Monday, October 31, 2011

Buried Alive!

The pathological fear of being buried alive is called taphophobia1 [from the Greek taphos, or grave]. Being buried alive seems like a fate worse than death, the stuff of nightmares and horror movies and Edgar Allan Poe short stories. What could be pathological about such a fear? When taken to extremes, it can become a morbid, all-consuming obsession. In 1881, psychiatrist Enrico Morselli wrote about "two hitherto undescribed forms of Insanity" (English translation, 2001):
As the result of some observations I have made in recent years, I propose to add two new and previously undescribed varieties to the various forms of insanity with fixed ideas, whose underlying phenomenology is essentially phobic. The two new terms I would like to put forward, following the nomenclature currently accepted by leading clinicians, are dysmorphophobia and taphephobia.

The first condition consists of the sudden appearance and fixation in the consciousness of the idea of one’s own deformity; the individual fears that he has become deformed (dysmorphos) or might become deformed, and experiences at this thought a feeling of an inexpressible ansieta (anxiety). The second condition, taphephobia, consists of the sick person’s being plagued, at his approach to the time of his own death, by a fear of the possibility of being buried alive (taphe, grave), this fear becoming the source of a terribly distressing anguish. It is not necessary for me to give a very detailed description of these two new forms of rudimentary paranoia I have discovered and named, since in so doing I would only be repeating descriptions that have long been available among the many and varied forms of paranoia in books and the most important journals of psychiatry; instead, I shall limit myself to making some general comments on the conditions.

The ideas of being ugly and of being buried whilst in a state of apparent death are not, in themselves, morbid; in fact, they occur to many people in perfect mental health, awakening however only the emotions normally felt when these two possibilities are contemplated. But, when one of these ideas occupies someone’s attention repeatedly on the same day, and aggressively and persistently returns to monopolize his attention, refusing to remit by any conscious effort; and when in particular the emotion accompanying it becomes one of fear, distress, anxiety and anguish, compelling the individual to modify his behaviour and to act in a pre-determined and fixed way, then the psychological phenomena have gone beyond the bounds of normal, and
may validly be considered to have entered the realm of psychopathology.
Dysmorphophobia has come to be known as body dysmorphic disorder, a preoccupation with perceived defects in one's appearance (Buhlmann & Winter, 2011).

Although taphophobia seems irrational now with modern definitions of brain death,2 it was a more prevalent (and realistic) fear in the 19th century. "Safety coffins" with air tubes, bells, flags, and burning lamps were a booming business. However, these contraptions failed to assuage an inventor with severe taphophobia (Dossey, 2007):

One of the most popular safety devices in Victorian England was the Bateson Revival Device, invented by George Bateson, who made a fortune in sales. The gadget came to be known as Bateson’s Belfry. It consisted of an iron bell mounted on the coffin lid just above the deceased’s head, with a cord connected to the hand “such that the least tremor shall directly sound the alarm.” Ironically, his invention did nothing to relieve his own all-consuming fear of premature burial. In 1886, driven mad by his dread, he committed suicide by dousing himself with linseed oil and setting himself on fire.

Would you rather burn to death or suffocate in a coffin? Excruciating physical pain vs. sheer panic,3 bloodied limbs, and mental anguish? Not a pleasant choice.


1 Also spelled taphephobia.

2 Which are still controversial, nonetheless (Teitelbaum & Shemi, 2011).

3 Well, not if you're The Bride in Kill Bill Vol. 2.


Buhlmann U, Winter A. (2011). Perceived ugliness: an update on treatment-relevant aspects of body dysmorphic disorder. Curr Psychiatry Rep. 13:283-8.

Dossey L. (2007). The undead: botched burials, safety coffins, and the fear of the grave. Explore (NY). 3:347-54.

Morselli, E., & Jerome, L. (2001). Dysmorphophobia and taphephobia: two hitherto undescribed forms of Insanity with fixed ideas. History of Psychiatry, 12 (45), 103-107 DOI: 10.1177/0957154X0101204505 [Introduction]

Morselli, E. (2001). Dysmorphophobia and taphephobia: two hitherto undescribed forms of Insanity with fixed ideas. History of Psychiatry, 12 (45), 107-114 DOI: 10.1177/0957154X0101204506 [Translation of original Italian]

Teitelbaum J, Shemi SD. (2011). Neurologic determination of death. Neurol Clin. 29:787-99.

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Saturday, October 29, 2011

The oldest remaining werewolf movie

-from the story by Dr. C.A. Hill, adapted by Bennett Cohen

"Deep in the fastness of the great Canadian forests."

Plot summary

Dick Bannister is the new field boss of the Ford Logging Company, a Canadian logging-crew during a time when conflicts with the powerful Consolidated Lumber Company, a bitter rival company, have turned bloody, like a private war. His boss, Miss Edith Ford, comes to inspect the lumberjack camp, bringing her doctor fiancé with her. Dick is attacked by his rivals and left for dead. His loss of blood is so great that he needs a transfusion, but no human will volunteer, so the surgeon uses a wolf as a source of the blood...

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Saturday, October 22, 2011

Activation of the Hate Circuit While Reading 'Depression Uncouples Brain Hate Circuit'

A recent article published in Molecular Psychiatry has the curious title, 'Depression uncouples brain hate circuit' (Tao et al., 2011). Hate circuit, you ask? Is there really any such thing? Is the existence of a distinctive brain circuit for hate so well-established that we ought to go about including it in the title of our papers? And what does it mean for this circuit to be uncoupled in depression? That depressed people no longer have coherent feelings of hatred?

The current article refers to the one prior fMRI study on the topic, which examined the 'Neural correlates of hate' (Zeki & Romaya, 2008). The 17 participants were chosen because they expressed intense hatred for a particular individual. Sixteen people hated an ex-lover or a competitor at work, and one person hated a famous political figure (see Hate On Halloween for details of that study). Participants viewed pictures of a person they hate, and the resultant BOLD signal changes were compared to when they viewed pictures of neutral people.

And the groundbreaking hypothesis? Love and hate might be represented by different brain states! Who knew?
We hypothesized that the pattern of activity generated by viewing the face of a hated person would be quite distinct from that produced by viewing the face of a lover.
The results identified 7 regions that were significantly more active for the Hated Face condition than for the Neutral Face condition. The flaming figure above illustrates a few of them, including the medial frontal gyrus [the anterior cingulate cortex (ACC) and the pre-SMA], the right putamen, and bilateral premotor cortex. The other regions were the frontal pole and our friend, bilateral insula [activated in all sorts of conditions from speech to working memory to reasoning to pain to disgust to the allure of Chanel No. 5 and "love" of iPhones]. An additional correlation analysis related degree of hatred to level of activation across 5,225 voxels (using an uncorrected statistical threshold of p≤0.01) and found three regions to be most related: right insula, right premotor cortex, and right ACC.

These results set the stage for the current study by Tao et al. (2011), which compared the resting state functional connectivity patterns between controls and severely depressed individuals. The "resting state" or "default mode network" (DMN) is the brain activity observed when there is no active task (Raichle et al., 2001). In other words, the participants are free to daydream about their lover or to think about dinner or to remember the amusing movie from last night or to focus on feelings of despair. A specific group of brain regions has been identified as the DMN, and these are deactivated when participants have to perform a demanding cognitive or perceptual task.

A new feature of the present study was the community mining algorithm used to determine coherent resting state networks among the 90 regions of interest (ROIs). First, a template was formed based on data from 37 healthy controls. Then the network connectivity for the control template was compared to that of two depressed groups: 15 unmedicated first-episode major depressive disorder (FEMDD) patients and 24 resistant major depressive disorder (RMDD) patients.

The 6 "communities" or resting state networks are illustrated below. Note that RS1/DMN (red in the top figure) isn't identical to the typical DMN (orange in the bottom figure).

Top: Adapted from Fig 1C (Tao et al., 2011). Left: Medial view of the surface of the brain. Right: The lateral view of the surface of the brain. Different colors represent different communities. Bottom: Adapted from Buckner et al. (2008).

One big difference between the two schemes is that the dorsal ACC /SMA active task network (blue in the bottom left figure) is part of the DMN in Tao et al.'s community structure (red in the top left figure).

But wait, where is the 'hate circuit'?? It emerged with some bizarre post hoc hand waving:
It can be seen from Figures 2, 3 and 4 that the strongest evidence for reduced connectivity compared with control subjects in both FEMDD and RMDD is that between the insula and putamen in both brain hemispheres (s=0.4 and 0.25 for FEMDD and RMDD, respectively). Additionally, the link between the left superior frontal gyrus and the right insula is also reduced (s=0.2991 and 0.2658). Thus, the links between the three main components of the ‘hate circuit’ have become largely uncoupled.
OK, I thought Zeki's 'hate circuit' included bilateral premotor cortex and the frontal pole, plus the putamen only in the right hemisphere. But somehow, the community mining algorithm determined that the insula [part of RSN4 - auditory network] has links with the putamen [RSN6 - subcortical network] and the dorsal superior frontal gyrus [RSN1 - DMN, and perhaps not the same area as in Zeki & Romaya] only in controls but not in the depressed participants. And this set of links in controls comprises the 'hate circuit' and nothing else.

Adapted from Fig 4a (Tao et al., 2011). The common links of the first-episode major depressive disorder (FEMDD) and resistant major depressive disorder (RMDD) networks. Red lines are links that appear in depression network only while blue lines are links that appear in normal template only. The widths of the lines are proportional to the scores.

I was critical of the original 'neural correlates of hate' study 3 yrs ago, but at least the authors never used the term 'hate circuit' in their paper1. Plus, they had something interesting to say about the overlap between brain regions engaged by looking at pictures of those you love and hate:
Our studies did indeed reveal a basic pattern. As far as we can determine, it is unique to the sentiment of hate even though individual sites within it have been shown to be active in other conditions that are related to hate. The network has components that have been considered to be important in (a) generating aggressive behavior and (b) translating this behavior into motor action through motor planning. Finally, and most intriguingly, the network involves regions of the putamen and the insula that are almost identical to the ones activated by passionate, romantic, love.
Call me a hater, but maybe the 'love circuit' has come undone in the depressive folks instead... But really, if a clinical group is lacking functional coupling between the insula and the putamen, it can mean any number of things, not only that their so-called 'hate circuit' is incoherent.2 Another important question emerges from the control data: what does it mean to have strong functional connectivity within the 'hate circuit' at rest? That you spend a lot of free time filled with hate? One of the authors, Professor Jianfeng Feng, had this to say:
MRI study finds that depression uncouples brain’s hate circuit

. . .

“The results are clear but at first sight are puzzling as we know that depression is often characterized by intense self loathing and there is no obvious indication that depressives are less prone to hate others. One possibility is that the uncoupling of this hate circuit could be associated with impaired ability to control and learn from social or other situations which provoke feelings of hate towards self or others. This in turn could lead to an inability to deal appropriately with feelings of hate and an increased likelihood of both uncontrolled self-loathing and withdrawal from social interactions. It may be that this is a neurological indication that is more normal to have occasion to hate others rather than hate ourselves.”
Now it is a seriously long stretch to conclude, from the present resting state fMRI data, that the depressed groups are impaired in controlling or learning from hate-filled social interactions, and as a consequence transform these disjointing feelings into self-loathing. Perhaps it will be more instructive to read about 'Demoralization: its phenomenology and importance' instead...


1 That phrase was reserved for the university press release, although it's unclear who was actually responsible for coining it.

2 While we're at it, why are the left inferior frontal gyrus (opercular), left precentral gyrus , right inferior frontal gyrus (opercular), and right supramarginal gyrus considered the "risk/action" circuit?


Buckner RL, Andrews-Hanna JR, Schacter DL. (2008). The brain's default network: anatomy, function, and relevance to disease. Ann NY Acad Sci. 1124:1-38.

Raichle ME, MacLeod AM, Snyder AZ, Powers WJ, Gusnard DA, Shulman GL. (2001). A default mode of brain function. Proc. Natl. Acad. Sci. 98: 676–682.

Tao, H., Guo, S., Ge, T., Kendrick, K., Xue, Z., Liu, Z., & Feng, J. (2011). Depression uncouples brain hate circuit. Molecular Psychiatry DOI: 10.1038/mp.2011.127

Zeki S, Romaya JP. (2008). Neural correlates of hate. PLoS One 3(10):e3556.

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Tuesday, October 11, 2011

Rising Mortality Rates for People with Serious Mental Illness

Fig 1 (Hoang et al., 2011). Trend in standardised 365 day all cause mortality ratio for all people discharged from hospital with principal diagnosis of bipolar disorder or schizophrenia.

The "mortality gap" is the differential between the mortality rates for the general population and for persons with serious mental illness (schizophrenia and bipolar disorder). A new study from England examined hospital records for psychiatric patients discharged between 1999 and 2006, and determined how many had died within one year (Hoang et al., 2011). The authors expected to see a drop in the mortality gap over time due to government programs:
Over the past decade several strategies have been implemented in England and Wales aimed at reducing the mortality gap between people with serious mental illness and the general population, including those to address deliberate self harm and to reduce suicide (7 8 9), to decrease smoking (10 11 12), alcoholism, and drug misuse (13 14) and to deal with other lifestyles associated with increased mortality (15 16). Recent studies have suggested that the rate of suicide has been stabilising among people with mental disorders as a whole (17 18 19 20 21); however, trends in mortality for people with schizophrenia or bipolar disorder remain poorly characterised, particularly the relative contributions of natural and unnatural causes. The United Kingdom government’s recent mental health strategy states that “more people with mental health problems will have good physical health” as one of its objectives, specifically stating that “fewer people with mental health problems will die prematurely” (22). It is therefore timely to review the level of and trends in these recognised inequalities.
However, as illustrated in Fig. 1 above, the opposite trend was observed, with increased mortality for those with schizophrenia and bipolar disorder. The standardized mortality ratios show a rise from ~30-60% greater than the general population to about double the population average:
For people discharged with schizophrenia, the ratio was 1.6 in 1999 and 2.2 in 2006 (P<0.001 for trend). For bipolar disorder, the ratios were 1.3 in 1999 and 1.9 in 2006 (P=0.06 for trend). Ratios were higher for unnatural than for natural causes. About three quarters of all deaths, however, were certified as natural, and increases in ratios for natural causes, especially circulatory disease and respiratory diseases, were the main components of the increase in all cause mortality.
These results are alarming (but not new, unfortunately) and similar to those reported by Chang et al. (2011) - see Improving the Physical Health of People With Serious Mental Illness. In that post, I mentioned the possible role of "second generation" or atypical antipsychotics, which can cause substantial weight gain and hence diabetes, hypertension, cardiovascular problems, high cholesterol, and stroke. To counteract these serious side effects, a regular part of mental health treatment should include programs that promote better physical health: smoking cessation and nutritionists and structured exercise classes in addition to standard psychiatric care and substance abuse treatment. For example, a six month intervention pilot study enrolled 63 overweight participants at psychiatric rehabilitation day programs and showed promising initial results (Daumit et al., 2010).

These concerns were mentioned earlier in a systematic review of the literature by Saha et al. (2007), who urged immediate action:
“in light of the potential for second-generation antipsychotic medications to further adversely influence mortality rates . . . optimizing the general health of people with schizophrenia warrants urgent attention.”


Chang CK, Hayes RD, Perera G, Broadbent MT, Fernandes AC, Lee WE, Hotopf M, Stewart R. (2011). Life expectancy at birth for people with serious mental illness and other major disorders from a secondary mental health care case register in London. PLoS ONE 6(5):e19590.

Hoang, U., Stewart, R., & Goldacre, M. (2011). Mortality after hospital discharge for people with schizophrenia or bipolar disorder: retrospective study of linked English hospital episode statistics, 1999-2006. BMJ, 343:d5422. DOI: 10.1136/bmj.d5422

Daumit GL, Dalcin AT, Jerome GJ, Young DR, Charleston J, Crum RM, Anthony C, Hayes JH, McCarron PB, Khaykin E, Appel LJ. (2010). A behavioral weight-loss intervention for persons with serious mental illness in psychiatric rehabilitation centers. Int J Obes (Lond). 35(8):1114-23.

Saha S, Chant D, McGrath J (2007). A systematic review of mortality in schizophrenia: is the differential mortality gap worsening over time? Arch Gen Psychiatry 64:1123-31.


October 10 was World Mental Health Day, an event designed to raise public awareness of mental health issues:
This year the theme is "Investing in mental health". Financial and human resources allocated for mental health are inadequate especially in low resource countries. The majority of low- and middle-income countries spend less than 2% of their health budget on mental health.

Many countries have less than one mental health specialist per one million population. Even a considerable part of the limited resources is spent on large mental hospitals and not for services delivered through community and primary health care.

We need to increase investment for mental health and to shift the available resources towards more effective and more humanitarian forms of services.
More information and links available at Providentia and The Amazing World of Psychiatry.

World Mental Health Day Blog Party, sponsored by Psych Central.

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Thursday, October 06, 2011

New York Times on Addiction and The Insula

In Clue to Addiction, Brain Injury Halts Smoking

Published: January 26, 2007

Scientists studying stroke patients are reporting today that an injury to a specific part of the brain, near the ear, can instantly and permanently break a smoking habit. People with the injury who stopped smoking found that their bodies, as one man put it, “forgot the urge to smoke.”

The finding, which appears in the journal Science, is based on a small study [Naqvi et al., 2007]. But experts say it is likely to alter the course of addiction research, pointing researchers toward new ideas for treatment.

While no one is suggesting brain injury as a solution for addiction, the finding suggests that therapies might focus on the insula, a prune-size region under the frontal lobes that is thought to register gut feelings and is apparently a critical part of the network that sustains addictive behavior.

Hey, wait a minute!

Didn't the NYT just publish an authoritative piece to the contrary? In You Love Your iPhone. Literally., Martin Lindstrom claimed the insula was a signifier of love and compassion, not addiction:
WITH Apple widely expected to release its iPhone 5 on Tuesday, Apple addicts across the world are getting ready for their latest fix.

But should we really characterize the intense consumer devotion to the iPhone as an addiction? A recent experiment that I carried out using neuroimaging technology suggests that drug-related terms like “addiction” and “fix” aren’t as scientifically accurate as a word we use to describe our most cherished personal relationships. That word is “love.”

. . .

But most striking of all was the flurry of activation in the insular cortex of the brain, which is associated with feelings of love and compassion. The subjects’ brains responded to the sound of their phones as they would respond to the presence or proximity of a girlfriend, boyfriend or family member.

OK, OK, we all know by now that royal proclamations of brain function based on logical fallacies and unpublished (and never-to-be-peer-reviewed) commercial studies are not to be believed. NYT did publish a retort to this silliness, a Letter to the Editor (The iPhone and the Brain) in which "Forty-five neuroscientists respond to a recent Op-Ed about using brain imaging to analyze our attachment to digital devices." We also know that the insula is activated in a substantial percentage of all neuroimaging studies (Yarkoni et al. 2011; PDF). Reflecting this ubiquity, The Neurocritic blog archive contains 73 unique posts with the word "insula."

But what of addiction and the insula? In their 2007 Science paper, Naqvi and colleagues performed a retrospective study of 69 stroke patients (all smokers): 19 with lesions in the insula and 50 with lesions elsewhere. The color coding in the figure below depicts the number of individuals with damage in specific brain regions.

Fig. 1 (Naqvi et al., 2007). Number (N) of patients with lesion in each of the regions identified in this study, mapped onto a reference brain. Boundaries of anatomically defined regions are drawn on the brain surface. Regions not assigned a color contained no lesions. (Top) All patients. The horizontal line marks the transverse section of the brain shown in the top row. The vertical line marks the coronal section shown in the bottom row. (Middle) Patients with lesions that involved the insula. (Bottom) Patients with lesions that did not involve the insula.

The likelihood of post-stroke smoking cessation did not differ between the insula and non-insula groups, but those with insula lesions who did quit smoking reported that it was easy to do so. The authors concluded that...
...smokers with brain damage involving the insula, a region implicated in conscious urges, were more likely than smokers with brain damage not involving the insula to undergo a disruption of smoking addiction, characterized by the ability to quit smoking easily, immediately, without relapse, and without persistence of the urge to smoke.
The problem with this assertion is that it relies on memory for events that occurred an average of 8 yrs earlier, which could be subject to recall bias (Vorel et al., 2007). A better design would be a prospective study that follows patients from the time of stroke and then assesses subsequent smoking behavior. In fact, Bienkowski et al. (2010) performed such a study and failed to see a difference between their insula and non-insula groups at a 3 month follow-up. This suggests that the insula does not play a special role in addiction.

What does this mean for iPhone love? Is Lindstrom right? Unlikely! He would have to demonstrate that insular strokes cause an inability to feel love for iPhones (or anything else, for that matter). Such a finding would suggest that an intact insula is necessary for the experience of love and compassion, and that the activity in his fMRI experiment was not a mere epiphenomenon.

In the real world of peer-reviewed neuroimaging research, however, that sort of converging evidence is rarely obtained.

Further Reading

NYT Editorial + fMRI = complete crap

the New York Times blows it big time on brain imaging

Neuromarketing means never having to say you're peer reviewed (but here's your NYT op-ed space)

fMRI Shows My Bullshit Detector Going Ape Shit Over iPhone Lust

...and pollyannaish comment by Martin Lindstrom

NYT Letter to the Editor: The uncut version

Articles on insular cortex from The Amazing World of Psychiatry: A Psychiatry Blog

The Insula Is The New Black...

No Longer an Island, the Insula Is Now a Hub of High Fashion


Bienkowski P, Zatorski P, Baranowska A, Ryglewicz D, Sienkiewicz-Jarosz H. (2010). Insular lesions and smoking cessation after first-ever ischemic stroke: a 3-month follow-up. Neurosci Lett. 478:161-4.

Naqvi, N., Rudrauf, D., Damasio, H., & Bechara, A. (2007). Damage to the Insula Disrupts Addiction to Cigarette Smoking. Science, 315 (5811), 531-534 DOI: 10.1126/science.1135926

Vorel SR, Bisaga A, McKhann G, Kleber HD.(2007). Insula damage and quitting smoking. Science 317:318-9; author reply 318-9.

Yarkoni T, Poldrack RA, Nichols TE, Van Essen DC, Wager TD. (2011). Large-scale automated synthesis of human functional neuroimaging data. Nat Methods 8:665-70.

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Saturday, October 01, 2011

Neuromarketing means never having to say you're peer reviewed (but here's your NYT op-ed space)

There's a truly hideous op-ed piece in the New York Times by neuromarketing guru Martin Lindstrom:
You Love Your iPhone. Literally.

Published: September 30, 2011

WITH Apple widely expected to release its iPhone 5 on Tuesday, Apple addicts across the world are getting ready for their latest fix.

But should we really characterize the intense consumer devotion to the iPhone as an addiction? A recent experiment that I carried out using neuroimaging technology suggests that drug-related terms like “addiction” and “fix” aren’t as scientifically accurate as a word we use to describe our most cherished personal relationships. That word is “love.”

. . .

Earlier this year, I carried out an fMRI experiment to find out whether iPhones were really, truly addictive, no less so than alcohol, cocaine, shopping or video games. In conjunction with the San Diego-based firm MindSign Neuromarketing, I enlisted eight men and eight women between the ages of 18 and 25. Our 16 subjects were exposed separately to audio and to video of a ringing and vibrating iPhone.

In each instance, the results showed activation in both the audio and visual cortices of the subjects’ brains. In other words, when they were exposed to the video, our subjects’ brains didn’t just see the vibrating iPhone, they “heard” it, too; and when they were exposed to the audio, they also “saw” it. This powerful cross-sensory phenomenon is known as synesthesia. [NOTE: Not necessarily. It could also be called cross-modal activation.]

But most striking of all was the flurry of activation in the insular cortex of the brain, which is associated with feelings of love and compassion. The subjects’ brains responded to the sound of their phones as they would respond to the presence or proximity of a girlfriend, boyfriend or family member.
Oh boy.... Reverse inference alert! Reverse inference alert! Lindstrom committed a logical fallacy - one cannot directly infer the participants' cognitive or emotional state from the observed pattern of brain activity in neuroimaging experiments. See papers by Aguirre (2003) and Poldrack (2006).

Fortunately, Everybody's a Neurocritic! Reputable academic neuroimaging gurus Russ Poldrack and Tal Yarkoni have already written posts about this debacle: NYT Editorial + fMRI = complete crap and the New York Times blows it big time on brain imaging. Here they note the completely erroneous assumption that activation of insular cortex = love. As Yarkoni says:
The insula is one of a few ‘hotspots’ where activation is reported very frequently in neuroimaging articles (the other major one being the dorsal medial frontal cortex). So, by definition, there can’t be all that much specificity to what the insula is doing, since it pops up so often.
In fact,
In Tal Yarkoni’s recent paper in Nature Methods [PDF], we found that the anterior insula was one of the most highly activated part of the brain, showing activation in nearly 1/3 of all imaging studies!
In days of yore, The Neurocritic wrote about The Right and The Good and The Insula:
[The insula]'s a pretty large area. Besides being crowned the "seat of emotional reactions" (whatever that means), portions of the insula have been associated with interoceptive awareness, visceral sensation, pain, autonomic control, and taste, among other things... a lot of other things. Do a search of the BrainMap database using just two of the many insular foci reported by the Caltech researchers [Hsu et al., 2008] and you'll see activations related to action execution, speech, attention, language, explicit memory, working memory, and audition.
Then Who Can You Trust? deconstructed a Science paper entitled The Rupture and Repair of Cooperation in Borderline Personality Disorder by King-Casas et al. (2008). The study examined how well individuals with borderline personality disorder trusted others in an economic exchange game (called, conveniently enough, the Trust Game). In brief,
The authors linked the insular activation to the detection of social norm violations in interpersonal contexts, concluding that individuals with BPD are deficient in this regard. But what are the participants really thinking about during the 4-8 sec interval following a stingy offer? Do we have yet another example of reverse inference here?

Below is a figure generated from entering the x, y, z coordinates from the right insular focus into the Sleuth program (available at, which searched the available database of papers for matches. The resulting list of coordinates and experiments was then imported into the GingerALE program, which performed a meta-analysis via the activation likelihood estimation (ALE) method (see this PDF). The figure illustrates that this exact same region of the right insula was activated during tasks that assessed speech, language, explicit memory, working memory, reasoning, pain, and listening to emotional music.

So there we have it. Let's all read a peer reviewed Nature Methods paper [PDF] instead of buying Buyology...

Oh, and let's all sign a Letter to the Editor of the NYT.


Aguirre GK (2003). Functional Imaging in Behavioral Neurology and Cognitive Neuropsychology. In: T.E. Feinberg & M.J. Farah (Eds.), Behavioral Neurology and Cognitive Neuropsychology. New York: McGraw Hill.

Hsu M, Anen C, Quartz SR. (2008). The Right and the Good: Distributive Justice and Neural Encoding of Equity and Efficiency. Science 320: 1092-1095.

King-Casas B, Sharp C, Lomax-Bream L, Lohrenz T, Fonagy P, Montague PR (2008). The Rupture and Repair of Cooperation in Borderline Personality Disorder. Science 321: 806-810.

Poldrack RA (2006). Can cognitive processes be inferred from neuroimaging data? Trends in Cognitive Sciences 10: 59-63.

Yarkoni T, Poldrack RA, Nichols TE, Van Essen DC, Wager TD. (2011). Large-scale automated synthesis of human functional neuroimaging data. Nat Methods 8:665-70.

Lobus insularis [Insula] (labels in English and Japanese)

According to Wikipedia, the insula "lies deep to the brain's lateral surface, within the lateral sulcus which separates the temporal lobe and inferior parietal cortex. These overlying cortical areas are known as opercula (meaning "lids"), and parts of the frontal, temporal and parietal lobes form opercula over the insula."

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