered this infectious plague all by himself. He hasn't noticed that many others before him have closely examined and criticized the misuse of brain science to sell self-help books or to advance an academic career. Even his neurowords are old, invented or popularized by other people. Raymond Tallis, for instance, is known for neurotrash and neuroscientism. But even Tallis didn't coin these words.1

Poole hasn't done his homework, which is unfortunate for someone who uses terms like "intellectual pestilence" as a casual insult. Perhaps he should know more about the fields he ridicules:

Happily, a new branch of the neuroscienceexplains everything genre may be created at any time by the simple expedient of adding the prefix “neuro” to whatever you are talking about. Thus, “neuroeconomics” is the latest in a long line of rhetorical attempts to sell the dismal science as a hard one; “molecular gastronomy” has now been trumped in the scientised gluttony stakes by “neurogastronomy”; students of Republican and Democratic brains are doing “neuropolitics”; literature academics practise “neurocriticism”. There is “neurotheology”, “neuromagic” (according to Sleights of Mind, an amusing book about how conjurors exploit perceptual bias) and even “neuromarketing”.

Let's see, Wired had a 1999 piece on neurotheology, and Sharon Begley wrote about it in 2001 (Your Brain on Religion: Mystic visions or brain circuits at work?). Neuroeconomics has been around since the late 1990s, and has desperately tried to distinguish itself from its more applied cousin (neuromarketing, a term coined in 2002).2 And lots of people, apparently, are doing “neurocriticism” of various sorts (e.g., this blog and neuro-lit-crit and Critical Neuroscience).

But here's Poole again:
Hoping it’s not too late to jump on the bandwagon, I have decided to announce that I, too, am skilled in the newly minted fields of neuroprocrastination and neuroflâneurship.
Why yes, it is a bit late to jump on the bandwagon...


Nonetheless, there are some wonderful quotes from Professor Paul Fletcher, who...
...gets “exasperated” by much popular coverage of neuroimaging research, which assumes that “activity in a brain region is the answer to some profound question about psychological processes. This is very hard to justify given how little we currently know about what different regions of the brain actually do.” Too often, he tells me in an email correspondence, a popular writer will “opt for some sort of neuro-flapdoodle in which a highly simplistic and questionable point is accompanied by a suitably grand-sounding neural term and thus acquires a weightiness that it really doesn’t deserve. In my view, this is no different to some mountebank selling quacksalve by talking about the physics of water molecules’ memories, or a beautician talking about action liposomes.”

But these important points get buried in the bile inflicted on Jonah Lehrer and Malcolm Gladwell. Haven't they been beaten to death already? And it's not at all clear why he would go after distinguished cognitive scientist Dr. Art Markman and lump him in with the highly discredited agenda of neurolinguistic programming:
Mastering one’s own brain is also the key to survival in a dog-eat-dog corporate world, as promised by the cognitive scientist Art Markman’s Smart Thinking: How to Think Big, Innovate and Outperform Your Rivals. The field (or cult) of “neurolinguistic programming” (NLP) sells techniques not only of self-overcoming but of domination over others.

Markman's book has different subtitles in the US and the UK, but it doesn't yammer on about neuro-anything, from what I can tell (and only mentions the word "brain" 7 times).

A number of neurobloggers and journalists have been tackling shoddy neuroscience for years, whether in journal articles or books or mainstream media.3The Neurocritic has extensive coverage of books [and other claims] by Louann Brizendine and Daniel Amen, for instance, along with copious criticism of media coverage and press releases that distort and exaggerate neuroscience findings.

Along with Mind Hacks, one of the major influences on this blog was Bad Neurojournalism (later renamed the Neuro-Journalism Mill), a collection of bad neuroscience journalism from 1998-2009, compiled by a comedian at the James S. McDonnell Foundation. A few examples (all definitely worth the click):
2000-10-28 Looking for That Brain Wave Called Love: Humanities Experts Use MRI's to Scan the Mind for the Locus of the Finer Feelings

2000-03-04 Men's Brains Have More Cells, Say Scientists Who Counted

2000-03-14 Just What's Going On Inside That Head of Yours? 4

There's always room for snarky new neurocriticism, Mr. Poole, but please realize that simplified pop visions of oxytocin and dopamine and mirror neurons have been under siege for years.

FYI - Steven Poole is the author of the forthcoming book “You Aren’t What You Eat”, which will be published by Union Books in October.


Footnotes

1For a short primer, we return to 2006 and the entertaining neuroword contest hosted by Neurofuture. Among the entries:

neurotrash: a group of attractive, progressive, and fashionable young neuroscientists of non-european heritage. (M. Miller)

neurosceptic: someone who doubts grand media claims made on behalf of neuroscience. (Vaughan Bell)

neurogibberish: Seemingly impressive jargon used by some neuroscientists to hide lack of real findings. (E.)

neuroessentialism: the belief in, or tactic of, invoking evidence, or merely terms, from neuroscience to justify claims at the psychological level. See also neuromysticism, neurobollocks. (Tom Stafford)

2According to Paul W. Glimcher:
Neuroeconomics is a purely academic discipline concerned with the basic mechanisms of decision-making. In contrast, Neuromarketing is a more applied field concerned with the application of brain scanning technology to the traditional goals and questions of interest of marketers, both those in academia and those in private industry. While these two disciplines are related, they are also very distinct. This is a distinction often overlooked by the popular media.

3Bad Science, BishopBlog, Daniel Bor, Ed Yong, LawsNeuroBlog, Mind Hacks, Neurobonkers, Neurophilosophy, Neuroskeptic, Neuron Culture, Oscillatory Thoughts, Scicurious, etc. [NOTE: I may keep adding to this list.]


4 The seductive allure of fMRI was initially revealed by the New York Times in 2000:
The technology is seductively easy to use, said Dr. Christopher Moore, a postdoctoral fellow at Massachusetts General Hospital in Boston who is carrying out a number of imaging studies. ''You can think of an idea, throw five friends into the scanner overnight and write up your results the next day. People don't have to think very hard about what they're doing.''

-from Just What's Going On Inside That Head of Yours?
By SANDRA BLAKESLEE
Published: March 14, 2000

Of Mice and Women: Animal Models of Desire, Dread, and Despair

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Scene from Mon Oncle d'Amérique by Alain Resnais


Dr. James G. Pfaus, a Professor of Psychology at Concordia University in Montreal, recently wrote a post in defense of Naomi Wolf's neuroscience acumen. This is understandable, as he was one of her main sources of scientific information about the "brain-vagina connection" in Vagina: A New Biography. Wolf, as you know, has been under fire for her simplistic and gendered treatment of cortisol and dopamine, as if these chemicals have highly specific effects on adult feminist women (and their vaginas), but no one else.1

Pfaus's general reply to that line of criticism is that we should let Wolf have poetic license with her storytelling:
Is Wolf right in regarding dopamine as the "ultimate feminist neurochemical"? It is certainly unlikely that sea slugs and nematode worms are feminists. But can't we allow an accomplished writer and social critic a little poetic leeway to make a point?

In Who's Afraid of the Vagina-Brain Connection? Pfaus also described some of his work on the sexual behavior of female lab rats:
Wolf's search took her, among other places, to my laboratory. We had been doing research on the role of clitoral and vaginocervical stimulation in the sex and reproductive lives of female rats, work that has been published in high-quality peer-reviewed scientific journals. This work revealed that such stimulation, when applied in the right way, induces a state of sexual reward that conditions place and partner preferences (the latter of which was unexpected in an allegedly promiscuous and polygamous species). Taken together with previous work from my laboratory showing the profound role of dopamine and opioid neurotransmitters in both male and female sexual behavior, and in the context of a more general scientific literature in animals and humans showing that blockade of those transmitters induces varying degrees of an "anhedonic" state akin to depression in which reward does not occur and animals do not focus their attention toward it anymore, it became clear to Wolf that these neurochemicals were important parts of the sexual desire and pleasure systems of the brain.  

Pfaus is a prolific scientist whose work ranges from basic animal models and translational research to establishing definitions for human sexual disorders. Now that more of Vagina is online at Amazon, I see that Wolf relied heavily on his research (he's mentioned 26 times), and that she cited many original sources from the scientific literature (albeit not always correctly).2

Which brings us to animal models for what we typically regard as profoundly human states: longing, angst, futility.  Or Desire, Dread, and Despair. The words don't easily lend themselves to rodent analogues, because they remind us of an unrequited crush or an existential crisis. Certainly, rats don't write love letters or read Kierkegaard or appreciate Expressionist art. Dark Night of the Soul (the original poem) was written by a Roman Catholic mystic to describe the painful journey of a bride (soul) in search of her groom (God). Today it indicates a spiritual crisis, a state of profound aloneness, a crushing existential despair.

The animal models of these states are more mundane and less abstract, yet important for potentially explaining the neural mechanisms underlying human suffering: addiction, anxiety, and depression. But are they really adequate stand-ins for the human condition? Of course not. My purpose here isn't to critique animal research, but rather to consider actual behaviors and how they map onto the terminology used to describe them.

Desire

For our present purposes, desire is defined in terms of sexual behavior. Specifically, sexual desire includes the anticipation of and motivation for participation in sexual activity. In rats, "Desire is inferred by certain measures, such as solicitations, rates of pacing (in which female rats control the initiation and rate of copulatory contact with male rats), and the strength of operant behavior aimed at acquiring sex partners" (Pfaus, 2006).

Modified from FIG. 1 (Pfaus, 2006). Incentive sequences for human and rat sexual behavior (modified from Pfaus et al., 1999). The behavioral stream moves from left to right, through appetitive, precopulatory, and consummatory phases of behavior. This conforms to the movement of animals from distal to proximal to interactive with respect to the sexual incentive.

In Fig. 1 we can see that female rat Excitement (grooming, investigation, motor activation) maps onto female human Sexual Desire (fantasy, excitement). Sexual fantasy is decidedly absent from the repertoire of rats, so conditioning and preference paradigms serve that purpose. Meanwhile, female rats show subsequent stages of defensiveness and lordosis, while female humans get to have orgasms. Fig. 2 in the Pfaus paper shows four panels of appetitive and consummatory measures of copulation in a pair of rats. Solicitation, investigation, running away, pursuit, lordosis, and mounting took all of 4 seconds. This goes on for several bouts until the male ejaculates. Wolf's "Goddess Array" is nowhere to be found.

Indeed, one of the places where Wolf went most astray in Vagina was in her wild extrapolations from the neurobiology of Pfaus's rats to the "Goddess Array" and what women need sexually: candles, flowers, music, or some other romantic gesture ("A whole set of words, actions, and gestures that women cannot do without"). Even if this were universally true, it obviously involves the kind of cognitive capacity well beyond rats.

Nonetheless, a major goal of the animal model is to serve as a preclinical testing ground for perceived sexual dysfunction in humans, including the categories of Hypoactive Sexual Desire Disorder (HSDD) and Female Sexual Arousal Disorders, which are distinct (and yet overlapping, according to some). In his accurately (but inelegantly) titled review Of rats and women: preclinical insights into the nature of female sexual desire, Pfaus (2006) stated:
Many clinicians and motivational theorists alike view desire as distinct from arousal in both animals and humans. This is apparent in the DSM’s categorization of arousal disorders distinct from desire disorders, a distinction that generally reflects blood flow to the genitals and erectile tissues versus a ‘psychological’ sexual interest in which individuals ‘want’ or ‘crave’ sex (Robinson & Berridge, 1993).

The neurochemical distinctions between ‘wanting’ [incentive salience] and ‘liking’ (in sum, dopamine vs. opioids) have been extensively studied by Kent Berridge and colleagues as applied to addiction. However, simplistic notions that low dopamine = low libido and depression in women (Wolf, p. 57) are not clearly supported by the literature.3

It's also important to note that HSDD is a controversial clinical diagnosis, one given to women who have a low (or nonexistent) libido and are distressed about it. However, desire is highly subjective, and what might be distressing to one woman is of no concern to another. Examining the causes of diminished sexual desire is critical, and these can include non-sexual health problems, menopause,4 a house full of kids, relationship issues, and having a crappy lover. Dr. Petra Boynton has written extensively about the problematic aspects of the HSDD diagnosis and the screening tools used to assess it, as well as the medicalization of sexuality for pharmaceutical marketing purposes.5

In general, you know that something is nosologically amiss when a review article claims that "Over 50% of women are believed to be affected by female sexual dysfunction" (Woodis et al., 2012). Which brings us to a state of dread...


Naomi Watts and Laura Elena Harring in Mulholland Drive


Dread

Desire can turn to dread very quickly in human relationships. This is also true in the rat mesolimbic dopamine system. Recent studies (e.g., Faure et al., 2008) have suggested that "desire" and "dread" reside in close proximity in the nucleus accumbens (NAc). Appetitive and aversive motivations can be elicited by manipulations of glutamate or GABA systems located only millimeters apart in the NAc.(Richard & Berridge, 2011):
NAc and dopamine-related circuits are best known for roles in appetitive motivation, but are also implicated in some forms of aversive motivation related to fear, stress, disgust, and pain. Within medial shell of NAc, neuroanatomical coding plays an important role in determining appetitive versus fearful valence of intense motivations generated by glutamate disruptions.

Scene from Rabbits by David Lynch

The measured behaviors in these experiments are actually called "desire" and "dread" (Richard & Berridge, 2011; 2012). Desire is the time spent eating food chow pellets, and dread (fear) is the time spent kicking up crushed corn cob bedding at threatening stimuli, a behavior known as defensive treading. The figure below shows an anterior-posterior gradient for desire and dread in the NAc medial shell. The glutamate AMPA receptor anatgonist DNQX was microinjected alone or in combination with D1/D2 dopamine antagonists into subregions of the NAc. Glutamate disruption in the anterior region induced eating, but glutamate disruption in the posterior region induced defensive treading. Both effects were reversed by dopamine antagonists, suggesting that the behaviors were mediated by dopamine.




Modified from Fig. 3 (Faure et al., 2008). Magnitude of increases in food intake (A) and defensive treading (B) behaviors elicited by DNQX, mixture, or vehicle microinjections in the anterior and posterior halves of the medial shell of the nucleus accumbens. *p< 0.05; **p< 0.01; #p< 0.05, anterior versus posterior. Error bars indicate SEM.


In real life, it seems that such anatomically discrete manipulations of NAc would not be the norm. This might suggest that a mixed feeling of desire and dread is more typical: you want to eat that donut bacon cheeseburger but fear the extra pounds (or a heart attack). Or you desire the sultry stranger who showed up in your shower but dread the consequences of unravelling the mystery (or at least you do in a David Lynch movie).




Fortunately, the NAc is sensitive to emotional context, so the "desire-dread" map can show plastic changes according to the current environment (Reynolds & Berridge, 2008). Under standard conditions (neither very safe nor very stressful), there's a yellow zone of ambiguity in the middle.

Figure 3 (Reynolds & Berridge, 2008). Summary map of glutamatergic valence generation in the medial shell. Purely appetitive sites are shown in green (where DNQX elicited only eating or drinking behaviors). Purely fearful sites are shown in red (where DNQX elicited only defensive-treading behavior). Ambivalent or mixed valence sites are shown in yellow (where DNQX microinjection elicited both appetitive-eating behavior and defensive-treading behavior from the same rat). The home environment expanded the purely appetitive zone compared with the standard environment, whereas the stressful environment (Iggy Pop music at 80-86 dB) expanded the fearful and ambivalent zones.


Ambivalent states are more computationally intensive for the Bayesian brain, and preferences for novel, surprising, and even inexplicable experiences (such as Mulholland Drive) present a challenge for Bayesian theorists and their "free energy principle" (see Free-energy minimization and the dark-room problem), which seeks to reduce uncertainty. Motivations aren't always clear-cut, even in rat NAc. Fortunately, the NAc doesn't exist in isolation, and top-down influences from medial prefrontal cortex can bias or suppress intense motivations (Richard & Berridge, 2012).

For other realms of dread, there's a very large literature on fear conditioning, as most of you know.

Despair

I'll end this essay on a brief note of despair. Rodent models of depression might be the largest of the three D's, in terms of neuroscience research (Cryan et al., 2002). In The Abject Self:Self-States of Relentless Despair, psychotherapist Dr. Kathleen Adams discusses the anguished experience of abject states in her patients:
In her opus on the powers of horror, Kristeva (1982) delineates a realm of preverbal experience permeated by affects of meaninglessness, dread, and horror. Her constructs of abject states and self-abjection are complex amalgams of identity, attachment disorganization, affect, and enactment.  ... Whereas the masochist suffers to gain nurture, the abject self suffers in the certain knowledge that he/she is beyond help.
...  In the grip of abject feelings, one feels unworthy, unlovable, and in utter despair about the situation ever changing.

That terrifying sense of existential dread and aloneness is not exactly captured by animal models of behavioral despair. There's a gaping chasm between Kristeva's abject states and depressive-like behaviors in mice exposed to chronic stress. The animals may give up in the forced swim test, but they're not filled with self-loathing in the face of their inadequacy.

I tried to write in greater detail about this topic in 2009 but gave up. In despair of ever finishing. The post was titled Is There a Valid Animal Model of Depression? but the literature was too large to sufficiently summarize in a single post. In fact, you might need an entire blog that touches on these issues, so head right over to Functional Neurogenesis to read the posts tagged anxiety/depression. Oh, and you can take a look at my early attempt from six years ago: Sad Cingulate on 60 Minutes and in Rats.


I don't care if you're sad
I don't care if you're heart is breaking
You soothe me and you turn me on
Speed and sleep

-Throwing Muses, Speed and Sleep



 

Footnotes

1 My pull quote from an initial read of the available excerpts was:
Dopamine is not a feminist neurotransmitter, unless snails and insects have been secretly reading Betty Friedan and listening to Bikini Kill.

2 However, the sources she used were misstated at times... as in this gift that just keeps giving (Vagina, p. 290):
Specific scents have been found to boost vaginal blood engorgement: cucumbers and Good & Plenty candies both are at the top of the vaginal-engorgement-activating scents, according to one study (and both are phallic in shape).
"Honey, I'm tired of the cucumber. Can we use the Good & Plenty tonight?" But seriously, she cited Zhou and Chen (2008) for this, which is incorrect. Who fact checked this book??

3 For example, in a group of individuals with Parkinson's disease (all of whom were under dopaminergic treatment), Celikel et al. (2008) found that: "Female patients had reduced sexual drive and they were less satisfied with orgasm, while male patients had easier orgasms than did the controls." Wolf cited a study that reportedly found "a link between well-functioning dopamine (and norepinephrine) systems and strong female sexual response" (p. 58), but the authors themselves did not observe that: "Our prediction that women with HSDD and FSAD would show substantially lower DA and NE responses to sexual stimuli was not supported" (Meston & McCall, 2005). Finally, the dopamine and norepinephrine reuptake inhibitor bupropion has been shown to improve sexual functioning in some studies of depressed humans, but it had no effect on sexual motivation and copulatory behavior in female rats (López et al., 2007). Also see a detailed post by David Dobbs, in response to Dr. Pfaus.

4 Naomi Wolf is about to turn 50, and I predict she's already working on a sequel to Vagina: A New Biography -- one that involves menopause. 

5 I've previously written about neuroimaging studies of Hypoactive Sexual Desire Disorder: Media HSDD: "Hyperactive Sexual Disorder Detection"  and Underwear Models and Low Libido.

6 Original by David Lynch, one of his photos from the collaborative work Dark Night of the Soul. Rodents extra.


References

Adams K (2011). The abject self: self-states of relentless despair. International journal of group psychotherapy, 61 (3), 332-64 PMID: 21728704

Celikel E, Ozel-Kizil ET, Akbostanci MC, Cevik A. (2008). Assessment of sexualdysfunction in patients with Parkinson's disease: a case-control study. Eur J Neurol.15:1168-72.

Cryan JF, Markou A, & Lucki I (2002). Assessing antidepressant activity in rodents: recent developments and future needs. Trends in pharmacological sciences, 23 (5), 238-45 PMID: 12008002

Faure A, Reynolds SM, Richard JM, & Berridge KC (2008). Mesolimbic dopamine in desire and dread: enabling motivation to be generated by localized glutamate disruptions in nucleus accumbens.  Journal of neuroscience, 28 (28), 7184-92 PMID: 18614688

López HH, Wurzel G, Ragen B. (2007). The effect of acute bupropion on sexual motivation and behavior in the female rat. Pharmacol Biochem Behav. 87:369-79.

Meston CM, McCall KM. (2005). Dopamine and norepinephrine responses to film-induced sexual arousal in sexually functional and sexually dysfunctional women. J Sex Marital Ther. 31:303-17.

Pfaus JG (2006). Of rats and women: preclinical insights into the nature of female sexual desire Sexual and Relationship Therapy, 21 (4), 463-476: 10.1080/14681990600967011

Reynolds SM, Berridge KC. (2008). Emotional environments retune the valence ofappetitive versus fearful functions in nucleus accumbens. Nat Neurosci. 11:423-5.

Richard JM, Berridge KC (2011). Nucleus accumbens dopamine/glutamate interaction switches modes to generate desire versus dread: D(1) alone for appetitive eating but D(1) and D(2) together for fear. Journal of Neuroscience, 31 (36), 12866-79 PMID: 21900565

Richard JM, Berridge KC (2012). Prefrontal Cortex Modulates Desire and Dread Generated by Nucleus Accumbens Glutamate Disruption. Biological psychiatry PMID: 22981656

Snyder JS, Soumier A, Brewer M, Pickel J, Cameron HA. (2011). Adult hippocampal neurogenesis buffers stress responses and depressive behaviour. Nature 476:458-61.

Wolf N (2012). Vagina: A New Biography. Ecco Press.

Woodis CB, McLendon AN, Muzyk AJ. (2012). Testosterone supplementation for hypoactive sexual desire disorder in women. Pharmacotherapy 32:38-53.

Zhou W, Chen D. (2008). Encoding human sexual chemosensory cues in the orbitofrontaland fusiform cortices. J Neurosci. 28:14416-21.


Untitled (Little Girl #1), Dark Night of the Soul6


Law and Order: Psychiatry Unit

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Crime dramas on American television are known for loosely adapting actual news stories "ripped from the headlines" and calling them fiction. Law and Order: Special Victims Unit is especially known for this pattern. For instance, in one episode last year a much beloved basketball coach who runs a charitable foundation was found guilty of sexually abusing his young players over the course of many years.


















In another episode, a well-known politician's long-kept secret is finally revealed after 13 years: the child he fathered with the family housekeeper.
















I thought I would do SVU executive producer Dick Wolf a favor and present a unique psychiatric case study that can be adapted for the small screen.  Since it's unknown to the American viewing public (and most everyone else), it will seem like a more original idea.


Patient Presenting with Stockholm Syndrome Ultimately Diagnosed with Münchausen Syndrome and Dissociative Identity Disorder

{SPOILER ALERT: it ends badly.}

A troika of unusual and spectacular psychiatric disorders was observed in one Dutch patient, as reported by Spuijbroek et al. (2012):
A young female of indeterminate age called a crisis hotline several times in the course of a month, giving accounts of severe sexual abuse, kidnapping by her father, and membership in a sect in the recent past. She spoke by preference to male staff members, was difficult to understand, and used a high-pitched, childlike voice. She provided different names and addresses that proved to be wrong. “God,” “men and women,” and “good and evil” were regular topics...

After a few weeks, she expressed suicidal feelings, saying she wished to go to God, and she agreed to be admitted to a local psychiatric hospital. She left, however, after 1 day. One month later, she was hospitalized again, using a different family name. She stated that she was 19 years of age and claimed to have been severely abused by her father and other sect members. ... Her isolation from the outside world, the power imbalance, her sympathy for her abusing father, and her unwillingness to escape the life-threatening situation were consistent with the clinical picture of Stockholm syndrome.

In cases of Stockholm syndrome, a person held hostage or captive comes to strongly identify and bond with her captor. Here, the patient claimed she was kidnapped into a religious cult and sexually abused, yet she felt sympathy for her abusers (which included her own father). However, it soon became apparent that she was not telling the truth:
At first, the personal information provided by the patient could not be verified. After several weeks,  however, her identity was revealed by police detection. The patient turned out to be a 27-year-old woman who had been reported missing 3 weeks earlier by her family. The patient had been receiving mental health care since childhood; she also had financial debts and was at risk of losing her housing. She had wandered about for several years, presenting regularly at various hospitals with a variety of somatic and psychiatric symptoms. She also frequently contacted the police with very detailed and alarming stories that were impossible to verify...

The patient at first seemed unaffected by the disclosure of her identity, but after some days she showed concern. She was uncomfortable at the reunion with her parents. Gradually her behavior changed: she answered to her own name now, and she would speak with female staff members. A few weeks later, the patient said that she could not remember anything about the period when she was admitted to the hospital...

Thus, paradoxical elements of both Münchausen Syndrome (deliberately fabricating an illness) and a dissociative disorder (involuntary rupture of memory, awareness, identity and/or perception) were observed. The diagnosis of Stockholm Syndrome was withdrawn, and psychotic disorders were ruled out:
...The patient did not report hallucinations. While her stories were often improbable, they were never bizarre, and no cognitive impairment was found. Given the many moments of acuity and social responsiveness displayed by the patient, the picture was inconsistent with schizophrenia. The family reported that the patient had fabricated fantastical stories since she was a little girl. Fugue-like states with periods of unexplained peregrination or wandering may have occurred as well. Nevertheless, the patient was regularly able to contact others, continuing her telephone calls to mental health workers and other health care professionals, in a very consistent way. After her identity was disclosed, “Munchausen syndrome,” with imitation of both mental and somatic conditions, turned out to be the most likely description of the patient’s condition.

An additional examination of the patient was conducted by specialists from a regional psychological trauma center... their assessment revealed the following cluster of severe dissociative symptoms: derealization, fugue, depersonalization, amnesia, identity confusion, pseudoepileptic seizures, sleep problems, and self-damaging behavior. Although it was recognized that the patient was suffering from pseudologia fantastica [pathological lying], her dissociative symptoms were regarded as serious and authentic...

The court ordered the patient to be hospitalized for 6 months. During this time she was prescribed a series of medications (including antidepressants, antipsychotics, and benzodiazepines), none of which were effective. She became suicidal. Although her suicide attempts were characterized as "ambivalent", it was unfortunate that she ultimately succeeded while in hospital:
After several months, suicidal tendencies and a desire for euthanasia were a regular topic of conversation for the patient. Several times during her hospitalization, she demonstrated overt suicidal behavior: two medication overdoses, once walking on railroad tracks, and twice putting a plastic bag around her head. These attempts seemed ambivalent, since the chance of detection by staff members was relatively high. The patient was placed in seclusion because of heightened suicidal risk several times, leading to increased fear and tension within the therapeutic relationship. After 7 months, the patient suicided on the ward by suffocation with a plastic bag...

The clinical case discussion ends with COMMENTARY by David A. Kahn, MD [imagine a voice-over by Rod Serling]:
Why have I been haunted by this case report of a mysterious, unfortunate woman who was never truly knowable? The treating staff was ambivalent in its diagnoses of both Munchausen syndrome, which is the intentional feigning of illness, and DID [dissociative identity disorder], or the unintentional adoption of two or more personalities or identities. These appear to be in contradiction, ironically a most accurate reflection of the emotions evoked by the patient who appeared both manipulative but also helplessly unable to control herself and tell a true story. Who was she? Did she know or not know? Was she putting them on, or was she actually unsure of who she really was? Her final act of suicide was a forceful if equally ambiguous communication, as non-verbal as her others, but the authors suggested that it indicated both a growing attachment to the first treatment team that would be lost with transfer to a specialized trauma program, and terror or rage at feeling either found out, or held captive. The first explanation, loss that could not be expressed in words, supports dissociation—an unconscious reaction to immense pain. The second explanation, exposure and entrapment, might suggest antisocial traces more consistent with Munchausen syndrome.

The expository feature of post-episode commentary by a medical expert would distinguish Law and Order: Psychiatry Unit from other series in the franchise. Or the show could be taken in a more haunting and profound direction, which would be a clear departure from the usual police procedural. The Psychiatric Twilight Zone, perhaps?


Reference

Spuijbroek EJ, Blom N, Braam AW, & Kahn DA (2012). Stockholm syndrome manifestation of Munchausen: an eye-catching misnomer. Journal of psychiatric practice, 18 (4), 296-303. PMID: 22805905

Surrealistic Imaging Experiment #1

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"The case against the realist position needs to be considered, after considering the materialist position. The latter, more poetic however than the former, admittedly implies on the part of a Man, a monstrous pride, but not a new and more complete degeneration. It should be seen, above all, as a welcome reaction against certain ridiculous spiritualist tendencies. Ultimately, it is not incompatible with a certain nobility of thought.

The realistic position, in contrast, inspired by positivism, from Thomas Aquinas to Anatole France, appears to me to be totally hostile to all intellectual and moral progress. It horrifies me, since it arises from mediocrity, hatred and dull conceit. It is what engenders all the ridiculous books, and insulting plays of our day. It feeds on newspaper articles, and holds back science and art, while applying itself to flattering the lowest tastes of its readers; clarity bordering on stupidity, the life lived by dogs."

-from the Surrealist Manifesto, by André Breton (1924)

Surrealism was a philosophical movement in art and literature that embraced the unexpected, the impossible, the dream-like elements hidden from waking life. The founder of surrealism was French writer and poet André Breton, who was trained in medicine, psychiatry, and Freudian psychoanalysis. He defined surrealism as "Pure psychic automatism by means of which one intends to express, either verbally, or in writing, or in any other manner, the actual functioning of thought. Dictated by thought, in the absence of any control exercised by reason, free of any aesthetic or moral concern." Breton clearly had no use for the realist position, which he viewed as a pox on society. Eighty-eight years later, he might find it ironic that surrealism itself is the subject of positivist thought and scientific investigation.


Does the brain process surrealistic art in a different fashion than realistic art? 

Why yes, one would expect that to be the case. Undaunted, Silveira and colleagues (2012) asked this question in a recent fMRI study. I would predict that surrealist art is more computationally intensive for the Bayesian brain, so there would be greater activation in regions associated with top-down visual processing in an attempt to construct a coherent meaning from an unusual image.1 There was a precedent for this position in a study that compared the activations produced while viewing possible and impossible objects (Wu et al., 2012). Briefly, regions in both the dorsal and ventral visual streams showed greater activation for impossible than for possible objects.2


The authors of the current study adopted a different perspective (so to speak):
While naturalistic paintings present the world in a habitual way, surrealistic paintings violate the expected frame of reference. Surrealistic paintings are characterised by presenting mainly recognisable objects but in constellations that do not exist in real life or that are impossible from a physical point of view. In presenting impossible scenes, these artworks prevent an effortless processing of information to come to a meaningful interpretation of the visual world. ... We hypothesised that percepts violating an expected percept cannot be integrated effortlessly into a frame of prior experiences or expectations and therefore also lack the potential for self-reference.As it has been assumed that cortical midline structures refer to such self-representations (Han and Northoff 2008), we expected naturalistic and surrealistic paintings to have different activations in these areas.

The major prediction was that surrealistic images cannot engender self-referential processing, so differences in cortical midline structures (medial prefrontal and posterior cingulate cortices) were expected, with no further mention of dorsal/ventral stream visual regions, top-down input from prefrontal cortex, networks for processing novelty, or lateral temporal regions associated with semantic processing.



















Figure S2 (Silveira et al., 2012). Reproductions of naturalistic and surrealistic artworks. N = naturalistic, S = surrealistic. N1: Edward Hopper “Sunday”. N2: Edward Hopper “Morning Sun”. N3: Eric Fischl “Japanese Bath”. N4: Francisco de Goya “La Cometa”. N5: Edward Hopper “Chop Suey”. N6: Francisco de Goya “Niños con Mastines”. N7: Edward Hopper “Summer Evening”. N8: Edward Hopper “Cape Cod Morning”. S1: René Magritte “Son of Man”. S2: Vladimir Kush “Pearl”. S3: Salvador Dalí “My Wife Nude”. S4: Max Ernst “Elephant Celebes”. S5: Vladimir Kush “Walnut of Eden”. S6: Giorgio de Chirico “Hector and Andromache”. S7: René Magritte “Le Prêtre Marié”. S8: Vladimir Kush “Departure of the Winged Ship”.


The final stimulus set of 8 realistic and 8 surrealistic paintings is shown above. These were selected from a larger set of images rated on valence, arousal, and familiarity by a separate group of participants. Highly familiar pieces were excluded.3 The control stimuli were homogeneous color fields. All pictures were matched in size, luminance, color saturation, and spatial frequency parameters. Each picture was presented 3 times, and the task was to make a binary decision about their reaction to the image: “Are you touched by the painting?” The subjects were equally affected by the realistic and surrealistic paintings, but took longer to decide on the realistic ones.

The major neuroimaging result was obtained using a subtraction analysis to compare the BOLD response to naturalistic vs. surrealistic paintings. There was significantly greater activation to the naturalistic pictures bilaterally in the precuneus (Brodmann area/BA 7) and medial occipital cortex (BA 17, 18, 19) and in the right middle temporal gyrus. It seemed that no brain areas showed greater activity while viewing the surrealistic images. In fact, the surrealistic pictures resulted in deactivation of the precuneus, medial occipital, and temporal regions when compared to the color field control condition.



Figure 1 (modified from Silveira et al., 2012). Neurometabolic level of processing for naturalistic versus surrealistic images. Sagittal section. Note: Prec = precuneus, MOC = medial occipital cortex.


Given some of the hypothesized roles of the precuneus, the authors' interpretation is plausible:
As a part of the cortical midline structures, precuneus activity has been suspected to be associated with visuo-spatial imagery, episodic memory retrieval, and even of what has been referred to as the “self ” (Cavanna and Trimble 2006). Episodic memory retrieval is very likely to be associated with top–down processing (Sestieri et al 2010). However, surrealist paintings are not only unfamiliar but also disturb our sense of consistency and coherence and may therefore also hardly be related to our sense of the self. The higher activation of the precuneus in the naturalistic condition supports the hypothesis that percepts matching expectations and therefore confirming specific aspects of reality can be linked both to
prior experiences and innate programmes of the representation of the visual world...

What doesn't make sense to me is why there were no visual areas that showed greater activation to the surrealistic images, as in the impossible object study (Wu et al., 2012). Furthermore, it is unclear why the processing of such marked visual/semantic incongruity would not activate any kind of "novelty" circuit in dorsolateral prefrontal cortex, temporal parietal junction, and hippocampus, or semantic regions in the lateral temporal lobe. A very interesting electrophysiological study (using non-invasive ERP recordings, or event-related potentials) found a component at 390 msec post-stimulus that was related to mismatches between scenes and objects, as shown below (Ganis & Kutas, 2003). The authors speculated that this N390 scene congruity response "reflects the action of visual scene schemata stored in the anterior temporal lobe."


 modified from Fig. 1 of Ganis & Kutas


A green apple floating in front of someone's face (S1), or a ship's sails made out of butterflies (S8), might involve a similar violation of visual scene schemata.

"We are still living under the rule of logic, that, of course, is what I am driving at. But in our day, logical procedures are only applicable in solving problems of secondary interest. The absolute rationalism still in fashion only allows us to consider facts directly related to our own experience. The aims of logic, in contrast, escape us. Pointless to add that our very experience finds itself limited. It paces about in a cage from which it is more and more difficult to free it. It leans, it too, on immediate utility, and is guarded by common sense. Under the flag of civilisation, accompanied by the pretext of progress, we have managed to banish from the spirit everything that might rightly or wrongly be termed superstition, fancy, forbidding any kind of research into the truth which does not conform to accepted practice. It was by pure chance, it seems, that a part of our mental world, and to my mind the most important, with which we pretended to be no longer concerned, was recently brought back to light."

-from the Surrealist Manifesto, by André Breton (1924)


Footnotes

1 So once again, we have a challenge for Bayesian theorists and their "free energy principle" (see Free-energy minimization and the dark-room problem), which seeks to reduce uncertainty.

2 See That's Impossible! How the Brain Processes Impossible Objects for details of that study:
The paper started by reviewing the basic neuroanatomy of the visual system and its division into dorsal ("where") and ventral ("what") visual streams. Objects are primarily represented in the ventral stream, and the lateral occipital complex (LOC) is one area that seems to be specialized for object recognition. The authors predicted that impossible objects would be difficult for the LOC to process; therefore, additional regions would be recruited...

What were the results? As predicted, regions in both dorsal and ventral visual streams showed greater activation for impossible than for possible figures: right superior parietal in the former and right fusiform and inferior temporal gyri in the latter.

 

3 The Magrittes weren't familiar? Especially “Son of Man”? Really?


References

Ganis G, Kutas M. (2003). An electrophysiological study of scene effects on object identification. Cog Brain Res. 16:123-44.

Silveira S, Graupmann V, Frey D, Blautzik J, Meindl T, Reiser M, Chen C, Wang Y, Bao Y, PöppeI E, Gutyrchik E (2012). Matching reality in the arts: self-referential neural processing of naturalistic compared to surrealistic images. Perception, 41 (5), 569-76 PMID: 23025160

Wu, X., Li, W., Zhang, M., Qiu, J. (2012). The neural basis of impossible figures: Evidence from an fMRI study of the two-pronged trident. Neuroscience Letters 508:17-21.



Yves Tanguy, Indefinite Divisibility (1942)

Surrealistic Imaging Experiment #2

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Scene from Le sang d'un poète (1930, Jean Cocteau) 1

"It is often said that The Blood of a Poet is a surrealist film. However, surrealism did not exist when I first thought of it."
-Jean Cocteau 2

In our second installment of Surrealistic Imaging Experiments, Marketing Professor Mohamed M. Mostafa of the Gulf University for Science and Technology in Kuwait was interested in how the brain processes Surrealistic imagery used in advertising (Mostafa, 2012). He approached the background to his topic and the fMRI study itself in a very different fashion from Silveira et al. (2012), who performed Surrealistic Imaging Experiment #1.

In that study, the authors hypothesized that humans cannot directly relate to surrealistic images because "percepts violating an expected percept cannot be integrated effortlessly into a frame of prior experiences or expectations and therefore also lack the potential for self-reference" (Silveira et al., 2012). Reduced activation in the precuneus to surrealistic relative to naturalistic pictures served as the major support for this contention. However, self-referential processing is also associated with other cortical midline structures (medial prefrontal and posterior cingulate cortices), which were not differentially activated here. Furthermore, there was no mention of top-down input from prefrontal cortex, networks for processing novelty, or lateral temporal regions associated with semantic processing. This seemed odd to me, as I expected that surrealistic paintings would require greater processing resources than realistic paintings.



Don't be lost in the weird world of investments.
Advertising Agency: Leo Burnett, São Paulo, Brazil


The Persistence of Memory in Advertising

In contrast to the restricted frame of reference presented above, Mostafa (2012) provides a historical background of Surrealism and summarizes the major themes and techniques used by iconic painters such as Salvador Dalí, René Magritte, and Giorgio de Chirico (who influenced the Surrealists). He extends the reach of surrealistic imagery to marketing and popular culture:
Today, the influence of Surrealism extends to cinema and advertising. Some Surreal advertisements create ambiguity by juxtaposing incongruous visual and verbal elements in a way that deliberately defies reason. It is not surprising that advertisers seek to create unique, unexpected and dreamlike images for use in promotions because advertisers often try to gain consumers' attention to fuel their fantasies and to induce them to view a product in a new light. For this reason, the casually Surrealist image has become, in particular, a stock-in-trade of the advertising industry (Macmillan 2000; Denny 2001).

Mostafa then segues into a review of neuromarketing and the brain imaging techniques used to probe the brains of consumers (fMRI, MEG, EEG). The aims of the study are articulated below:
...no previous studies have focused solely on investigating how consumers' brains process Surrealistic imagery in advertising. In this study, we aim to fill this void by investigating the neural correlates of Surrealistic imagery in advertising. More specifically, we aim to:

1.
identify cortical areas that selectively respond to Surrealistic imagery in advertising and
2.
test whether the elaboration and surprise hypotheses are supported within advertising context.3
Then, the specific hypotheses of the experiment are clearly elaborated after a review of the relevant literature:
H1: Surrealistic imagery in advertising will elicit more activation in brain areas associated with novelty detection such as the inferior frontal gyrus (IFG) and the anterior cingulate cortex (ACC).

H2: Surrealistic imagery in advertising will elicit more activation in brain areas associated with emotional responses such as the thalamus and the amygdala.

H3: Surrealistic imagery in advertising will elicit more activation in brain areas associated with episodic-memory retrieval such as the precuneus and the parietal cortex.

As for the methodological details, the participants were 18 right-handed English speakers in their 20s. None were experts in art history. The experimental task (passive picture viewing) used a 2 x 2 factorial design of (1) Surrealistic advertisements (novel, repeated) and (2) congruent advertisements (novel, repeated).

novel congruent    repeated congr   novel surrealistic   repeated surreal

Figure 1 (Mostafa, 2012). Stimuli and presentation sequence.


Thus, the author took into account both stimulus novelty and stimulus repetition (using a modified adaptation design), the latter to examine a form of priming in which a relative reduction in neural activity is observed when a stimulus is repeated. The stimulus set of Silveira et al. (2012) might have been better matched on size, luminance, color saturation, and spatial frequency parameters, but each of their 16 stimuli were repeated 3 times. There could have been differential priming effects for surrealistic vs. naturalistic images, but we don't know. On the other hand, the presentation parameters and number of stimuli in Mostafa's study weren't clear to me, either. 4

Briefly, the results confirmed the major hypotheses:
Surrealistic imagery elicited greater activation in several brain areas including the parietal cortex (BA 1, 2, 3), the precuneus (Brodmann area (BA) 7), the lateral parietal cortex (BA 39/40), the prefrontal cortex (BA 6/9), the IFG (BA 45/46), the ACC (BA 24), the insula (BA 13) and the amygdala. This result suggests that, compared to other types of advertisements, Surrealistic advertisements are processed in different functional brain pathways. This finding lends strong support to the elaboration and surprise hypotheses, which postulate that incongruous stimuli elicit increased processing that leads to more distinct and robust memory traces.

The novelty and distinctiveness of the Surrealistic images presented here in Surrealistic Imaging Experiment #2 required greater subcortical and cortical processing resources (including in the precuneus) than did the congruent images, in contrast to the detachment and alienation suggested by Surrealistic Imaging Experiment #1. How do we account for this discrepancy? What is the logical explanation?

"Our brains are dulled by this incurable mania for reducing the unknown to the known, to the classifiable. The desire for analysis wins out over feeling. It results in lengthy statements whose persuasive force derives from their very strangeness, and only impress the reader by recourse to an abstract vocabulary, which is moreover quite ill-defined."

-from the Surrealist Manifesto, by André Breton (1924)


Don't be lost in the weird world of investments.
Advertising Agency: Leo Burnett, São Paulo, Brazil


Footnotes

1 From Blood of a Poet: spectator as spiritualist
The film is essentially an exploration into the creative process; a self-conscious exploration of the subconscious, even the unconscious. Cocteau states that he was not thinking while he made the film but allowed images and ideas to present themselves to him, almost like the improvisation of a Jazz musician. Cocteau repeatedly spoke in interviews of the mysterious other self within an artist, saying that a poet (and by this he means artist of any genre) is a medium for the strange force which exists within him. He doesn’t shape this force, but rather the force shapes him. “My relationship with the work was like that of a cabinet maker who puts together the pieces of a table whom the spiritualists, who make the table move, consult”
2 This sly comment from Cocteau is not true; André Breton wrote the Surrealist Manifesto in 1924.

3 On memory, bizarreness, elaboration and surprise:
Prior behavioral research has also investigated visual imagery mnemonics and Surrealism in advertising. This line of research suggests that Surrealistic advertisements are likely to be processed more extensively than non-Surreal advertisements. For example, O'Brien and Wolford (1982) suggested that bizarre images increase the distinctiveness of items. Houston, Childers, and Heckler (1987) found that pictorial information incongruent with prior expectation is more difficult to comprehend and stimulates more elaborate internal processing. Behavioral support for bizarreness effect is based on both the elaboration hypothesis (Merry 1980; Wollen and Cox 1981) and the surprise hypothesis (Hirshman, Whelley, and Palu 1989). The elaboration hypothesis suggests that incongruous stimuli elicit extra processing because such stimuli are more difficult to make sense within the context of expected semantic norms.
4 It doesn't seem like the contrasts presented in Table 1 and Figs. 5 and 6 were corrected for multiple comparisons, which is a problem. The Silveira et al. (2012) study was methodologically superior in this specific realm.


References

Mohamed M. Mostafa (2012). The persistence of memory: an fMRI investigation of the brain processing of Surrealistic imagery in advertising. Journal of Marketing Communications DOI: 10.1080/13527266.2011.653688

Silveira S, Graupmann V, Frey D, Blautzik J, Meindl T, Reiser M, Chen C, Wang Y, Bao Y, PöppeI E, Gutyrchik E (2012). Matching reality in the arts: self-referential neural processing of naturalistic compared to surrealistic images. Perception 41:569-76.



Absurdly low consumption. The Polo BlueMotion.
Advertising Agency: DDB, Berlin, Germany

Savoir Faire or Savant?

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Is amygdala volume correlated with social network size or with special talents in autism spectrum disorders? Or both??


The amygdala is a subcortical structure located within the medial temporal lobes. It consists of a number of different nuclei, or collections of neurons delineated by commonalities in morphology and connectivity. The amygdala is best known for major roles in fear conditioning (Paré et al., 2004) and responding to emotional stimuli more generally (Phelps & LeDoux, 2005), but its functions extend beyond that.

A presentation at the recent Society for Neuroscience meeting in New Orleans reported on MRI data obtained from Dr. Temple Grandin, the famous and talented Professor of Animal Science at Colorado State (Cooperrider et al., 2012):
Dr. Temple Grandin: A neuropsychological and multimodal neuroimaging case study of a savant with autism

. . .

Results: Dr. Grandin’s left lateral ventricle showed much more leftward volumetric asymmetry than controls. Her left cerebral white matter volume and bilateral entorhinal cortex thickness were much greater compared to controls. Her fusiform gyrus thickness was much less than the control mean. She had greater left lateral ventricle, intracranial, left cingulate, bilateral amygdala, and bilateral entorhinal cortex volumes. White matter microstructural differences were found for Dr. Grandin in multiple brain regions, including those known to relate to language function and facial information processing. ... The neuropsychological assessment indicated superior visuospatial and nonverbal reasoning abilities...

Virginia Hughes wrote a splendid summary of the study, which is not yet published in a peer-reviewed journal.

An earlier experiment was conducted with another very talented autistic savant (Corrigan et al., 2012):
The subject of this study is a 63-year-old, right-handed male with savant syndrome and a long-standing diagnosis of ASD.1 Institutionalized as a child, he has lived semi-independently as an adult, working for more than 30 years in dishwashing jobs. This individual is gifted with several special skills. One area of considerable talent is in music. He has perfect pitch and plays several musical instruments, of which his favorite is the accordion. He has substantial abilities with languages and can engage in basic conversations in twelve different languages. He also has remarkable abilities with sound imitation. His most exceptional ability, however, is in the area of art. ... He has become a highly regarded and accomplished graphic artist, whose works have been recognized through numerous exhibitions nationally as well as publication in a book. His medium is paper with pencil, marker, and crayon. His interest is in drawing collections, usually quite large, of items such as tools, birds, instruments, trains, flowers, and shoes, among many others. He takes a special interest in categorizing the physical world.

The volumes of his amygdala and caudate were both larger than values in the normative literature, and a strong right-sided asymmetry was seen for both structures (Corrigan et al., 2012). Hippocampal volumes did not differ from control values.

Although these two single-case studies were of exceptional people who may not be characteristic of the general ASD population, it was notable that both individuals had larger amygdalae than controls. Is this a surprising finding, in light of recent results on the correlations between amygdala volume and social network size in control participants? Surely the average neurotypical college student has a larger Social Network Index of offline contacts (Bickart et al, 2011) and more Facebook friends (Kanai et al., 2012) than the average person with ASD?
Grandin says, “the part of other people that has emotional relationships is not part of me” and she has neither married nor had children. ... She describes socializing with others as “boring” and has no interest in reading or watching entertainment about emotional issues or relationships.

In an earlier post on the Bickart article (More Friends on Facebook Does NOT Equal a Larger Amygdala), I noted that bigger is not always "better" (see Fig. 2 below):
One prominent example is the finding of larger amygdalae in children (and adults) with autism (Howard et al., 2000; Mosconi et al., 2009). However, the literature on this issue is variable (and voluminous)...2 More consistent are observations of increased amygdala volumes in generalized anxiety disorder (Etkin et al., 2009; Schienle et al., 2010). In rats, chronic stress causes hypertrophy (enhanced dendritic arborization) of pyramidal and stellate neurons in the basolateral nucleus of the amygdala (Vyas et al., 2002).


Modified from Fig. 2 (Howard et al., 2000). Volume estimation of the amygdala by the stereological point counting method. Section area estimation of posterior, middle, and anterior amygdala sections, using a regular array of test points. Section areas are increased in autism compared to controls.

A further interpretive conundrum is presented by the variety of conditions that are associated with increased amygdala volume: first-episode patients with nonschizophrenic psychoses, women high in harm avoidance, learning disabled adolescents at high risk of schizophrenia, adopted Romanian adolescents who experienced severe early institutional deprivation, and political conservatism.3
Most of those things are not especially fantastic for an active social life...

Autism is often considered as a disorder of microcircuitry and of long-range connections, so determining the structural and functional connectivity of the amygdala with other brain regions is crucial. One view holds that "underconnectivity" is a characteristic feature of the brains of those with autism, although recently this hypothesis has been called into question.

A new study from Bickert and colleagues (2012) followed up on their previous morphometric work and examined the functional connectivity of the amydala in relation to offline social network size in a group of 30 young adults (19 of whom had been in their previous experiment). Two separate groups of subjects, a "discovery sample" (n=89) and a "replication sample" (n=83) were scanned with fMRI at rest to establish the large-scale amygdala networks related to social cognition.

In brief, three networks were identified: (1) the ventrolateral amygdala and "perception" network (connected with lateral orbitofrontal cortex); (2) the medial amygdala and "affiliation" network (connected with ventromedial prefrontal cortex); and (3) the dorsal amygdala and "aversion" network (connected with dorsal anterior cingulate cortex).














Figure 1 (Bickert et al., 2012). Hypothetical topographic model of amygdala subregions and their affiliated large-scale networks subserving social cognition. A schematic of (a) the amygdala subregions in coronal view that we hypothesize are anchors for (b) three large-scale networks subserving processes important for social cognition. Ins, insula; SS, somatosensory operculum; dTP, dorsal temporal pole; cACC, caudal anterior cingulate cortex; rACC, rostral anterior cingulate cortex; sgACC, ubgenual anterior cingulate cortex; MTL, medial temporal lobe; FG, fusiform gyrus; vTP, ventral temporal pole; vlSt, ventrolateral striatum; vmSt, ventromedial striatum.


In the experimental sample (n=30), stronger intrinsic connectivity within the "perception" and "affiliation" networks was correlated with larger real-life social networks, but connectivity within the "aversion" network was not. A thorough evaluation of the methods used to establish these relationships is beyond the scope of this post, but an important question remains: can the current results inform the patterns of amygdala connectivity observed in participants with autism?


Footnotes

1 Although not specifically named, the participant was Gregory Blackstock, author of Blackstock's Collections: The Drawings of an Artistic Savant.


2 In fact, recent meta-analyses suggest that individuals with ASD may have smaller amygdala volumes than controls (Cauda et al., 2011; Via et al., 2011). On the other hand, the literature on early childhood hypertrophy of the amygdala in autism seems consistent (Mosconi et al., 2009). But another study in adolescents and adults with Asperger syndrome observed larger amygdala volumes than in controls (Murphy et al., 2012).

3 This study was published in a newspaper, not in a peer reviewed journal (see Left Wing vs. Right Wing Brains).


References

Bickart, K., Hollenbeck, M., Barrett, L., & Dickerson, B. (2012). Intrinsic Amygdala-Cortical Functional Connectivity Predicts Social Network Size in Humans. Journal of Neuroscience, 32 (42), 14729-14741. DOI: 10.1523/JNEUROSCI.1599-12.2012

Bickart KC, Wright CI, Dautoff RJ, Dickerson BC, Barrett LF. (2011). Amygdala volume and social network size in humans. Nat Neurosci. 14:163-4.

Cauda F, Geda E, Sacco K, D'Agata F, Duca S, Geminiani G, Keller R. (2011). Greymatter abnormality in autism spectrum disorder: an activation likelihoodestimation meta-analysis study. J Neurol Neurosurg Psychiatry 82:1304-13.

J.R. Cooperrider, E.D. Bigler, J.S. Anderson, S. Doran, C. Ennis, N. Adluru, A.L. Alexander, A.L. Froehlich, M.B.D. Prigge, J.E. Lainhart. Dr. Temple Grandin: A neuropsychological and multimodal neuroimaging case study of a savant with autism. Program No. 18.08. 2012 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2012. Online.

Corrigan, N., Richards, T., Treffert, D., & Dager, S. (2012). Toward a better understanding of the savant brain, Comprehensive Psychiatry, 53 (6), 706-717. DOI: 10.1016/j.comppsych.2011.11.006

Etkin A, Prater KE, Schatzberg AF, Menon V, Greicius MD. (2009). Disrupted amygdalar subregion functional connectivity and evidence of a compensatory network in generalized anxiety disorder. Arch Gen Psychiatry 66:1361-72.

Howard MA, Cowell PE, Boucher J, Broks P, Mayes A, Farrant A, Roberts N. (2000). Convergent neuroanatomical and behavioural evidence of an amygdala hypothesis of autism. Neuroreport 11:2931-5.

Kanai R, Bahrami B, Roylance R, Rees G. (2012). Online social network size isreflected in human brain structure. Proc Biol Sci. 279:1327-34.

Mosconi MW, Cody-Hazlett H, Poe MD, Gerig G, Gimpel-Smith R, Piven J. (2009). Longitudinal study of amygdala volume and joint attention in 2- to 4-year-old children with autism. Arch Gen Psychiatry 66:509-16.

Murphy CM, Deeley Q, Daly EM, Ecker C, O'Brien FM, Hallahan B, Loth E, Toal F, Reed S, Hales S, Robertson DM, Craig MC, Mullins D, Barker GJ, Lavender T, Johnston P, Murphy KC, Murphy DG. (2012). Anatomy and aging of the amygdala andhippocampus in autism spectrum disorder: an in vivo magnetic resonance imagingstudy of Asperger syndrome. Autism Res. 5:3-12.

Paré D, Quirk GJ, Ledoux JE. (2004). New vistas on amygdala networks in conditioned fear. J Neurophysiol. 92:1-9.

Phelps EA, LeDoux JE. (2005). Contributions of the amygdala to emotion processing: from animal models to human behavior. Neuron 48:175-87.

Schienle A, Ebner F, Schäfer A. (2010). Localized gray matter volume abnormalities in generalized anxiety disorder. Eur Arch Psychiatry Clin Neurosci. Sep 5. [Epub ahead of print].

Via E, Radua J, Cardoner N, Happé F, Mataix-Cols D. (2011). Meta-analysis of graymatter abnormalities in autism spectrum disorder: should Asperger disorder besubsumed under a broader umbrella of autistic spectrum disorder?Arch Gen Psychiatry 68:409-18.

Vyas A, Mitra R, Shankaranarayana Rao BS, Chattarji S. (2002). Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. J Neurosci. 22:6810-8.

Tenure-Track Position in Neuroetiquette and Gender Theory

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Department of Critical Socioneurobiology.

Pending approval of departmental funds, the North Dakota School for Social Research is seeking outstanding candidates for its newly developed Interdisciplinary Program in Architecture, Kitchen Design, Sociology of Gender Roles, and Neuroimaging. State-of-the-art Siemens MAGNETOM 7T MRI and 306-channel planar dc-SQUID Neuromag Vectorview MEG facilities available. Start-up funds of $50K provided. Requirement to teach 3 classes per semester, including Statistics, Introduction to Celebrity Chefs, and Advanced Techniques in Optogenetics. The successful Assistant Professor candidate will be expected to obtain NEA funding, publish in high-impact science journals, give a Top 10 TED talk, and negotiate a major book deal before receiving tenure. Experience as a nationally syndicated advice columnist preferred.

Send CV, design portfolio, writing samples, research manifesto, and 10 letters of recommendation to: Chair of Search Committee, Department of Critical Socioneurobiology, North Dakota School for Social Research. Address inquiries to: neuroetiquette_and_gender_theory@ndsfsr.edu.

NDSFSR is an Equal Opportunity Employer.

Neuroetiquette and Neuroculture

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Discover neuro-etiquette: fork and knife in action


Are neuroscientists taking jobs away from philosophers, sociologists and gender theorists?
"We need a neurocultural manifesto because the brain has been put forward by others as foundational for knowing about the self and social life, because neuroscientists are being asked to be the philosophers, sociologists and gender theorists of our era - they are being asked to do our jobs - and are responding with enthusiasm, and also because brain matter is mattering."

- from Neurocultures Manifesto by Victoria Pitts-Taylor.

In case you haven't realized yet, my job posting for a Tenure-Track Position in Neuroetiquette and Gender Theory was a spoof. The details were inspired by the highly unrealistic expectations of academia and by a disparate collection of neurowords.
  • Neuroetica -- I initially had a tough time decoding this word, translating its orthography to phonology and semantics. Neurorotica? Neuroetiquette? No, neuroetica is an Italian word from an article in Neuoethics that takes "a Look at the Development of the Italian Debate on Neuroethics." 

  • Neuroetiquette -- Much to my dismay, a writer at New York Etiquette Guide had already coined the word 'neuro-etiquette' in her blog post on neuroplasticity, learning to play the piano, and how to properly hold your knife and fork.

  • Neuroculture -- Etiquette is part of culture, of course. One encounters the word 'neuroculture' in many online discourses, from the tenets of the Neurocultures Manifesto to David Dobbs' blog Neuron Culture to the lifestyle marketing claim that Neuro Gasm Is Part Of The New Neuro Culture.

I think the neuro-panic among social scientists is overblown. How many philosophers, sociologists, and gender theorists are unemployed because their respective departments have decided to hire neuroscientists instead? How many developmental neurobiologists have applied for this Instructor of Philosophy position at Rochester Community and Technical College? Will a cognitive neuroscientst be able to teach transnational feminism or postcolonial feminism, queer theory, and critical race theory in the Women's and Gender Studies Program at Illinois State University?


Are we living in a neuroculture?

Daniel Buchman and David Dobbs asked that question two years ago. Their answers were "yes" and "of course we do!" More recently, a conference on Culture, Mind, and Brain: Emerging Concepts, Methods, Applications was held at UCLA:
The aim of this 2-day conference is to highlight emerging concepts, methodologies and applications in the study of culture, mind, and brain, with particular attention to: (1) cutting-edge neuroscience research that is successfully incorporating culture and the social world; (2) the context in which methods are used as well as the tacit assumptions that shape research questions; and (3) the kinds and quality of collaborations that can advance interdisciplinary research training. 
To find out what happened, you can check out the Conference Blog, Neuroanthropology, and Somatosphere. Ultimately, it sounds like we can all get along.

All sarcasm aside, I am in favor of multidisciplinary research. And I strongly endorse critical thinking about neuroscience. However, some self-appointed pontificators want to strip the brain of any power over human thought. At those times, it's good to see a defence of cognitive neuroscience. I'm starting a backlash against the anti-neuro backlash. After nearly 7 years of critical neuroblogging, it might be time for a change: The Neurocomplimenter.


But I never tire of highlighting those neuro-analogies that go over the top...
Discover neuro-etiquette: fork and knife in action

by Lyudmila Bloch, Etiquette Expert New York City

From the frontiers of neuroscience research, we know that our brain can change, reorganize, adapt, learn, and reprogram itself to a new “wiring” regardless of our age, previous experience, or current challenges.

A revolutionary discovery in neuroscience, called neuroplasticity, has confirmed that our brain is not a fixed, hardwired machine but rather vital and tirelessly evolving organ in our body. Experiments and clinical trials over the past two decades, conducted by the best minds in neuroscience, have discovered that our amazing brain, with proper rewiring and targeted conditioning, can master the most difficult of tasks at any age. Astonishing progress in overall functioning and new- skills acquisition show this master organ to be nothing short of, well, miraculous!

Leading behavioral psychologists and scientists have been collaborating, trying to understand the process of how a human brain learns and how it acquires new skills.
. . .

Any new skill or task we try to learn, including the proper use of diningutensils – so essential to our dining etiquette -- will entail the same kind of diligence in practicing, over and over, a “balancing exercise” -- holding your fork and knife correctly.

Got Brains? License Plate

Blow Your Mind with Hostile THINKIES


(Every Day Is) Halloween

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New research provides fresh evidence that bogus press releases may depend largely on our biological make-up

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This Is Your Brain On Press Releases: Neuroscience Reveals Brain Differences Between Writers and Consumers

ScienceDally (Nov. 1, 2012)— New research from the University of South Carolina provides fresh evidence that writing bogus press releases days before the U.S. Presidential Election may depend largely on our biological make-up. That's because the brains of self-identified University Press Offices and the Discerning General Public are hard-wired differently and may be naturally inclined to hold varying, if not opposing, perceptions and values. This study showed a strong link with broad ideas of truth with Press Offices and a strong link with tight ideas of truth with the Discerning Public.












Democrat Brain, Republican Brain

It's no coincidence that the University of South Carolina chose to issue a news release on the purported "hard-wired" differences between the brains of Democrats and Republicans -- based on unpublished data -- a mere five days before the U.S. presidential election.

The parody lede above sticks closely to the simplistic story that American voters are "born that way" and have little choice over their hopelessly opposed views. Here's the original:

This Is Your Brain On Politics: Neuroscience Reveals Brain Differences Between Republicans and Democrats

ScienceDaily (Nov. 1, 2012) — New research from the University of South Carolina provides fresh evidence that choosing a candidate may depend largely on our biological make-up. That's because the brains of self-identified Democrats and Republicans are hard-wired differently and may be naturally inclined to hold varying, if not opposing, perceptions and values. This study showed a strong link with broad social connectedness with Democrats, and a strong link with tight social connectedness with Republicans.

With the U.S. presidential election just days away, new research from the University of South Carolina provides fresh evidence that choosing a candidate may depend more on our biological make-up than a careful analysis of issues.

That's because the brains of self-identified Democrats and Republicans are hard-wired differently and may be naturally inclined to hold varying, if not opposing, perceptions and values. The USC study, which analyzed MRI scans of 24 USC students, builds on existing research in the emerging field of political neuroscience. 

Next comes the confident (yet uninformative) obligatory quote from the expert:
"The differences are significant and real," said lead researcher Roger Newman-Norlund, an assistant professor of exercise science in the Arnold School of Public Health and the director of USC's new Brain Stimulation Laboratory.

What is the peer-reviewed source for this quote? There is none. Not even a conference presentation. Do we learn much about the experimental methods, questionnaires, or specific imaging results? No. All we get is a bunch of popular buzz words: Mirror neurons. "Resting state." Social connectedness.
The study focused on the mirror neuron1 system, a network linked to a host of social and emotional abilities. After declaring their political affiliations, the subjects were given questionnaires designed to gauge their attitudes on a range of select political issues. Next, they were given "resting state" MRIs which made it possible to analyze the strength of connections within the mirror neuron system in both the left and right hemispheres of their brains; specifically the inferior frontal gyrus, supramarginal gyrus and angular gyrus.
[NOTE: I inserted the links. Are those anatomical regions really going to mean something to the average reader? Would they even know that the latter two gyri are in the parietal lobe?]

The results found more neural activity in areas believed to be linked with broad social connectedness in Democrats (friends, the world at-large) and more activity in areas linked with tight social connectedness in the Republicans (family, country). In some ways the study confirms a stereotype about members of the two parties -- Democrats tend to be more global and Republicans more America-centric -- but it actually runs counter to other recent research indicating Democrats enjoyed a virtual biological lock on caring for others.

You mean, there are well-established and specific brain regions linked to the possession of broad (or tight) social connections? What do these terms actually mean, beyond friends/world vs.family/country? And please, point us to the actual research showing that Republicans are biologically incapable of caring for others... [The Republican Brain?].

Next we have the obligatory overblown implications:
While political neuroscience and study is still largely in its infancy, the implications for future races could be big as politicians and campaign strategists learn how to exploit brain differences to make more effective, biologically targeted appeals to voters.

We've seen this before. The Political Brain. This is Your Brain on Politics (we all know how that one turned out -- Politics and the Brain). How Neuromarketers Tapped the Vote Button in Your Brain to Help the GOP Win the House.


Then what little information we have about the actual scientific results (different functional connectivity patterns in resting state fMRI in Republicans and Democrats??) appears to be overinterpreted (and attributed to mirror neurons, of course):
The research also suggests that maintaining an open mind about political issues may be easier said than done. In fact, bridging partisan divides and acting contrary to ideological preferences likely requires going against deeply ingrained biological tendencies. And while there is evidence that mirror neuron connections can change over time, it's not something that happens overnight, Newman-Norlund said.

"The (brain) differences could be a result of genetics, experiences, or a combination of both," he said. "It takes a lot of effort to see the other side and we're not going to wake up one day and all start getting along."

It could be that Professor Newman-Norlund actually holds a more nuanced view than is depicted here.2 How does this press release (and its opportunistic timing) benefit him or serve as a credit to the University of South Carolina?  In the end, you might ask, "hey Neurocritic, why have you devoted so many pixels to this one simplistic and misleading news blurb, out of thousands?" 3 It's because the science promotion industry hasn't learned anything. I feel like I'm writing on the same themes as four (and five) years ago...


Footnotes

1 First observed in the ventral premotor area F5 of macaque monkeys, mirror neurons increase their rate of firing when the animal performs an action, and when the animal watches someone else perform the action (Rizzolati et al, 1996). They've also been observed in the inferior parietal lobe (and even in the primary motor cortex of monkeys. There's little convincing evidence of their existence in humans (from intracranial neuronal recordings), and that evidence implicates hippocampal neurons, which is problematic for the whole concept. Instead, a range of brain areas show "mirror neuron-like" responses in fMRI studies, hence the name "mirror neuron system." Greg Hickok has been a leading critic of the mirror neuron theory of action understanding.

2 For a good example of this, see Biology and ideology: The anatomy of politics.

3 Instead of writing about, let's say, Day of the Dead or the mistaken personality attributes of black cats?

Cotard's Syndrome: Not Pretending That We're Dead

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Playing dead game --  A craze called the "playing dead game" has swept this nation where people of all ages stage elaborate death scenes everyplace.


Believing That We're Dead

Cotard's Syndrome is the delusional belief that one is dead or missing internal organs or other body parts (Debruyne et al., 2009). Those who suffer from this "delusion of negation" deny their own existence. The eponymous French neurologist Jules Cotard called it le délire de négation ("negation delirium").

Cotard's syndrome has been observed in mentally ill persons with psychotic disorders (such as schizophrenia and psychotic depression), as well as in neurological patients with acquired brain damage. In a review of 100 cases, Berrios and Luque (1995) found that:
Depression was reported in 89% of subjects; the most common nihilistic delusions concerned the body (86%) and existence (69%). Anxiety (65%) and guilt (63%) were also common, followed by hypochondriacal delusions (58%) and delusions of immortality (55). An exploratory factor analysis extracted 3 factors: psychotic depression, Cotard type I and Cotard type II. The psychotic depression factor included patients with melancholia and few nihilistic delusions. Cotard type 1 patients, on the other hand, showed no loadings for depression or other disease and are likely to constitute a pure Cotard syndrome whose nosology may be closer to the delusional than the affective disorders. Type II patients showed anxiety, depression and auditory hallucinations and constitute a mixed group.

In their overview, Debruyne et al., 2009 presented two cases with distinctively different outcomes:
1. An 88-year-old man with mild cognitive impairment was admitted to our hospital for treatment of a severe depressive episode. He was convinced that he was dead and felt very anxious because he was not yet buried. This delusion caused extreme suffering and made outpatient treatment impossible. Treatment with sertraline, 50 mg, and risperidone, 1 mg, resulted in complete remission of the depressive episode and nihilistic delusions...

2. A 46-year-old woman with known rapid-cycling bipolar disorder ... presented with a depressive episode with psychotic features. Her nihilistic delusions were compatible with Cotard’s syndrome. She had the constant experience of having no identity or “self” and being only a body without content. In addition, she was convinced that her brain had vanished, her intestines had disappeared, and her whole body was translucent. ... The following pharmacologic treatments previously had been used to treat this patient, without consistent effect: lithium, valproate, carbamazepine, haloperidol, olanzapine, risperidone, clozapine, pimozide, sulpiride, clomipramine, sertraline, paroxetine, fluoxetine, citalopram, mirtazapine, and venlafaxine. Electroconvulsive therapy (ECT) was also used without effect. The nihilistic delusions disappeared in this patient, but a mood switch to a hypomanic episode occurred...
In the 46 year old patient, MRI and SPECT findings were negative, but her neuropsychological testing was suggestive of right hemisphere dysfunction.


Delusions of Death in a Patient with Right Hemisphere Infarction

Does the right hemisphere play a unique role in maintaining a sense of self? A new case study by Nishio and Mori (2012) described a 69 year old patient who suffered a stroke affecting portions of the right frontal, temporal, and parietal lobes and right thalamus. A neurological exam a week later revealed severe hemispatial neglect of the left side of space, left sided weakness, motor neglect of his left limbs, and impaired senses of pain, cold, touch, vibration, and position on the left side of his body. These symptoms are typical of such a large right hemisphere lesion (see below).1


FIGURE 1. (Nishio & Mori, 2012). Magnetic resonance images of the patient’s brain, taken just after the onset of the stroke. The right side of the brain appears on the left side of the scans. A, Transverse diffusion-weighted images show fresh infarcts involving the right-frontal, temporal, and parietal lobes and thalamus.


What was unusual were other aspects of his behavioral presentation:
...He criticized his doctors, nurses, and rehabilitation therapists, and complained bitterly about the hospital’s food and oxygen. He falsely believed that his brother-in-law, previously a director of another hospital, was to blame for this hospital’s flaws. He was treated with mianserin (10 mg/day) and quetiapine (25 mg/day); his irritability and agitation subsided within 2 to 3 weeks. During that time, we became aware that the patient was suffering from several delusional misidentifications. He thought that Kim Jong-il, then the leader of North Korea, was staying on the floor below his own, and that his physical therapist was a grandson of Puyi, the last Emperor of China...

A month after the onset of his symptoms, by which time his motor and cognitive symptoms had gradually improved, he began complaining regularly of feelings of unreality, and asked his wife whether he was alive or dead. He said to his doctor, “I guess I am dead. I’d like to ask for your opinion.” Later, his conviction about death became firmer. He said, “My death certificate has been registered. You are walking with a dead man,” and “I am dead. I will receive a death certificate for me from my doctor and have to bring it to the city office early next week.”

His discussion of his demise was not associated with a depressed mood or feelings of fear. When his doctor asked him whether a dead man could speak, he understood that his words defied logic, but he could not change his thinking.

As time passed, his delusions of death dissipated, yet in retrospect he characterized these delusions as real:
His delusion of being dead and his feelings of depersonalization gradually subsided and disappeared 4 months after the stroke. One year after the stroke, however, he still believed in the truth of the memories that he had formed during his delusional state. He said, “Now I am alive. But I was once dead at that time,” and “I saw Kim Jong-il in the hospital where I stayed.”

The authors discussed the case in relation to other delusional misidentification syndromes such as Capgras syndrome, where the patient believes their loved ones have been replaced by nearly identical duplicates or impostors. One functional interpretation of Capgras is that a disconnection between facial recognition and affective processes has occurred, such that the person no longer experiences the feelings of familiarity and warmth towards their significant others. In a similar fashion, some cases of Cotard could result from a lack of familiarity with or detachment from one's self, which is then interpreted as being dead or no longer existing.

Why did this particular patient show the Cotard delusion, whereas other people with similar right hemisphere strokes have not? Where is the pathology in psychiatric patients with Cotard's, who comprise the bulk of case reports? For that matter, will we be able to develop neuroscientific explanations for these questions and construct something resembling a functional neuroanatomy of the self?

Are you really your connectome??



L7 - Pretend We're Dead, directed by Modi Frank.


Footnote

1Interestingly, the patient seemed to present with a relatively pure case of Cotard type I. His delusion was restricted to death, as he did not deny the existence of body parts or of his left-sided weakness. Both of these are relatively common with similar right hemisphere strokes.
The patient did not show asomatognosia (lack of awareness about the condition of part or all of his body), anosognosia (lack of awareness of his disability) for hemiplegia, or somatoparaphrenia (denial that a limb or a whole side belonged to his body).


References

Berrios GE, Luque R. (1995). Cotard's syndrome: analysis of 100 cases. Acta Psychiatr Scand. 91:185-8.

Debruyne H, Portzky M, Van den Eynde F, Audenaert K (2009). Cotard's syndrome: a review. Current psychiatry reports, 11 (3), 197-202. PMID: 19470281

Nishio Y, Mori E (2012). Delusions of Death in a Patient with Right Hemisphere Infarction. Cognitive and behavioral neurology. PMID: 23103861



Playing dead -- Chuck Lamb is the “dead body guy”. He enjoys playing dead and his tryings to “perform” in movies made him more famous than his actually doing that.

The Neuroscience of Speed Dating Choice

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Can brain activity measured while rating potential dates predict later choices at speed dating events?

Haven't you lay awake at night wondering if 36 voxels in your rostromedial prefrontal cortex (RMPFC) can predict your future romantic decisions? If you have, you're in luck. Cooper and colleagues (2012) conducted an fMRI study to answer this burning question in the affirmative.
"and then I asked him with my eyes to ask again yes and then he asked me would I yes to say yes my mountain flower and first I put my arms around him yes and drew him down to me so he could feel my breasts all perfume yes and his heart was going like mad and yes I said yes I will Yes." 

-James Joyce, Ulysses

OK, so maybe nothing that dramatic emerged after your 5 min date at the Campus Rec Center...

This might be hard for me, but I'll try to seriously convey the major point of the study: how does the brain form first impressions of potential romantic partners? My immediate retort to the experimental approach is why would you ever think that 36 voxels in one brain area (and 34 in another) can drive such a complicated decision??

But that was the finding of this paper, which was published in the Journal of Neuroscience.

To describe the methods in brief, 39 single young heterosexual adults participated in a scanning session where they viewed photographs of their potential dates and rated them on on three dimensions:
a “first-impression”(FI) rating with the scale “How much would you like to date this person?,” as well as separate ratings of physical attractiveness (Att) and likability (Like).

After scanning, the same photos were rated again on scales that assessed potential romantic desirability: “How physically attractive is this person?” and “How much do you think you would like this person?”  Another 112 young adults also participated in the behavioral part of the study, but not the fMRI part.

For analysis, the authors estimated four models:
  1. Basic decision, two predictors: partners who were later pursued and those who were rejected.
  2. Similar but controlled for reaction time (RT) to the FI decision. This will become important, as we'll see below.
  3. Regions that correlated with subjective desirability ratings: single predictor for all partners with two parametric modulators: one for subjective physical attractiveness (Att) and one for subjective likeability (Like).
  4. Adjustment for partner and relationship effects: single predictor for all partners with two parametric modulators: one for the consensus judgment (hot or not) and one for individual preference (idiosyncratic choice).

Let's look at the results for the basic decision (A) and for subjective attractiveness (B) in the figure below.



Modified from Fig. 2 (Cooper et al.,  2012). Neural predictors of subsequent decision compared with areas mediating judgments of physical attractiveness. A, Brain regions showing greater responses at the time of first viewing for faces of individuals that are subsequently selected as a potential romantic partner, compared with those who were not. Paracingulate cortex (circled) is the only activated region that significantly independently correlates with subsequent decision in a multiple regression including all activated regions. B, Brain regions positively correlating with subjective ratings of physical attractiveness for each partner. C, Overlap between brain regions related to decision and those related to attractiveness, showing substantial overlap between these variables in the paracingulate cortex. All images thresholded at p< 0.001 voxelwise with extent threshold set to control whole-brain FWE at p< 0.05. Color bars indicate t statistic.


The circled area (A) is called paracingulate cortex by these authors and dorsal anterior cingulate cortex (ACC) by many others. The paracingulate is the only region that correlated with subsequent dating decisions. However, the dorsal ACC is activated in a whole host of situations (Botvinick, 2007; Posner et al., 2007). An explanation for this is well beyond the scope of a single blog post. The big blob (B) correlated with physical attractiveness, and (C) shows the overlap between these two.

It was important to control for the RT of first impression decisions because activity in the ACC is sensitive to "time on task," or how long it takes to process or respond to a stimulus. This means that the ACC shows greater activity when RTs are long. This is a confound for many studies that examine response conflict, or interference, like the well-known Stroop task (RED, BLUE, etc.).  If you control for longer RTs that are inevitable in tasks like the Stroop, the interference effect in the ACC goes away (Carp et al., 2010). Hence, the paracingulate could merely be responsive to making dating decisions that are sometimes ambiguous or difficult.

The table below shows that wasn't entirely the case, but the magnitude of the paracingulate activation was diminished when RT was controlled. This wasn't true of two other brain regions (ventral visual cortex, medial precuneus), which weren't even discussed in the paper.



Modified from Table 2 (Cooper et al.,  2012). Activations correlated with subsequent decisions/ratings. [NOTE: compare the two hearts.]


As a final comparison, let's look at activations sensitive to universal hotness vs. idiosyncratic choice. Our friend the paracingulate responded to objective attractiveness, as judged by the entire group of participants. In contrast, another region — 36 voxels in the rostromedial prefrontal cortex — responded to whether the potential partner was desirable to a specific participant.



Modified from Fig. 4 (Cooper et al.,  2012). Distinct regions of medial prefrontal cortex mediate effects of consensus judgments and individual preferences.A, Region of paracingulate cortex significantly correlated with consensus judgments for decisions (i.e., partners who were more frequently pursued). B, A distinct region of RMPFC was correlated with individual preferences.


Overall, the authors have tried to convince us that neural activity in two small regions of the brain mediate first impressions and can predict whether or not we'll pursue contact with a potential romantic partner at a speed dating event. Somehow I think we're missing something here... namely how these medial PFC regions interact with the rest of the brain while making these snap decisions. Not to mention how this intersects with our past experience and future goals.


References

Botvinick MM. (2007). Conflict monitoring and decision making: reconciling two perspectives on anterior cingulate function. Cogn Affect Behav Neurosci. 7(4):356-66.

Carp J, Kim K, Taylor SF, Fitzgerald KD, Weissman DH. (2010). Conditional Differences in Mean Reaction Time Explain Effects of Response Congruency, but not Accuracy,on Posterior Medial Frontal Cortex Activity. Front Hum Neurosci. 4:231.

Cooper, J., Dunne, S., Furey, T., O'Doherty, J. (2012). Dorsomedial Prefrontal Cortex Mediates Rapid Evaluations Predicting the Outcome of Romantic Interactions Journal of Neuroscience, 32 (45), 15647-15656 DOI: 10.1523/JNEUROSCI.2558-12.2012

Posner MI, Rothbart MK, Sheese BE, Tang Y. (2007). The anterior cingulate gyrus andthe mechanism of self-regulation. Cogn Affect Behav Neurosci. 7(4):391-5.










The Journal of Neuroscience Speed Dating is a specialty journal in The Journal of Speed Dating Studies series.

Vicodin for Social Exclusion

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Cyberball (with apologies to Kipling D. Williams).


Cyberball (not the Atari version) is a virtual game designed by social psychologists to be a model for social rejection and ostracism (Williams et al., 2000). The study participant is led to believe they are playing an online ball-tossing game with other people, who then proceed to exclude them from the game. The resultant negative feelings are meant to be a proxy for ostracism based on fundamental attributes such as race, disability, physical appearance, homelessness, etc. This simple game has lead to a burgeoning cottage industry on social pain and its close resemblance to physical pain.


Social Pain and Physical Pain Are Not Interchangeable

That statement may sound obvious to you, but an increasing number of neuroimaging studies would have us believe otherwise. Whenever I read an article proclaiming that "the brain bases of social pain are similar to those of physical pain" (Eisenberger et al., 2003), I am reminded of how phenomenologically DIFFERENT they are. Waking up from general anesthesia and feeling undermedicated for surgery that took your body apart and put it back together again feels absolutely nothing like being rejected by your long-term partner. Your anterior insula and anterior cingulate cortex might be very busy in both cases, but they're also activated in many different situations (Yarkoni et al, 2011).

Indeed, of the 2238 total papers in the BrainMap neuroimaging database, 735 of them contain the search term 'anterior cingulate' (see also Shackman et al., 2011). Besides pain and emotion, the behavioral domains that activate this brain region include motor learning, language, speech, explicit memory, working memory, bladder control, thirst, sexuality, and perception in all five senses. Sure, the affective components of pain might show some overlap with physical pain (Kross et al., 2011), but distinct networks are likely responsible for the unique aspects of these different qualia.1


The Aversive Brain

Hayes and Northoff (2012) described a core brain network involved in the processing of aversive stimuli (or states) that can be either painful or non-painful in nature. They relied on evidence from both the human and animal literatures. Aversion here refers to more than social and physical pain, and includes avoidance of stimuli that are unpleasant, frightening or disgusting. Meta-analysis of human neuroimaging data showed overlap in some of the structures involved in non-painful aversion and physical pain (shown in green below), which accounted for 35% of Aversion-related voxels and 24% of Pain-related voxels. These overlapping regions included mid-cingulate cortex, posterior cingulate cortex, anterior insula, right ventrolateral prefrontal cortex (PFC), dorsomedial PFC, thalamus, midbrain, secondary motor cortex, and areas related to memory (right hippocampus/parahippocampal gyrus) and even reward (dorsal striatum).2

It is important to note here that some of the social pain darlings (mid-cingulate cortex, anterior insula, right ventrolateral PFC) are also activated by unpleasant pictures, sounds, and smells.

- click on image for a larger view -


Fig. 2 (Hayes & Northoff, 2012). Overlap of pain- and aversion-related networks in humans. Results of meta-analyses for human pain- (blue) and aversion- (yellow) related studies (top row), overlapping activations (green; top row and isolated in bottom row), and a corresponding table of associated brain regions. All results are family-wise error rate whole-brain corrected at p < 0.05


Furthermore, although there was substantial overlap between Aversion and Pain, 65% and 76% of all activations (respectively) were not shared. Structures uniquely activated by Aversion included the amygdala, hypothalamus, more anterior regions of the anterior cingulate, and another reward-related area (ventral striatum). Brain regions uniquely activated by Pain included the cerebellum, rostral pons, somatosensory cortex, posterior insula, and yet another dopamine-rich, reward-related area (ventral tegmental area).3

Dave J Hayes, co-author of the study, wrote about this fruitful cross species network approach to The Aversive Brain in his blog.


But Depression Hurts, doesn't it?

It sure does according to Lilly, who would also like us to believe that their drug Cymbalta (duloxetine, an SNRI antidepressant) will cure your aches and pains along with your depression. But Duloxetine Does Not Relieve Painful Physical Symptoms in Depression, according to a meta-analysis of five available studies (Spielmans, 2008).

How much overlap is there between brain activity associated with physical pain and feelings of sadness? To answer this question, I performed a meta-analysis of my own that made use of the BrainMap database of published neuroimaging experiments. Using GingerALE software, I did two activation likelihood estimate (ALE) meta-analyses to look at brain regions activated by experimental manipulations to induce physical pain and sadness (see Laird et al., 2005 for methodological details of ALE). In brief, the procedure involves three steps to determine the likelihood of activation across experiments:
  1. ALE and Testing Significance: Compute the ALE values for each voxel in the brain and performs a test to determine the null distribution of the ALE statistic at each voxel.
  2. Thresholding: Take the P values from the previous step and computes the threshold for the ALE map using the Tom Nichol’s FDR algorithm.
  3. Cluster Analysis: Perform cluster analysis on the thresholded map, based on the minimum volume that is specified in the previous step.

Using Sleuth to search the BrainMap database revealed 94 papers related to pain perception or pain monitoring/discrimination, which involved 1334 subjects, 345 experimental contrasts, and 3455 locations.4 The search for sadness identified 58 papers involving 1159 subjects, 193 experimental contrasts, and 1204 locations. The pinkish-colored regions in the figure below show the overlap between sadness (in blue) and pain (in red) — which is not very extensive! The slices were selected to highlight overlap in anterior cingulate (Left), mid-insula and basal ganglia (Middle), and anterior insula (Right).


The main points here are that:
  • Sadness is represented quite differently from physical pain.
  • The shared physical pain-social pain network also includes aversive responses to unpleasant sensory stimuli. Which are not painful.

So any treatment designed to ease the unpleasantness of physical pain would not help the concomitant  feelings of sadness, at least not directly. But treatments for social pain could generalize to the non-painful aversion network: disgusting and disturbing things might not seem as bad, either.

Have there been any effective manipulations to ease social pain? One unlikely study claimed that acetaminophen reduced the pain of social rejection (Dewall et al., 2010).  I was quite skeptical of this study, as outlined in Suffering from the pain of social rejection? Feel better with TYLENOL®:
 In Experiment 1, 30 participants (24 women, 6 men) took one 500 mg acetaminophen pill immediately after waking up and another 500 mg an hour before going to sleep (1,000 mg per day for 3 weeks). The other 32 participants (24 women, 8 men) took the same dosing of placebo for 3 weeks. Each evening, subjects filled out the the Hurt Feelings Scale (the "today" version) to report how much social pain they had experienced that day. Despite the fact that the half life of acetaminophen is 4 hours, it took about 10 days for the drug group to report significantly lower hurt feelings than the placebo group. The difference on day 21 was greatest (p < .005). However, the difference in change-over-time slopes between the two groups was only marginally significant (p ≤ .10). The explanation of the time course for these effects was unclear...
 Or as Time writer Maia Szalavitz said in a comment on the post:
This study would have made sense if they used opioids, which are known to reduce the emotional aspect of physical pain. There's also a high concentration of opioid receptors in the cingulate. Of course, the result wouldn't have been novel or surprising: junkies wouldn't exist if opioids didn't kill emotional pain.

Indeed, if acetaminophen could numb emotional pain, this would have been discovered by addicts by now. The fact that the drug remains boringly OTC suggests that this effect is either so small it can only be detected in the lab or nonexistent as the blog suggests.

Buffer the Pain Away5

This brings us to a new study (by one of the same authors) that administered transcranial direct current stimulation (tDCS) over right ventrolateral PFC and reported a reduction in negative feelings caused by exclusion in a game of Cyberball  (Riva et al., 2012). This article, like the acetaminophen one, was published Psychological Science.


Rather than launch into a full-scale summary of this study, I refer the interested reader to a post by Andrew Wilson Psychological Science...meet me at camera 3, which is not about this paper but summarizes some of the general issues that can be seen in 2-3 page short reports in Psych Science.

As for the specific findings of Riva et al. (2012), beyond asking whether all five of the rating scales confirmed the result (rather than just the two reported), I wonder about the specificity of the response to social exclusion. In other words, would tDCS reduce reactions to aversive stimuli in general (as noted above)? What do you think, does right frontal tDCS improve functioning in other domains? What do we know about its mechanisms of action?

And finally, do you buy the premise that social exclusion hurts, literally?


Footnotes

1 According to the Stanford Encyclopedia of Philosophy:
Philosophers often use the term ‘qualia’ ... to refer to the introspectively accessible, phenomenal aspects of our mental lives. ... Disagreement typically centers on which mental states have qualia, whether qualia are intrinsic qualities of their bearers, and how qualia relate to the physical world both inside and outside the head. The status of qualia is hotly debated in philosophy largely because it is central to a proper understanding of the nature of consciousness. Qualia are at the very heart of the mind-body problem. 

2 Presumably, the vast majority of subjects were not masochists or gluttons for punishment.

3 Another complicating factor is that this so-called "Pain Matrix" might not be specific to pain at all, but may instead reflect responses to highly salient stimuli in different modalities (Iannetti & Mouraux, 2010).

4 Compare this to 6 yrs ago, when my analysis for physical pain yielded only 35 studies (see Hypnosis and Pain Control).

5 OR you could F**k the Pain Away...

...as Peaches would say.


References

Dewall CN, Macdonald G, Webster GD, Masten CL, Baumeister RF, Powell C, Combs D, Schurtz DR, Stillman TF, Tice DM, Eisenberger NI. (2010). Acetaminophen reduces socialpain: behavioral and neural evidence. Psychol Sci. 21:931-7.

Eisenberger NI, Lieberman MD, Williams KD. (2003). Does rejection hurt? An FMRI study of social exclusion. Science 302:290-2.

Hayes, D., Northoff, G. (2012). Common brain activations for painful and non-painful aversive stimuli. BMC Neuroscience, 13 (1) DOI: 10.1186/1471-2202-13-60

Iannetti GD, Mouraux A. (2010). From the neuromatrix to the pain matrix (and back). Exp Brain Res. 205:1-12.

Kross E, Berman MG, Mischel W, Smith EE, Wager TD. (2011). Social rejection sharessomatosensory representations with physical pain. Proc Natl Acad Sci 108(15):6270-5.

Laird AR, Fox PM, Price CJ, Glahn DC, Uecker AM, Lancaster JL, Turkeltaub PE, Kochunov P, Fox PT. (2005). ALE meta-analysis: controlling the false discovery rate and performing statistical contrasts. Hum Brain Mapp. 25:155-164.

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