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Should a book chapter be republished as a peer-reviewed article with no attribution?

UPDATE (10/23/2013): The authors have commented to offer their explanation for the omitted attribution.

An entire book chapter from a popular science trade book has been published as an "Original Research Article" in Frontiers in Psychiatry. The article appears as part of a Research Topic on Alternative Models of Addiction in Frontiers in Addictive Disorders and Behavioral Dyscontrol, a specialty section within Frontiers in Psychiatry.

I downloaded the provisional PDF and was initially tipped off by the curious citation style and copious use of footnotes, unlike the standard reference list seen in journal articles (e.g., APA format). I looked for a mention of the published book but could not find it anywhere. Perhaps this will be corrected in later editions of the article (if any).

The book is copyrighted (see below), but the nearly identical article is covered by a Creative Commons agreement, which states that the open-access text can be freely cited with attribution.

- click on images to enlarge -

Here's the Introduction, which is identical to Chapter 3 of the book (see above image).

But here's an abstract that might be unique to the Frontiers article (Satel & Lillienfeld, 2013):
The notion that addiction is a ''brain disease'' has become widespread and rarely challenged.The brain disease model implies erroneously that the brain is necessarily the most important and useful level of analysis for understanding and treating addiction. This paper will explain the limits of over-medicalizing -- while acknowledging a legitimate place for medication in the therapeutic repertoire -- and why a broader perspective on the problems of the addicted person is essential to understanding addiction and to providing optimal care. In short, the brain disease model obscures the dimension of choice in addiction, the capacity to respond to incentives, and also the essential fact people use drugs for reasons (as consistent with a self-medication hypothesis). The latter becomes obvious when patients become abstinent yet still struggle to assume rewarding lives in the realm of work and relationships. Thankfully, addicts can choose to recover and are not helpless victims of their own ''hijacked brains.''

Below is page 6 of the Provisional PDF.

Compare to pages 51 and 52 of the book.

Chapter 3, page 51

Chapter 3, page 52

This is such an egregious violation that I suspect it must be some sort of a mistake. I've had my differences of opinion with the book's authors,1 but I don't want to be seen as harboring animus to discredit them.2 Which is why I'm not repeatedly calling them out by name in the post (though it's obvious who they are). I do feel somewhat bad about the whole situation, and will post an addendum to clear up any misunderstandings, or any subterfuge by an unknown third party. I've contacted the journal editor, and will keep you posted.


1I do agree with some parts of the book's agenda (and in fact the authors include Mind Hacks, Neuroskeptic, and The Neurocritic in their Acknowledgments -- which is good, since many of their examples are from our blogs). But I disagree in particular with their idea that shaming addicts is helpful (and also with their stance on property dualism). See these posts:

The Destructive Power of Shame


All Washed Up

Finding Middle Ground on Neuroscience, by Daniel Lende

Book Review: Brainwashed, by Neuroskeptic

2Full disclosure: I also know that the first author is affiliated with the American Enterprise Institute, a conservative think tank ideologically opposed to my political beliefs.


Satel S, Lilienfeld SO (2013). Brainwashed: The Seductive Appeal of Mindless Neuroscience. Basic Books.

Satel S, Lilienfeld SO (2013). Addiction and the Brain-Disease Fallacy. Frontiers in Addictive Disorders and Behavioral Dyscontrol.  doi: 10.3389/fpsyt.2013.00141

Blurred Lines: The Science Blogosphere and the Borasphere

Hey, hey, hey

                      Hey, hey, hey

                             Blurred Lines
                                     ------Robin Thicke

full size image atScienceBloggingHR.jpg
One depiction of the science blogosphere (~2010), by Brian Reid

This is a post about the neuroscience blogosphere. It exists as a loose entity separate from the infographic above. Oh, there are a few stray overlaps here and there. But not many.

I was initially going to call this post Parallel Lines.

The story is subjective. It's told from one point of view. Mostly mine. So it's the perspective of a blogger who is a scientist. Not a science writer. Not exactly a "science communicator" either. Not part of a blog network. One who has never attended ScienceOnline. Therein lies the rub, the reason my ilk don't exist on infographics.

The Science Blogosphere

Other stories, many sad and angering and tragic tales, should really take precedence now. Stories of blurred lines and clearly crossed lines. Recent instances of censorship and harassment have deeply affected that parallel community, the one that dominates the discourse on science blogging. The reverberations have been felt far and wide. Perhaps the ongoing conversations about racism and sexism and sexual harassment and abuse of power will lead to positive lasting changes.

Time will tell.

graphic from the Journal of Feelsynapsis

The Borasphere

Bora Zivkovic was an incredibly influential, powerful, and prolific presence in the science blogging world, especially in the US. He was the community manager for the Scientific American Blog Network. He built it nearly from scratch. He encouraged and promoted a large number of young talented writers (most of whom were women).1 He was a manager / organizer of the ScienceOnline conference, the Open Laboratory anthologies, and the ScienceSeeker website.

He was known as The Blogfather. In 2010, he described the Changing Science Blogging Ecosystem in 8,247 words (mostly in terms of the ScienceBlogs network). In 2012 he went further and got to define what a science blog is and to write their history (6,868 words).

Many people came to confuse the Borasphere with the totality of the Science Blogosphere. Blogs that fell outside his sphere of influence barely existed. Should any one person be this powerful?

Blurred Lines

The Bora story above uses past tense verbs because everything changed October 16 to October 18.  Bora was forced to resign his positions when detailed accounts of sexual harassment came to light. While he devoted years to the cause and contributed many great things to science blogging at large, his legacy is tainted by these inappropriate violations of trust.

There is another tale that has not been told. It is not mine to tell. It exists in the realm of sheer speculation and might be better left unsaid.

Here's where the neuro/psych blogging comes in.

Laura Helmuth is the only person who's hinted at it publicly (that I know of), in her excellent piece at Slate:
At the most reprehensible end of the spectrum of possible explanations, Zivkovic is a predator who surrounded himself with inexperienced women because he considered them easy prey. Or perhaps he has some mental health problems with impulse control.  

Some of his behavior might be consistent with bipolar disorder, with mania/hypomania in particular. Bora was a chronobiologist who studied circadian rhythms in animals. He was also extremely knowledgeable about Lithium, Circadian Clocks and Bipolar Disorder and wrote lengthy posts on the topic. He was very prolific and energetic. Blog Around the Clock has an obvious double meaning.

If true, this DOES NOT excuse his behavior, but it may provide a possible explanation. You see, hypersexuality is a common symptom in those experiencing a hypomanic episode:

B. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree: 
(1) inflated self-esteem or grandiosity
(2) decreased need for sleep (e.g., feels rested after only 3 hours of sleep)
(3) more talkative than usual or pressure to keep talking
(4) flight of ideas or subjective experience that thoughts are racing
(5) distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli)
(6) increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation
(7) excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, or foolish business investments)

The Neuroscience Blogosphere

On October 14, Adam J Calhoun wrote a provocative post asking Why is there no neuroscience blogosphere?
Obviously, there are tons of great neuroscience blogs out there – I’m not even going to try to list them because they are numerous and I don’t want to accidentally leave one out. But there does not seem to be a blogosphere. To get all middle school on you, Wikipedia defines the blogosphere as the collection of all blogs and their interconnections, implying that they exist as a connected community.

When I look around at the Economics blogosphere, I see a lot of give-and-take between blogs. One blog will post an idea, another blog will comment on it, and the collective community has a discussion. I see this discussion, to a greater or lesser extent, in the other communities I follow: math, physics, and ecology. Yet missing in all this is neuroscience, and perhaps biology in general. Why is this?

. . .

Are biologists just less interested in discussing broad ideas? I wouldn’t think so, but I don’t see any equivalent to, say, Dynamic Ecology, where discussions on neuroscience ideas big and small can kick off. I think the closest we get is the Neuroskeptic/critic axis.

Well, I was very flattered indeed to be part of the axis of evil...

One thing I've tried to do in my many years of neuroblogging is to provide a loose sense of community by the mere aggregation of independent, non-network neuroscience and psychology blogs. The impetus for this was the rise in number, prominence, and clout of the blogging networks in 2010, and a definition of science blogging that excluded our voices. We're in the @neuroghetto, folks. This alternate history is recounted in Independent Neuroblogs as part of the science blogging ecosystem.

Obviously, many excellent network-based blogs have long been part of Adam's neuroscience blogosphere too, and some of these straddle multiple worlds.2  I'm not here to be exclusionary.

In general, I’d rather be critiquing the latest faux pas in neuro/psych research then blathering on about the current state of the blogosphere (i.e., blogging about blogging).3 But with all these recent events I felt like my head was going to explode.  I wish everyone well.


1This caused #RipplesOfDoubt.

2 Foremost among them (in my mind) is Scicurious, who was an early protégé of Bora. In fact, I waited for her thoughtful response to the scandal before posting anything myself. Very insightful commening as well; this comment by Razib Khan was especially notable.

3 There’s nothing inherently wrong in blogging about blogging, but it’s usually not my thing.

                                              Hey, hey, hey

DARPA allocates $70 million for improving deep brain stimulation technology


In what appears to be an exclusive story, the New York Times has reported that the Defense Advanced Research Projects Agency (DARPA) will spend $70 million over the next 5 years to further develop and improve deep brain stimulation (DBS) techniques. This funding is part of President Obama's BRAIN Initiative.

Agency Initiative Will Focus on Advancing Deep Brain Stimulation

Published: October 24, 2013
. . .

The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology.

Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.”

And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.”

The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation.

The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought.

I couldn't find a news announcement on DARPA's website or a request for research proposals. The program hasn't even been mentioned in their Twitter feed!


On the other hand, the NIH Director's BRAIN Advisory Committee issued its Interim Report (PDF) on September 16. The report is focused primarily on animal models, including improved technologies for recording neuronal activity and manipulating circuit function. Section 6d mentions Devices for Monitoring and Stimulating the Human Brain, but mostly in the context of recruiting patients as research participants.1

DARPA tends to fund, shall we say, very ambitious (and unorthodox) research projects. For BRAIN, they want to develop a device that can monitor and detect the symptoms of a psychiatric illness, deliver appropriate DBS, and record neural activity to determine whether the treatment was successful.2 The article continues:
Darpa’s goal would require solving several longstanding problems in neuroscience, one of which is to develop a detailed model of how injuries or illnesses like depression manifest themselves in the systems of the brain.

The next step is to create a device that can monitor the signs of illness or injury in real time, treat them appropriately and measure the effects of the treatment. The result would be something like a highly sophisticated pacemaker for a brain disorder.

Darpa is asking for research teams to produce a device ready to be submitted to the Food and Drug Administration for approval within five years.

“Is it overambitious? Of course,” said Dr. Mayberg, adding that working with the brain is “a slow process.” But she said that it was an impressive first investment and that the clear emphasis on human illness was “stunning.”

The driving force of the research program is to improve treatments for combat veterans who suffer from mental and physical conditions. These are pressing needs for DARPA, problems that warrant immediate solutions. This is one government agency that doesn't want to wait around for “a slow process” to yield results...

ADDENDUM: For more information, read A Tale of Two BRAINS: #BRAINI and DARPA's SUBNETS


1 Oddly, theNYT article says NIH "has not decided on its emphasis, appears to be aiming for basic research, based on the recommendations from a working committee advising the agency." I thought the 58 page report provided detail on NIH's emphasis.

2 Perhaps they would also like a device to predict (and prevent) criminal offending, like in this rough sketch:
Is it possible for a brain scan to predict whether a recently paroled inmate will commit another crime within 4 years? A new study by Aharoni et al. (2013) suggests that the level of activity within the anterior cingulate cortex might provide a clue to whether a given offender will be rearrested.

Dress this up a bit and combine with a miniaturized brain-computer interface that continuously uploads EEG activity to the data center at a maximum security prison. There, machine learning algorithms determine with high accuracy whether a given pattern of neural oscillations signals the imminent intent to reoffend that will trigger deep brain stimulation in customized regions of prefrontal cortex, and you have the plot for a 1990s cyberpunk novel.



Image credits.Left:SUBNETS program (DARPA). Right:BRAIN interim report presentation (NIH).

In April, the White House announced the $100 million Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative. The goals of this bold new research effort are to "revolutionize our understanding of the human mind and uncover new ways to treat, prevent, and cure brain disorders like Alzheimer's, schizophrenia, autism, epilepsy, and traumatic brain injury." A series of high-profile journal articles traced the genesis of this initiative from the Brain Activity Map idea to develop nanotechnologies and "image every spike from every neuron" (Alivisatos et al., 2012) to its current emphasis on neural circuits and systems neuroscience more broadly construed (Insel et al., 2013). In the first year (FY 2014),1 $50 million will be allocated to DARPA and $40 million to NIH.2

The two federal agencies have taken starkly different approaches to the challenge, in terms of timing and scope. They also address different levels of nervous system function. Both are ambitious, but one surpasses earlier calls for a "moon shot" to the mind.  IF successful,3 it would render much of pre-clinical neuroscience research quaint and obsolete (except for providing mechanistic details).

The Tale of Two BRAINS

1. The National Institute of Health (NIH) sponsored a series of meetings and solicited public feedback. The NIH Director's BRAIN Advisory Committee issued its Interim Report (PDF) on September 16. The report focuses primarily on animal models, including improved technologies for recording neuronal activity and manipulating circuit function.4 Here are the high-priority research areas for FY 2014:
#1.  Generate a Census of Cell Types.
#2.  Create Structural Maps of the Brain. 
#3.  Develop New Large-Scale Network Recording Capabilities.
#4.  Develop A Suite of Tools for Circuit Manipulation.
#5.  Link Neuronal Activity to Behavior.
#6.  Integrate Theory, Modeling, Statistics, and Computation with Experimentation.  
#7.  Delineate Mechanisms Underlying Human Imaging Technologies.
#8.  Create Mechanisms to Enable Collection of Human Data.
#9.  Disseminate Knowledge and Training.
These are very ambitious projects, each delineated in more detail in the full report (PDF). However, the NIH has yet to issue a Request for Applications that outlines the requirements for grant proposals submitted through this program.

2. On the other hand, the Defense Advanced Research Projects Agency (DARPA) announced their goals for the BRAIN Initiative via the New York Times on October 24 and and issued a broad agency announcement (call for proposals) on October 25. The focus is on developing technologies and treatments that use deep brain stimulation (DBS), which has been highly successful in Parkinson's Disease.

There are 3 Technical Areas that are covered in the announcement. All applicants must address Area One, and teams of investigators are encouraged to address all three.
TA One is comprised of clinical trials in order to establish mechanistic models of awake, behaving human brain activity.

TA Two encompasses the hardware development component in order to create safe and effective sensing and stimulation systems.

In TA Three, investigators will use human-relevant animal models [primates, not rodents] to generate safety and efficacy data as well as establish preliminary theories and rapidly prototype hypotheses regarding the links between neural data and clinical outcomes. 
To elaborate, over a 5 year period, the successful applicants must conduct clinical trials in human patients with 7 specified psychiatric and neurological disorders (not including PD), some of which have never been treated with DBS. The successful teams will use devices that both stimulate and record neural activity, and provide real-time data that can be decoded as reflecting a particular behavioral state... basically, a futuristic implant that can adjust its own stimulation parameters based on how the patient is doing. At least, that's how I interpret it.

Brainstorm (1983). Brain-computer interfaces have improved a bit in the last 30 yrs.

Systems-Based Neurotechnology for Emerging Therapies (SUBNETS)

Let's take a closer look at TA One of DARPA's SUBNETS program.
SUBNETS is distinct from current therapeutic approaches as it seeks to develop the ability to create a closed-loop diagnostic and therapeutic system. Through measuring pathways involved in complex systems-based brain disorders such as depression, compulsion, debilitating impulse control, and chronic pain, SUBNETS will attempt to establish the capability to record and model how these systems function in both normal conditions, among volunteers seeking treatment for unrelated neurologic disorders, as well as impaired clinical research participants. SUBNETS will then use these models to determine appropriate therapeutic stimulation methodologies that meet guidelines for both safety and efficacy in human participants. These models will be adapted onto next-generation, closed-loop neural stimulators that exceed currently developed capacities for simultaneous stimulation and recording and provide a research investigator, a clinician, and a human research participant with the ability to record, analyze, and stimulate multiple brain regions for therapeutic purposes.

Seven disorders are targeted: Post-Traumatic Stress Disorder (PTSD), Major Depression, Borderline Personality Disorder (BPD), General Anxiety Disorder (GAD), Traumatic Brain Injury (TBI), Substance Abuse/Addiction, and Fibromyalgia/Chronic Pain. To the best of my knowledge, there is no published literature on DBS for PTSD, BPD, GAD [as opposed to OCD], or TBI [except for minimally conscious state]. At clinicaltrials.gov, a Pilot Study of DBS of the Amygdala for Treatment-Refractory Combat PTSD was withdrawn prior to enrollment. There's one DBS trial for TBI that aims to enroll 5 patients over a 4 year period. I couldn't find anything for BPD or GAD (although these disorders might possibly be comorbid in some patients treated for depression or OCD).

With this starting point in mind...
All proposers must address each of the conditions described above by the end of Phase Two of this program. If, through the course of Phase One, a given condition is demonstrated to not be amenable to modeling and intervention as described in this BAA, performers will be allowed to describe an alternative condition.

Here are the milestones for Phase One (24 months):
  • Generate models for two DSM diagnosis categories chosen from: (A) Major Depression, (B) PTSD, (C) General Anxiety Disorder, (D) Borderline Personality Disorder.
  • Generate models for one disrupted neurologic of physiologic system chosen from: (A) Fibromyalgia/Chronic Pain, (B) TBI, (C) Substance Abuse/Addiction.
  • Demonstrate ability to intraoperatively relieve symptom severity with computer in the loop (measured through neural signature of disease as well as phenotypic presentation).
  • Evaluate the effects of intraoperative stimulation on symptomology at four hours, 24 hours, and 72 hours through neural recordings and behavioral experiments.

For Phase Two (36 months):
  • Refine models from Phase One.
  • Generate models for remaining two DSM diagnosis categories and two neurological/physiological systems.
  • Demonstrate ability to intraoperatively relieve symptom severity with device in the loop (measured through neural signature of disease as well as phenotypic presentation).
  • Demonstrate ability to chronically relieve symptom severity over 14 day window.
  • Demonstrate ability to provide therapy in response to stimuli in free-living environment.

So perhaps every major DBS center (e.g., Emory, University of Toronto, UCLA, Oxford, Brown, Butler, Cleveland Clinic, Mayo Clinic, Stanford, Johns Hopkins, Bonn, Magdeburg, Amsterdam, etc.) can work together to develop appropriate models for all the disorders and choose precise target locations. Then they'd need to collaborate with the brain decoding crowd, BCI developers, and William Gibson.


1 Stanford professor and working group co-chair Bill Newsome said:
"The government shutdown will very definitely affect BRAIN--will bring it to a complete halt in fact. To write good proposals, to get them evaluated, to get the money committed for this next year flowing, that’s a long process--even with the NIH process moving at warp speed, it takes the better part of a year. We on the working group, we delivered our end of the bargain. NIH wants to deliver on its end of the bargain, but they simply can’t do it if they’re sitting at home on an unwanted furlough."

2 Plus $20 million to NSF (Samuel et al., 2013) and over $120 million from private foundations.

3 I hate to be a wet blanket, but don't see how the entire DBS research community could achieve some of the Phase 2 goals within 5 years. I'm not alone in this. Dr. Helen Mayberg, one of the researchers most qualified to submit a proposal to DARPA, said:
“Is it overambitious? Of course,” said Dr. Mayberg, adding that working with the brain is “a slow process.” But she said that it was an impressive first investment and that the clear emphasis on human illness was “stunning.”

4 One section of the report mentions Devices for Monitoring and Stimulating the Human Brain, but mostly in the context of recruiting patients as research participants (not in developing technologies or treatments... which is covered by DARPA).

Further Reading

Agency Initiative Will Focus on Advancing Deep Brain Stimulation

BRAIN Initiative Interim Report: A Readers Guide

BRAIN Initiative Links at Empirical Planet

BAM and BRAINI links at Nucleus Ambiguous

From BAM to The BRAIN Initiative: A clearer view of a major neuroscience enterprise

Neuroscience thinks big (and collaboratively).

Scientific priorities for the BRAIN Initiative.

The challenge of connecting the dots in the B.R.A.I.N.


Alivisatos AP, Chun M, Church GM, Greenspan RJ, Roukes ML, & Yuste R (2012). The brain activity map project and the challenge of functional connectomics. Neuron, 74 (6), 970-4 PMID: 22726828

Insel TR, Landis SC, & Collins FS (2013). Research priorities. The NIH BRAIN Initiative. Science, 340 (6133), 687-8 PMID: 23661744

Marie Laveau Conjures a Horde of Avenging Zombies


In American Horror Story: Coven, New Orleans Voodoo Queen Marie Laveau casts a spell to avenge the brutal lynching of an African American high school boy in 1961. She's calling up the undead.

The zombie resurrection starts with one hand poking through the dirt, followed by the slow but steady emergence of a marauding horde. This may not be an entirely accurate scenario, however, since most cemeteries in New Orleans are above ground. The stone crypts and mausoleums are tourist attractions, with Marie Laveau's tomb being a particular favorite.

The four white racists try in vain to dispense with the intruders, to no avail. Silly rednecks! Don't you know that guns are useless against zombies? They'll just tear you limb from limb. It's a bloody awesome scene!

Marie Laveau is played by the fabulous Angela Bassett.

Ailurophobia (fear of cats) and the ability to sense their presence


Here's a leftover Halloween treat from American neurologist Silas Weir Mitchell (1829–1914).1 Mitchell was an illustrious physician known for discovering complex regional pain syndrome, coining the term "phantom limb", and prescribing the sexist "rest cure" (bed rest) for 19th century nervous maladies.2 His work on the treatment of neurasthenia and hysteria had an influence on Sigmund Freud, although the treatments were medical in nature and not psychoanalytic.

In 1902, he consulted on a case of a young female patient who had an extreme fear of cats, and claimed she could always tell if one was nearby. Mitchell was skeptical, and he wrote about his doubts in an entertaining fashion (Mitchell, 1905):
She declared that she could always detect the presence of an unseen and unheard cat. Since, however, she was constantly announcing the presence of a cat, it was not surprising that, like a clock that has stopped and tells the time correctly twice in the twenty-four hours, her occasional successes confirmed her belief. Her failures had of course no contradictory value.

Nevertheless, he became curious about this general phenomenon. Three years later, he reported the results from a self-selected sample who responded to a series of questions about cats (Mitchell, 1905). Specifically, he was searching for people who were afraid of cats.
A. 1. Have you any antipathy to cats?
     2. Are you subject to unusual feelings or symptoms in the presence of a cat?
     3. What are these?
     4. Does the presence of a tiger in a menagerie affect you as do cats?
     5. Can you account for your cat fear by anything obvious, as, for example, any incident of childhood?
     6. At what age did you first discover your peculiarity as to cats?

B. 1. Are you surely aware of the presence of a cat when it is not in sight, or known to be near?
     2. If yes, give the evidence, your own, and that of others as to the fact.
     3. What feelings or symptoms make you sure of the cat's presence?
     4. Is it the cat odor?
     5. How long have you had this peculiarity? 

Ailurophobia (the irrational fear of cats) is a type of specific phobia, one less common than the fear of spiders or snakes. Since this was 1905, Mitchell couldn't embed a poll at his LiveJournal or use SurveyMonkey. Instead, he published the questions in the journal Academic Medicine. The responses were impressive in number, in my view, but suffered from some of the same pitfalls you might expect from an internet poll:
The request was widely copied, and I received 159 replies from persons in America, England and Germany. Many were from well-known persons — professors, army officers, physicians and the like. About a third were valueless. A few were from men or women who were personally well known to me, and who I am certain may be trusted.

Some responses were thrown out because the individual suffered from asthma — a trivial explanation for the ability to sense an unseen cat. The reactions of the non-asthmatic individuals were typically immediate:
There may be only fear, terror, disgust; there may be added chilly sensations, horripilation, weakness, locked jaw, or, as in one case, fixed, open jaw, rigidity of arms, pallor, nausea, rarely vomiting, pronounced hysteric convulsions and even temporary blindness. These pass away with removal of the cat, but in a few examples leave the sufferer nervously disturbed for a day. Two report themselves as apt to have dreams of cats, what one of them calls "cat-mares."

The affliction did not differentiate between men and women, although women often suffered from more "extreme symptoms" (according to Mitchell). But even a macho military man, a big game hunter of tigers, was not spared from the terror of domestic house cats.

When asked whether there was a specific incident that caused their fear, the majority could not name a single one. Three mentioned a scary incident in childhood and one "a prenatal incident affecting the mother. Nothing of value was obtained." There was no attempt to provide a psychoanalytic explanation for ailurophobia.

Mitchell identified 27 cases of cat phobia with what he deemed a credible ability to detect an unseen cat in the room, who were without asthma and who denied any ability to smell the hidden creature. He appears to have conducted some experiments with concealed cats, but he doesn't want to bore us with any of the methodological details:
I should overload my paper if I were to relate in detail the cases in which cats were concealed in order to test the disbelieved capacity to detect them when not in sight and in which the hidden cat was at once known to be near. One or two permit of doubt; others are unassailable.

Assuming "unassailable" is accurate (a strong assumption), how were these people able to know a cat was nearby? Mitchell favored the ability to detect an odor that did not reach conscious awareness:
There may be olfactory emanations distinguished by some as odors and by others felt, not as odors, but only in their influential results on nervous systems unusually and abnormally susceptible. No other explanation seems to me available...

What he cannot explain, however, is why the irrational fear of cats developed in the first place. But leave it to a Freudian psychoanalyst in the 1950s to come up with a sexual explanation...

Ailurophobia and Ornithophobia (Cat Phobia and Bird Phobia)

Mitchell made a horrible mistake with his "rest cure" (which was depicted in The Yellow Wallpaper), but at least his didn't try to blame cat phobia on Mommy or Daddy. That angle was covered by Louis S. London almost 50 years later (London, 1952). First, he reviewed the [fortunately] meager psychoanalytic literature of the day, and found two examples: a supposedly paraphilic 48 year old woman who "identified herself with the cat, an embodiment of infantile, criminal ideas, a force which repressed sexual interest" and a 41 year old man with bird phobia in "in which a large homosexual component and identification with the father were found."

London was the author of a slew of books on [supposedly] abnormal sexual behavior and sexual deviations, so you know where this is headed. His published case of interest here is that of dual animal phobia in a 25 year old female patient (London, 1952). She hated her mother, of course. In brief, "her phobias symbolized fear of genitals and constituted the cause of her marked sexual frigidity." The presentation of her sexual history is downright embarrassing (and unbelievable), so I won't recount it here. Suffice it to say that she probably made things up to please/shock/alienate her psychiatrist:
During analysis, the patient, supporting her procrastination by a plea of amnesia for sexual events, did not disclose anything about sexuality until 75 sessions had passed. She was so reluctant to give information about her sex life that she sent the analyst a letter reporting some of her experiences.

The analyst, however, ignored the letter and waited for the woman to speak freely of the matters she had described in writing.

She was married to a man who was a terrible lover. She hated being a housewife and wanted to work outside the home. However, the explanations for her unhappiness were frigidity and latent homosexuality, respectively. The history devolves and London's explanations become more and more preposterous:
She became frightened whenever she saw a strange woman. This fear, representing fear of latent homosexuality, was similar to her fear of birds... It was especially strong when she was in the presence of women who were angry.

The kicker, though, is the opinion expressed by the patient's surgeon:
In the middle of analysis she developed acute abdominal pains. The possibility of a psychogenic etiology was considered, but the acuteness of the pain, coupled with the fact that her mental condition had improved, made this improbable. She was sent to an internist who made a diagnosis of appendicitis and advised an operation. He scoffed at the psychoanalytic treatment she had been getting.

Then we have two pages about dreams (none of which contained cats or birds, but the interpretations did dwell on "sadistic and bisexual conflicts"). And then we get the final pronouncement:
The cats and birds [not snakes] were symbols of the phallus, and she feared them because she feared heterosexuality. This is interwoven with her sexual frigidity with the consequent clinical picture shown in this paper.

But there's more! There's an Epilogue. London interviews the patient 14 years later. She's no longer afraid of cats and birds, yet she's still disinterested in sex with her husband. So much for a causal connection...


1 The contemporary actor of the same name is a descendent.

2 I recommend a post by Dr. Romeo Vitelli for those interested in learning more about The Bed Rest Cure prescribed to writer Charlotte Perkins Gilman.


Louis S. London, M.D. (1952). Ailurophobia and ornithophobia. The Psychiatric Quarterly 26: 365-371.

S. WEIR MITCHELL, M.D. (1905). OF AILUROPHOBIA AND THE POWER TO BE CONSCIOUS OF THE CAT AS NEAR, WHEN UNSEEN AND UNHEARD. Transactions of the Association of American Physicians 20:  4-14.

Now Is That Gratitude?


Now is that Gratitude,
Or is it really love?
Some kind of reality
That fits just like a glove

--Danny Elfman, Gratitude

Praise and condemnation serve a powerful purpose in our social and internal lives. They prop us up and tear us down. We reward ourselves (and others) when we perform good deeds, give a pat on the back for a job well done. Conversely, we punish bad behavior. Some people are more vengeful than others when they're wronged; other individuals might be more inclined to blame themselves, even when it's not their fault.

Laws and religions and etiquette and complex ethical systems enforce the rules of behavior. For most human beings of a certain age, moral emotions are the result of abiding by or violating these social norms. Moral emotions can be defined as “those emotions that are linked to the interests or welfare either of society as a whole or at least of persons other than the judge or agent” (Haidt, 2003). They can entail reacting to events that don't directly involve the self, as in the case of sympathy or contempt.

Zahn and colleagues (2013) refer to these feelings and reactions as moral sentiments, “following philosophers of the Scottish enlightenment who pointed to their role as key motivators of moral behaviour (Bishop, 1996).” In a recent study, they conceptualized four of these moral sentiments in a 2 x 2 grid, depending upon whether the emotion involved praise or blame, of oneself or of another (Zahn et al., 2013).

                          SELF       OTHER    
PRAISE      Pride       Gratitude
BLAME      Guilt        Indignation

Their goal was to determine whether there are individual differences in regional gray matter volumes associated with self-reports on the Value-related Moral Sentiment Task, which attempts to quantify personally felt human emotions.

Moral Phrenology

Does the tendency to experience each of these moral sentiments correlate with the size of different regions of the brain? The strong form of this question assumes the brain is modular and divisible into separate regions that oversee distinct processes. It also reflects a belief in the “brain is like a muscle” analogy, with discrete regions growing larger with use and smaller with disuse. In Franz Gall's original formulation of phrenology, there were 27 “organs” or mental faculties that could be measured by palpating bumps on the skull. The list of faculties was further refined and developed by Spurzheim (1815), Combe (1834 & 1847), and Lundie (1844). 1

Phrenological Chart, via Wikimedia Commons

For example, the organ of Benevolence is “situated at the upper part of the frontal bone... When it is large, the frontal bone rises with an arched appearance; when small, the forehead is low and retreating.”

Zahn et al. (2013) didn't palpate bumps on the skull, of course. Instead, they used voxel-based morphometry (VBM) to quantify regional gray matter (GM) volumes in 63 participants. In turn, these GM volumes were related to scores for each moral sentiment, controlled for positive and negative valence (Zahn et al., 2013):
We examined the effects of each moral sentiment measure (e.g. pride-proneness) on GM volume across the whole brain while using the other moral sentiment of equal valence (e.g. gratitude-proneness) as a covariate of no interest to control for effects of valence. We thus used two separate models to test for positive and negative emotions. All reported results were thus partial effects of one moral sentiment controlled for the adjusted effect of the equal-valence moral sentiment.

The Value-related Moral Sentiment Task (VMST) consists of 180 descriptions of positive or negative interactions between a participant and their best friend in which either they (self-agency, N=90), or their best friend (other-agency, N=90), acted in accord with (N=90) or counter to (N=90) social and moral values. The four conditions thus measured proneness to:
  1. Pride (POS_SELF): positive self-agency (e.g. ‘Yourself acting in a generous way towards Sam [best friend]’)
  2. Gratitude (POS_OTHER): positive other-agency (e.g. ‘Sam acting in a generous way towards you’)
  3. Guilt (NEG_SELF): negative self-agency (e.g. ‘Yourself acting in a stingy way towards Sam’)
  4. Indignation (NEG_OTHER): negative other-agency (e.g. ‘Sam acting in a stingy way towards you’)
The task was to choose the most fitting label (pride, gratitude, embarrassment[not examined here], guilt, indignation/anger, or none/other) for what they'd feel in response to each example. Participants then rated the unpleasantness or pleasantness of their projected feelings on a scale of -4 to +4.

Based on the authors' previous studies, the set of a priori brain regions of interest (ROIs) included anterior temporal lobes, posterior superior temporal sulcus/temporo-parietal junction, frontopolar cortex, dorsolateral prefrontal cortex (PFC), ventromedial PFC, lateral orbitofrontal cortex, dorsomedial PFC, insula, amygdala, basal ganglia, septum, hypothalamus, and ventral tegmental area.

However, there was no relationship at all between gray matter volumes in these predicted regions and any of the moral sentiments. Therefore, the correlations between 13 ROIs and scores for 4 moral sentiments yielded no significant results.

Instead, larger right inferior temporal cortex volumes were associated with the propensity to experience Gratitude (Fig. 1c), while smaller precuneus and cuneus volumes were associated with greater Pride-proneness (Fig. 1d). This is very surprising, since the cuneus contains primary visual cortex (Area V1, aka Brodmann area 17 in primates). Why would humble people have larger primary visual cortices? Because they spend more time looking at the outside world?

The Guilt-proneness and Gratitude-proneness voxels in the dorsolateral PFC (Figs. 1a and 1b) were not significant after correction for multiple comparisons.

Fig. 1 (Zahn et al., 2013). Individual differences were depicted as increases (yellow) or decreases (blue) in GM volume that were associated with proneness to experience a specific moral sentiment on the experimental task in N=63 participants.

Since the straightforward VBM analyses were a complete bust, the authors did post-hoc analyses in the subset of subjects who participated in an earlier fMRI study, evaluating individual differences in  guilt-related BOLD responses and their relationship to GM volumes. I won't discuss that here.

How do the authors explain Figure 1? Clearly, their predictions did not pan out. 2 After ruling out low statistical power as an issue, they put forth their best explanation: neuroanatomical differences cannot explain individual variation in responses on the VMST.
An alternative explanation which we favour is that structural variability in brain regions critical for specific moral sentiments is low between healthy participants, because high psychosocial functioning may not allow for large variations in structural anatomy within brain systems critical for moral motivations.

This doesn't stop them for offering highly speculative explanations for some of their findings (namely, the claim that gratitude might recruit visual imagery to a greater extent than pride):
We interpret the finding that individuals with higher GM volume within posterior cortical areas showed lower proneness to respond with pride and higher proneness to respond with gratitude as possibly being related to differences in reliance on visuo-spatial representations of morally salient scenes associated with these different types of feelings. A well-developed posterior cortical system may facilitate construction of detailed scenes which could play a more important role for experiencing gratitude than pride.

Now Is That Gratitude?

The present study illustrates the folly of modern-day moral phrenology. You can't measure the size of the anterior insula and determine whether someone is a self-righteously indignant person, or believe that the organ of gratitude is housed in the right inferior temporal cortex. Gratitude is a complex emotion that plays a huge role in positive psychology. You can be grateful for the weather or for your standard of living. Is praise of another person a valid operational definition of Gratitude as a moral sentiment? Or is this another form of wishful thinking, like the critical positivity ratio of 2.9013 (Brown et al., 2013)?


1For all phrenology all the time, see The History of Phrenology on the Web, by John van Wyhe.

2The authors made the following specific predictions:
...based on evidence from patient lesion studies (Moll et al., 2011) and fMRI (Takahashi et al., 2004; Moll et al., 2007; Kedia et al., 2008; Zahn et al., 2009b), we hypothesized associations of frontopolar GM volume with guilt-proneness. Based on recent studies, we further expected the importance of subgenual parts of the anterior cingulate (Zahn et al., 2009a, b) and the septal region (Zahn et al., 2009b; Moll et al., 2011) for individual variation on guilt-proneness. In contrast, we expected lateral orbitofrontal/insular areas to be associated with indignation-proneness based on an fMRI study directly probing indignation (Zahn et al., 2009b), a study in which this region showed activation for decisions based on moral anger (Moll et al., 2006), and evidence that a lateral orbitofrontal region was selectively more activated for other-critical feelings (anger and disgust) vs prosocial moral feelings including guilt (Moll et al., 2007). Our hypotheses for pride- and gratitude-proneness were less well supported due to a relative scarcity of evidence. Our main expectations were that pride-proneness and gratitude-proneness should be related to differences within mesolimbic and basal forebrain areas, specifically the hypothalamus, ventral tegmental area (VTA) and septal area (Zahn et al., 2009b).


Haidt, J. (2003). The moral emotions. In R. J. Davidson, K. R. Scherer, & H. H. Goldsmith (Eds.), Handbook of affective sciences. Oxford: Oxford University Press.(pp. 852-870).

Zahn R, Garrido G, Moll J, & Grafman J (2013). Individual differences in posterior cortical volume correlate with proneness to pride and gratitude. Social Cognitive and Affective Neuroscience PMID: 24106333

But when I think of you
And what you've done to me
You took away my hope
You took away my fantasy
I was set up for pride
The world was in my hands
I lived way at the top
In castles made of sand

--Danny Elfman, Gratitude

(Oooh) I dream of you sometimes

New Deep Brain Stimulation System Measures Neurotransmitter Release


Wireless Instantaneous Neurotransmitter Concentration Sensing System (WINCS) Patient Module printed circuit board & sterilizable case. (Fig. 1, Kimble et al. 2009).

Last month, the New York Times reported that the Defense Advanced Research Projects Agency (DARPA) will spend $70 million to further the development of technologies that use deep brain stimulation (DBS), which has been highly successful in treating Parkinson's Disease (PD). The SUBNETS program (Systems-Based Neurotechnology for Emerging Therapies) is part of the BRAIN Initiative that aims to "revolutionize our understanding of the human mind."

DARPA issued their call for proposals on October 25. My original take was that the goals were overly ambitious and nearly impossible to achieve within the specified time frame:
To elaborate, over a 5 year period, the successful applicants must conduct clinical trials in human patients with 7 specified psychiatric and neurological disorders (not including PD), some of which have never been treated with DBS. The successful teams will use devices that both stimulate and record neural activity, and provide real-time data that can be decoded as reflecting a particular behavioral state... basically, a futuristic implant that can adjust its own stimulation parameters based on how the patient is doing. At least, that's how I interpret it. 

How close are we to seeing a DBS implant that not only stimulates neural tissue, but also records electrical or chemical signals and then uses this information to adjust the stimulation parameters? Closer than I originally suspected. A recent Nature News article reported on the Mayo Clinic's efforts to develop a DARPAesque, state-of-the-art implant that aims to track brain signals in real time:
Researchers hope that the device will identify the electrical and chemical signals in the brain that correlate in real time with the presence and severity of symptoms, including the tremors experienced by people with Parkinson’s disease. This information could help to uncover where and how DBS exerts its therapeutic effects on the brain, and why it sometimes fails, says Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minnesota, who is leading the project.
. . .

...Using a method called fast-scan cyclic voltammetry, the device applies a localized voltage change in the brain. This transiently pulls electrons off certain neurotransmitters — the brain chemicals that activate or inhibit neurons — giving rise to electrical currents that can be measured. Each neurotransmitter molecule produces a different electrochemical signature, which can be used to identify it and estimate its concentration every 10 milliseconds.

Studies in awake behaving rats have used fast-scan cyclic voltammetry to measure phasic dopamine release associated with burst firing (Robinson et al., 2003).

Fig, 3 (Robinson et al., 2003). Heterogeneity of electrically evoked dopamine release in the nucleus accumbens of a freely moving rat.

Further information about the device is provided in this article from the Mayo Clinic, which indicates that the WINCS has already been tested in 15 human patients with Parkinson's disease or essential tremor. The study registered in clinicaltrials.gov is described as an Efficacy Study whose primary purpose is basic science:
Neurotransmitter Measurements Using Wireless Instantaneous Neurotransmitter Concentration System (WINCS) During Deep Brain Stimulation Neurosurgery

In this study, the investigators will monitor extracellular neurotransmitter levels using a probe that is able to perform real time electrochemical detection during deep brain stimulation surgery. The overall question this study is designed to answer is: Are there neurotransmitters released during deep brain stimulation?

Interestingly, the primary outcome measure is adenosine1 release recorded by WINCS, and the secondary outcome measure is dopamine release (pre-, during, and post-DBS, over a time frame of 30 min). Adenosine A2A antagonistsmay extend the duration of action of L-dopa, a primary treatment for PD. Preliminary studies in rats were able to detect subsecond dopamine and adenosine release at an implanted sensor in the striatum during high-frequency stimulation of ascending fibers (Kimble et al., 2009). It seems the early results in patients were also successful in measuring neurotransmitter release.

The WINCS will be integrated with another device, the MINCS (Mayo Investigational Neuromodulation Control System), which is optically linked to WINCS. The entire system is being tested in animal models to deliver brain stimulation wirelessly.

Fig 1B (Chang et al., 2013). Photograph of the MINCS-WINCS hardware showing relative size, optical connection, and recording and stimulating electrode leads. ADC = analog-to-digital converter; DAC = digital-to-analog converter; LPF = low-pass filter; MC = microcontroller; TIA = transimpedance amplifier; V/I Sense = voltage/current sense. Numbers 1 and 4 indicate the microcontrollers; 2 and 3 are the Bluetooth modules.

These developments in DBS devices for Parkinson's disease are very impressive indeed, but DARPA wants to go 7 steps further by developing similar closed-loop systems for use in Post-Traumatic Stress Disorder (PTSD), Major Depression, Borderline Personality Disorder (BPD), General Anxiety Disorder (GAD), Traumatic Brain Injury (TBI), Substance Abuse/Addiction, and Fibromyalgia/Chronic Pain. As I said previously:
To the best of my knowledge, there is no published literature on DBS for PTSD, BPD, GAD [as opposed to OCD], or TBI [except for minimally conscious state]. At clinicaltrials.gov, a Pilot Study of DBS of the Amygdala for Treatment-Refractory Combat PTSD was withdrawn prior to enrollment. There's one DBS trial for TBI that aims to enroll 5 patients over a 4 year period. I couldn't find anything for BPD or GAD (although these disorders might possibly be comorbid in some patients treated for depression or OCD).

Although there is a tremendous amount yet to learn about Parkinson's, much more is known about the pathophysiology of PD than of any of the disorders listed above. But given the list of speakers at a recent Society for Neuroscience symposium on the Mechanisms of Deep Brain Stimulation Efficacy in Neuropsychiatric Disorders, scientists and clinicians at Mayo, Emory, Butler/Brown, and Case Western are certainly working on these problems. $70 million from DARPA would sure come in handy, even if the ambitious endpoints are unattainable within 5 years.


1Caffeine is an adenosine antagonist, but the drugs used as adjunct therapies in PD are istradefylline and preladenant.


Chang SY, Kimble CJ, Kim I, Paek SB, Kressin KR, Boesche JB, Whitlock SV, Eaker DR, Kasasbeh A, Horne AE, Blaha CD, Bennet KE, & Lee KH (2013). Development of the Mayo Investigational Neuromodulation Control System: toward a closed-loop electrochemical feedback system for deep brain stimulation. Journal of Neurosurgery. PMID: 24116724

Kimble CJ, Johnson DM, Winter BA, Whitlock SV, Kressin KR, Horne AE, Robinson JC, Bledsoe JM, Tye SJ, Chang SY, Agnesi F, Griessenauer CJ, Covey D, Shon YM, Bennet KE, Garris PA, & Lee KH (2009). Wireless Instantaneous Neurotransmitter Concentration Sensing System (WINCS) for intraoperative neurochemical monitoring. Conference proceedings: Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 2009, 4856-9. PMID: 19963865

Robinson DL, Venton BJ, Heien ML, Wightman RM. (2003). Detecting subsecond dopamine release with fast-scan cyclic voltammetry in vivo. Clin Chem. 49:1763-73.

Nature News link via @GholsonLyon

Confessions of a Prosocial Psychopath


Many neuroscientists have been howling about the media coverage surrounding a new book written by UC Irvine Professor Emeritus, Dr. James H. Fallon. This is because unbeknownst to himself for 58 years (or apparently to anyone else, for that matter), he was secretly a psychopath. How did he finally discover this? Did he complete the Psychopathy Checklist and score over 30?


Instead, he diagnosed himself as a psychopath on the basis of his PET scan.

Compared to a control brain (top), neuroscientist James Fallon’s brain (bottom) shows significantly decreased activity in areas of the frontal lobe linked to empathy and morality—anatomical patterns that have been linked with psychopathic behavior. Image via James Fallon in The Smithsonian.

This is a case of reverse inference, assuming that a certain pattern of brain activity indicates a particular behavioral state (or in this case, a specific psychiatric diagnosis). While it may be true at the group level that activity in the ventromedial prefrontal cortex is decreased in psychopaths, it's not possible to diagnose an individual on this basis (at least not with our current state of knowledge).

In fact, Fallon himself initially doubted the ugly possibility that he's lacking in empathy, morality and self-control:
In [his book], Fallon seeks to reconcile how he—a happily married family man—could demonstrate the same anatomical patterns that marked the minds of serial killers.

“I’ve never killed anybody, or raped anyone,” he says. “So the first thing I thought was that maybe my hypothesis was wrong, and that these brain areas are not reflective of psychopathy or murderous behavior.”

Not with certainty, they're not. The Smithsonian article continues:
Eventually, based on further neurological and behavioral research into psychopathy, he decided he was indeed a psychopath—just a relatively good kind, what he and others call a “pro-social psychopath,” someone who has difficulty feeling true empathy for others but still keeps his behavior roughly within socially-acceptable bounds.

A "prosocial psychopath"? Isn't this an oxymoron? Aren't psychopaths antisocial by definition? Eventually, he came to doubt the classification scheme. Psychopathy doesn't appear in the DSM...
...in part because it encompasses such a wide range of symptoms. Not all psychopaths kill; some, like Fallon, exhibit other sorts of psychopathic behavior.

“I’m obnoxiously competitive. I won’t let my grandchildren win games. I’m kind of an asshole, and I do jerky things that piss people off,” he says. “But while I’m aggressive, but my aggression is sublimated. I’d rather beat someone in an argument than beat them up.”

This is psychopathy??

(Perhaps) in response to a snarky query on Twitter ("There goes Hare's PCL"[to paraphrase]), Dr. Fallon noted:

But he looks like such a genial fellow!

Taking a quick look insideThe Psychopath Inside (p. 26), we learn that Fallon viewed himself as a "nice, regular guy" who was popular and able to form close friendships with women.1 Should we rely on his brain scan, or on his behavior, when applying such a stigmatizing label?

Confessions of an Extremely Antisocial Female Psychopath

Another book published this year would make an interesting pairing with Fallon's personal discovery neuroscience / memoir: Confessions of a Sociopath, by the anonymous "M. E. Thomas". If you want narcissistic antisocial [but nonviolent] braggadocio, this is the book for you.2 For starters, the author is female, placing her in the minority of those with antisocial personality disorder. She's also a Mormon law professor in California.

"Ms. Thomas" wears the stigmatized behaviors as a badge of pride, although she erroneously calls herself a "sociopath" (which doesn't exist as a diagnostic label). But what do I know? She's SO brilliant – she passed the bar exam without even studying (while everyone else was crying):
I loved getting high marks in school; it meant I could get away with things other students couldn't. When I was young, what thrilled me was the risk of figuring out just how little I could study and still pull off the A. It was the same for being an attorney. During the California bar exam, people were crying from the stress. The convention center where the exam took place looked like a disaster relief center; people made desperate attempts to recall everything they had memorized over the prior eight weeks—weeks that I spent vacationing in Mexico. Despite being woefully ill-prepared by many standards, I was able to maintain calm and focus enough to maximize the knowledge I did have. I passed while others failed.

And she's oh so charming!
You would like me if you met me. I have the kind of smile that is common among television show characters and rare in real life, perfect in its sparkly teeth dimensions and ability to express pleasant invitation. I'm the sort of date you would love to take to your ex's wedding—fun, exciting, the perfect office escort. And I'm just the right amount of successful so that your parents would be thrilled if you brought me home.

But the best take on the book comes from Patrick Bateman, who reviews it for Slate:
I take the elevator up to my apartment and wash my hands and sit in my cream leather chair and chase an Adderall with a J&B and read the book in one sitting. It begins with a psychological evaluation that describes M.E. Thomas as a “prototypical psychopathic personality” manifesting “a ruthless and calculating attitude toward social and interpersonal relationships, and a relative immunity to experiencing negative emotions.” ...
. . .

...She’s into “the fine art of ruining people,” according to the title of Chapter 7. She seduces with charisma, and she cunningly covers her hollowness with superficial charm. She’s a “Nietzschean machine.”

And she violates social norms like it’s her job. Emotionally she takes no prisoners: The high school teacher she falsely accuses of harassment, the friends whose boyfriends she sleeps with just because she can, the colleagues she mind-fucks—they’re all just roadkill...

I'd much rather read Fallon's memoir. He sounds like an upstanding and sympathetic guy, despite the fact that he's related to Lizzy Borden.

Further Reading

The Disconnection of Psychopaths

Born This Way?

I Feel Your Pain... and I Enjoy It

Can Brain Activity Predict Criminal Reoffending?

Are Cognitive Factors Related to Criminal Reoffending?

"None of us are saints"

The Stylized Neuroscience of Psychopaths


1 Interestingly, on page 28 we learn that he developed OCD in junior high, in particular an obsession with Catholicism and morality.

2 Confessions of a Glib Blogger: I haven't read either book.

The Phases of Shopping Addiction


The blight of Black Friday is upon us. What better time to look at a recent paper on compulsive shopping?

Sohn and Choi (2013) adopted a qualitative approach and recruited a small group of Korean housewives with problematic shopping habits via consumer news websites. These nine women ranged in age from 28 to 40. The authors identified their target group as individuals with compulsive buying disorder, who reported a "preoccupation with shopping, pre-purchase tension or anxiety, and sense of relief following the purchase defined by Faber and O’Guinn (1992)." The participants all had high scores on the Faber and O’Guinn 14 item "compulsive buying checklist."

The authors conducted in-depth 2 hour interviews with each participant and analyzed the data according to a six-step contents analysis (Kim et al. 1999) that derived concept clusters, subcategories, and categories. Of note are these Five Sequential Phases of Shopping Addiction (Sohn & Choi, 2013):

Phase 1. Retail therapy,Filling up emptiness with shopping”
Phase 2. Denial,Ignoring overconsumption”
Phase 3. Debt-ridden,Ran out of money, while nothing left”
Phase 4. Impulsive buying,Driving ones-self to hasty buying”
Phase 5. Compulsive buying,It is crazy but I cannot stop”

Accompanying these phases are 5 themes, 15 subthemes, and 43 codes (shown in detail below).

- click on image for a larger view -

Do you have a strong urge to purchase the latest Xbox One or PS4 before they sell out? Would you feel anxious if you didn't get one? If so, then you may be in Phase IV, Impulsive Buying.

But if you go to the mall every morning and shop online every day, it's all over. You've reached Phase V, Compulsive Buying.


Sang-Hee Sohn and Yun-Jung Choi (2013). Phases of Shopping Addiction Evidenced by Experiences of Compulsive Buyers. International Journal of Mental Health and Addiction DOI: 10.1007/s11469-013-9449-y

men are map readers and women are intuitive, but bloggers are fast

Connection-wise analysis for males and females (Ingalhalikar et al., 2013).

Blink and you've missed it! Is the news cycle over already? I've been too busy real-working under my rock.
The hardwired difference between male and female brains could explain why men are 'better at map reading'

A pioneering study has shown for the first time that the brains of men and women are wired up differently which could explain some of the stereotypical differences in male and female behaviour, scientists have said.

Researchers found that many of the connections in a typical male brain run between the front and the back of the same side of the brain, whereas in women the connections are more likely to run from side to side between the left and right hemispheres of the brain.
. . .

“In women most of the connections go between left and right across the two hemispheres while in men most of the connections go between the front and the back of the brain,” [Ragini Verma] said.

Because the female connections link the left hemisphere, which is associated with logical thinking, with the right, which is linked with intuition, this could help to explain why women tend to do better than men at intuitive tasks, she added.

“Intuition is thinking without thinking. It's what people call gut feelings. Women tend to be better than men at these kinds of skill which are linked with being good mothers,” Professor Verma said.

Ha, ha, ha! You can't be serious, Professor Verma...

And then we have this gem from the Guardian:
Male and female brains wired differently, scans reveal
. . .

Ragini Verma, a researcher at the University of Pennsylvania, said the greatest surprise was how much the findings supported old stereotypes, with men's brains apparently wired more for perception and co-ordinated actions, and women's for social skills and memory, making them better equipped for multitasking.

"If you look at functional studies, the left of the brain is more for logical thinking, the right of the brain is for more intuitive thinking. So if there's a task that involves doing both of those things, it would seem that women are hardwired to do those better," Verma said. "Women are better at intuitive thinking. Women are better at remembering things. When you talk, women are more emotionally involved – they will listen more."

She added: "I was surprised that it matched a lot of the stereotypes that we think we have in our heads. If I wanted to go to a chef or a hairstylist, they are mainly men." [NOTE: the study population ranged in age from 8 to 22, and I don't think sexual orientation was reported... if we're going to talk stereotypes.]

Within one day of the paper's publication in PNAS (Ingalhalikar et al., 2013), critical blog posts were streaming in to counter the gender stereotypes spouted by the authors themselves. It's the mad new world of rapid-fire post-publication peer review! Trial by Twitter and blog and PubPeer.

I almost feel sorry for the authors, like they've been living in rosy days of yore and weren't aware of the looming backlash, not only to their soundbytes, but to their science.

Although I wasn't able to write a proper post about the paper myself, I suppose I should feel proud that such a community of critics sprang into action on such short notice. PNAS has certainly been target of mine for oh, almost 8 years now...


asking questions about men and women by looking at teenagers

A quick moan about ‘male’ and ‘female’ brains

Are men better wired to read maps or is it a tired cliché?

New insights into gendered brain wiring, or a perfect case study in neurosexism?

How social media is transforming scientific debate, on Storify.

Men, Women, and Big PNAS Papers

Getting in a Tangle Over Men’s and Women’s Brain Wiring

What's For Breakfast? Fried Girl and Boy Brainz! How Men's And Women's Brains are Dramatically Different And What It All Means.

Discussion at PubPeer

ADDENDUM (Dec 5 2013, 9:45PM)

Brain scans prove there is no difference between male and female brains

We don't have to "wire" our children's brains to reinforce gender stereotypes

So my mushy head is 'hardwired' for girly things, is it? If this is science, I am Richard Dawkins

Extra, Extra! Scientists misunderstand own research!

Study: Male, Female Brains Wired Differently

About that PNAS Article: Journalism and Neurosexism
[Figure 1] is a fascinating example of a series of ontological, technological, and statistical translations leading to a 'wiring diagram', i.e. an ostensibly metaphoric image standing in for a series of evidently absent but detectible and determinative differences. These differences in wiring are then cast into normative social frames and categories. ...

...Now I could be mistaken here - the paper is very dense. But to me, the authors appear to have imagined a Platonic ideal brain connectome that is uni-sexed. One has to ask then: could there be 95 different regions of interest that show the brains are more alike then we thought - probabilistically that is! If not, then it would seem that their model doesn't really reflect the one with which they began.


M. Ingalhalikar, A. Smith, D. Parker, T. D. Satterthwaite, M. A. Elliott, K. Ruparel, H. Hakonarson, R. E. Gur, R. C. Gur, R. Verma (2013). Sex differences in the structural connectome of the human brain. PNAS.DOI: 10.1073/pnas.1316909110

The Manifestation of Migraine in Wagner's Ring Cycle


German Composer Richard Wagner (1813-1883) wasn't the healthiest guy. He suffered from heart disease, skin disorders, acute infections, minor ailments, and most prominently, recurring headaches – the “main plague” of his life (Göbel et al., 2013). He complained of “Headache, ‘sick headache,’ ‘dyspepsia,’ ‘nervousness,’ melancholy, insomnia, indescribable suffering... Wagner had all of them all of the time” (Gould, 1903).

Wagner wrote many letters to his doctor, Dr. Pusinelli, over a 35 year period (Gould, 1903):
They begin with, "I have headache," and continue with complaints of bad weather and bad health; of growing old and loss of joy (aged 33 years); of increase of illness; working at composition with consequent frightful suffering; with prayers for peace, peace; moans at the uselessness of life; regrets at inability to get a good photograph; and sleeplessness. Baths and douches drive him nearly crazy. There is longing for his natural joyfulness; reiteration of physical and mental exhaustion; the thought of suicide; emphasis of his irritability and of his inability to write another line, etc.

A new article in the Christmas edition of BMJ by a trio of Göbels (Göbel, Göbel, & Göbel, 2013) focuses on Wagner's migraines and how he incorporated the attacks and auras into his operas. The specific example of interest is the opera Siegfried (1876), which is the third part of the Ring Cycle.
The first scene of act 1 of the opera Siegfried provides an extraordinarily concise and strikingly vivid headache episode. The music begins with a pulsatile thumping, first in the background, then gradually becoming more intense. This rises to become a directly tangible almost painful pulsation. While the listener experiences this frightening headache sensation, Mime is seen pounding with his hammer, creating the acoustic trigger for the musically induced throbbing, painful perception. At the climax Mime cries out: “Compulsive plague! Pain without end!”

A contemporary staging of Siegfried by Anthony Pilavachi portrays the character of Mime as a scientist in a white lab coat (see video below). Göbel et al. (2013) identify a “migraine aura leitmotif” that occurs in act 1, scene 3. It depicts the visual disturbances that accompany migraine aura. Mime sings, “Loathsome light! Is the air aflame? What is it flaring and flashing, glittering and whirring, what is swirling and whirling there and flickering around? It glistens and gleams in the sunlight’s glow. What is it rustling and humming and blustering there?”

Wagner's disabling migraines contributed to a 12 year disruption in his work on Siegfried, which was finally completed in 1871 and first staged in 1876. He wrote of his struggles in one of his many letters, this one to Franz Liszt in January 1857 (Gould, 1903):
My health, too, is once more so bad that for ten days after I had finished the sketch for the first act of Siegfried, I was literally not able to write a single bar without being driven away from my work by a most alarming headache. Every morning I sit down, stare at the paper, and am glad enough when I get as far as reading Walter Scott. The fact is I have once more overtaxed myself, and how am to recover my strength? With Rheingold I got on well enough but the Valkyrie caused me much pain. At present my nervous system resembles a pianoforte very much out of tune. 

The Göbels summarize their paper in the video below.

Here's hoping that your holiday season is headache-free!


Carl H Göbel, Anna Göbel, Hartmut Göbel (2013). “Compulsive plague! pain without end!” How Richard Wagner played out his migraine in the opera Siegfried BMJ DOI: 10.1136/bmj.f6952

George M Gould (1903). THE ILL-HEALTH OF RICHARD WAGNER. Lancet DOI: 10.1016/S0140-6736(01)34061-8 

BRAIN Initiative Funding Opportunites at NIH


National Institutes of Health (NIH) has finally released detailed descriptions for six separate funding opportunities in support of the BRAIN Initiative. If you're big on cells, circuits, and/or technologies, one of these programs could be for you. NIH hopes to award $40 million by the end of the fiscal year (September 30, 2014). The application deadlines are all in March 2014.

In October, Defense Advanced Research Projects Agency (DARPA) announced that it would spend $70 million over the next five years to develop and improve deep brain stimulation (DBS) techniques. The approaches of the two agencies are quite different, as outlined in this post.

The NIH Director's BRAIN Advisory Committee issued its Interim Report (PDF) on September 16. The report focused on animal models, including improvement of technologies for recording neuronal activity and manipulating circuit function. The new Requests for Applications (RFAs) reflect the high-priority research areas for FY 2014. Here are concise summaries of the new funding opportunities from the White House:
  • Generate an inventory of the different types of cell types in the brain
  • Develop new tools to analyze the complex circuits that are responsible for brain function by delivering  genes, proteins and chemicals to particular cells
  • Develop new approaches to record the activity of large numbers of neurons in any location in the brain, and improve existing technologies so they can be widely adopted by neuroscientists
  • Understand large-scale neural circuits by integrating experimental, analytical, and theoretical approaches
  • Form teams to develop the next generation of non-invasive imaging technologies

As you can see, Cellular/Molecular and Systems/Circuits neuroscience researchers will benefit the most, along with engineers, physicists, and other technology-development types.

Here are the RFA summaries from NIH:
  • Transformative Approaches for Cell-Type Classification in the Brain (RFA-MH-14-215) – aims to pilot classification strategies to generate a systematic inventory/cell census of cell types in the brain, integrating molecular identity of cell types with connectivity, morphology, and location. These pilot projects and methodologies should be designed to demonstrate their utility and scalability to ultimately complete a comprehensive cell census of the human brain.

  • Development and Validation of Novel Tools to Analyze Cell-Specific and Circuit-Specific Processes in the Brain (RFA-MH-14-216) – aims to develop and validate novel tools that possess a high degree of cell-type and/or circuit-level specificity to facilitate the detailed analysis of complex circuits and provide insights into cellular interactions that underlie brain function. A particular emphasis is the development of new genetic and non-genetic tools for delivering genes, proteins and chemicals to cells of interest; new approaches are also expected to target specific cell types and or circuits in the nervous system with greater precision and sensitivity than currently established methods.

  • New Technologies and Novel Approaches for Large-Scale Recording and Modulation in the Nervous System (RFA-NS-14-007) – focuses on development and proof-of-concept testing of new technologies and novel approaches for large scale recording and manipulation of neural activity, with cellular resolution, at multiple spatial and/or temporal scales, in any region and throughout the entire depth of the brain. The proposed research may be high risk, but if successful could profoundly change the course of neuroscience research.

  • Optimization of Transformative Technologies for Large Scale Recording and Modulation in the Nervous System (RFA-NS-14-008) – aims to optimize existing and emerging technologies and approaches that have the potential to address major challenges associated with recording and manipulating neural activity. This FOA is intended for the iterative refinement of emergent technologies and approaches that have already demonstrated their transformative potential through initial proof-of-concept testing, and are appropriate for accelerated engineering development with an end-goal of broad dissemination and incorporation into regular neuroscience research.

  • Integrated Approaches to Understanding Circuit Function in the Nervous System (RFA-NS-14-009) – focuses on exploratory studies that use new and emerging methods for large scale recording and manipulation to elucidate the contributions of dynamic circuit activity to a specific behavioral or neural system. Applications should propose teams of investigators that seek to cross boundaries of interdisciplinary collaboration, for integrated development of experimental, analytic and theoretical capabilities in preparation for a future competition for large-scale awards.

  • Planning for Next Generation Human Brain Imaging (RFA-MH-14-217) – aims to create teams of imaging scientist together with other experts from a range of disciplines such as engineering, material sciences, nanotechnology and computer science, to plan for a new generation of non-invasive imaging techniques that would be used to understand human brain function. Incremental improvements to existing technologies will not be funded under this announcement.

Is this a call for DARPA-lite projects? Or for proposals as far-fetched as calcium imaging in humans? As the RFA explains...
The long-term objective is to develop tools for the precise imaging of molecules, cells, and circuits in the human brain.  Applications submitted in response to this R24 FOA should support the formation and development of interdisciplinary teams that will plan innovative approaches to substantively expand the ways by which brain structure and function can be imaged in humans.  These R24 awards will support planning activities such as meetings, prototype development projects and small scale pilot studies in mammals or humans that would provide proof of principle for transformative approaches to assessing human brain structure and function.  The proposed concepts are expected to be high-risk, high-impact, and disruptive (c.f. C. Christensen “The Innovator's Dilemma”, 1997; http://en.wikipedia.org/wiki/Disruptive_innovation).

What might these [post-]BOLD new BRAIN scanners of the future look like? This question was addressed by practiCal fMRI in September:
This week's interim report from the BRAIN Initiative's working group is an opportunity for all of us involved in fMRI to think seriously about our tools. We've come a long way with BOLD contrast to be sure, even though we don't fully understand its origins or its complexities. ...

I can't help but wonder what my fMRI scanner might look like if it was designed specifically for task. Would the polarizing magnet be horizontal or would a subject sit on a chair in a vertical bore? How large would the polarizing magnet be, and what would be its field strength? The gradient set specifications? And finally, if I'm not totally sold on BOLD contrast as my reporting mechanism for neural activity, what sort of signal do I really want? In all cases I am especially interested in why I should prefer one particular answer over the other alternatives.

Note that I'm not suggesting we all dream of voltage-sensitive contrast agents. That's the point of the BRAIN Initiative according to my reading of it. All I'm suggesting is that we spend a few moments considering what we are currently doing, and whether there might be a better way...

Further Reading

DARPA allocates $70 million for improving deep brain stimulation technology


New Deep Brain Stimulation System Measures Neurotransmitter Release

Anyone who is awarded one of these #BRAINI grants is free to use this nifty badge on all their promotional materials and publications.

The BRAIN Initiative badge is awarded by President Obama to research supported by his $100 million #BRAINI. This bold new research effort will include advances in nanotechnology and purely exploratory efforts to record from thousands of neurons simultaneously.

When Waking Up Becomes the Nightmare: Hypnopompic Hallucinatory Pain


Most of us have had frightening nightmares – someone is chasing after us trying to kill us, or the world is coming to an end. Other disturbing dreams are based on real life anxieties– our partner leaves us, we lose our job, we become homeless. One specific psychiatric condition includes nightmares as part of the diagnosis. Individuals with post-traumatic stress disorder (PTSD) often have terrible nightmares that relive the traumatic event (Pigeon et al., 2013)

We're always glad to wake up from such nightmares, whether they were of the supernatural or mundane or terrifying variety. "Thank god it was only a dream," we say.

But what if waking up from sleep was the nightmare? Hypnopompic hallucinations are unusual sensory phenomena experienced just before or during awakening. Their better known mirror image, hypnagogic hallucinations, are vivid and frightening episodes of seeing or hearing or feeling phantom sensations while falling asleep (or in early stage 1 sleep). Both are frequently associated with sleep paralysis, the terrifying condition of being half awake but unable to move. This is because the complete muscle atonia typically experienced during REM sleep has oozed into lighter stages of non-REM sleep.

Hypnagogic and hypnopompic hallucinations are usually associated with narcolepsy, but 37% of a representative community sample reported frequent hypnagogic hallucinations, and 12.5% reported hypnopompic hallucinations (Ohayon et al., 1996).1 This went well beyond the low incidence of narcolepsy in that population. Both types of hallucinations were more common in those with insomnia, excessive daytime sleepiness, anxiety disorders, and depression (according to self-report).

Night Terrors 1, by Beth Robinson

Nocturnal Episodes of Pain and Screaming

A new case study in the journal Sleep (Mantoan et al., 2013) reports on the terrifying hypnopompic hallucinations of a 43 year old woman who experiences intense limb pain when waking up, which vanishes within 30 seconds. This is a very unusual manifestation of a non-REM parasomnia, a sleep disorder involving partial arousal during the transition between non-REM and wakefulness. The phenomenology might be best characterized as a night terror.

According to the case report (Mantoan et al., 2013), the patient had...
...a history of nocturnal screaming episodes within 1–2 h of sleep onset from the age of 30 years. Her husband was habitually awoken by his wife screaming loudly, usually flapping either her right or left hand against the bed in a semi-purposeful fashion. Her husband reported that the events were sometimes heralded by an inspiratory sigh, she looked terrified and would not respond to him. The screaming would usually last 5–10 sec, and she would then complain to her husband of intense pain affecting the fingers of either hand or arm and occasionally her legs, with no associated numbness or paraesthesia. She would become fully orientated within 30 sec and would be partially amnesic for the event, but would recall an accompanying sense of “fighting to stay alive” associated with intense panic and often accompanied by fast regular palpitations. Otherwise no dream mentation or visualizations were reported in association with the episodes.

She initially had these episodes monthly, but they increased in frequency to 2-5 times a week with 1-2 episodes per night.
She was unable to identify any triggers for the episodes, and neither she nor her husband considered her to be stressed, anxious, or depressed. There was no history of sleep violence, sleep sex, sleep eating, or any other NREM parasomniac automatisms. 

The authors could not identify any standard physical source for the pain. Thoracic outlet syndrome, cervical radiculopathy, focal nerve entrapment, and median neuropathy (carpal tunnel syndrome) were all ruled out.

Pharmacological treatments were unsuccessful. A low dose (0.5–1 mg) of clonazepam was poorly tolerated (it made her feel depressed) and had no effect on her symptoms. Paroxetine was poorly tolerated (due to sedative effects), and gabapentin was also a complete failure. Trazodone, a sedating antidepressant most often prescribed for insomnia, actually made the symptoms worse.

An MRI ruled out a thalamic or hypothalamic lesion. Sleep EEG revealed sudden arousals from deep sleep, accompanied by looks of pain and/or fear on the patient's face. The episodes were consistent with a NREM parasomnia. In the example below, the patient was shaking her arm – muscle activity (EMG) is shown in the green trace.

adapted from Fig. 1B (Mantoan et al., 2013). EEG showing delta waves of stage 3 sleep before an episode of arousal with shaking of one arm and looks of fear. Channels 1-12 are EEG; channels 13 and 14 are electro-oculogram (EOG) activity; channel 15 is electromyography (EMG); channel 16 is electrocardiogram (ECG); channel 17 is oxygen saturation by pulse oximetry (SpO2).  {click on image for a larger view}

What did the doctors do to help this poor woman? Nothing, it seems. A few more musculoskeletal causes need to be ruled out.

The authors end on a vague note about the possible mechanism(s):
In conclusion, to our knowledge this is the first report of a NREM parasomnia associated with painful paroxysms, for which we postulate the following underlying pathophysiological mechanism: an internal or external stimulus triggers arousal, facilitating the activation of innate motor pattern generators in the brainstem and activating somatosensory cortical areas to produce hypnopompic hallucinatory pain.

So instead of the more typical visual hallucinations, the patient experiences pain hallucinations that originate.... where?? It seems to me that the sleep EEG could be analyzed more thoroughly, beyond merely ruling out seizure occurrence. Perhaps another imaging modality like PET could be tried (PET would be quieter than fMRI and would better tolerate movement). Identifying the neurophysiological correlates of her phantom night terror pain would provide a fascinating glimpse into a highly unusual sensory phenomenon.2

Further Reading

The Phenomenology of Pain During REM Sleep

The Neurophysiology of Pain During REM Sleep


1 The questions asked in the telephone interviews by Ohayon et al. (1996) were:
(a) Do you experience at least twice a week the following perceptions?

(i) the realistic feeling that someone or something is present in the room
(ii) a vivid experience of being caught in a fire
(iii) a vivid experience that you are about to be attacked
(iv) a vivid experience that you are flying through the air
(v) the feeling that you will soon fall into an abyss
(vi) the feeling that shadows or objects are moving and distorting.

(b) Do you experience other types of vivid perceptions?

(c) Can you specify the type of perception?

(i) auditory
(ii) visual
(iii) kinetic (involving movement)
To me, the most surprising part of the survey is that 37% reported these phenomenon at sleep onset twice a week for the past year. This contrasts sharply with only 0.04% reporting symptoms of narcolepsy.

2 I've occasionally felt pain in dreams that vanished upon awakening, but I'm pretty sure the episodes occurred during REM (or another stage of dreaming sleep), because visual narrative content was associated with the episodes. Those experiences were clearly not night terrors, and very different from what was reported in the case study.


Mantoan L, Eriksson SH, Nisbet AP, & Walker MC (2013). Adult-onset NREM parasomnia with hypnopompic hallucinatory pain: a case report. Sleep, 36 (2), 287-90 PMID: 23372277

Ohayon MM, Priest RG, Caulet M, & Guilleminault C (1996). Hypnagogic and hypnopompic hallucinations: pathological phenomena? The British journal of psychiatry, 169 (4), 459-67 PMID: 8894197

Pigeon WR, Campbell CE, Possemato K, Ouimette P. (2013). Longitudinal relationships of insomnia, nightmares, and PTSD severity in recent combat veterans. J Psychosom Res. 75:546-50.

The Sleep Paralysis Project

The Creativity of Denial


Never Forget Srebrenica, by Scott McIntyre. A Bosnian Muslim man makes his way past the caskets of those killed in the Srebrenica genocide of July 1995.

Horrible, unspeakable memories will forever haunt the psyches of many survivors of war, genocide, and other atrocities. But what is behind the systematic denial of crimes against humanity?

The Science of Hatred

What makes humans capable of horrific violence? Why do we deny atrocities in the face of overwhelming evidence? A small group of psychologists say they are moving toward answers. Is anyone listening?

By Tom Bartlett

The former battery factory on the outskirts of Srebrenica, a small town in eastern Bosnia, has become a grim tourist attraction. Vans full of sightseers, mostly from other countries, arrive here daily to see the crumbling industrial structure, which once served as a makeshift United Nations outpost and temporary haven for Muslims under assault by Serb forces determined to seize the town and round up its residents. In July 1995 more than 8,000 Muslim men, from teenagers to the elderly, were murdered in and around Srebrenica, lined up behind houses, gunned down in soccer fields, hunted through the forest.

This stunning article in The Chronicle of Higher Education focuses on studies of intergroup conflict, in particular the work of Sabina Cehajic-Clancy, a Bosnian social psychologist. “It is unbelievable the extent and amount of creativity that people possess when it comes to denying,” she said.

Sadly, this sort of research is seriously undervalued in psychology:
Studying conflict can be a draining, thankless endeavor. Government officials rarely turn to social psychologists for advice on how to end war or cool simmering tensions. Within psychology, research on intergroup conflict is not a speedy route to professional acclaim. The fieldwork can be arduous and expensive. Funds are hard to come by, and so is publication in top journals. You’d be better off surveying undergraduates about their dating preferences or dietary habits.

How Can We Forget?

** This post is meant to be read in tandem with its more complimentary cousin,Electroconvulsive Therapy Impairs Memory Reconsolidation, atThe Neurocomplimenter. **

spECTrum 5000Q® ECT device (MECTA)

Bad memories haunt a significant number of people with serious mental illnesses, such as chronic major depression and post-traumatic stress disorder (PTSD). If it were possible to undergo an experimental procedure that selectively impairs your memory for an extremely unpleasant event, would you do it? If this sounds like the plot of Eternal Sunshine of the Spotless Mind, you're not alone.

A pet peeve of mine is reference to this excellent but far-fetched film in scientific journals and popular media coverage of “memory erasure.” The idea that it's possible to selectively remove a complex autobiographical memory that has become intimately entwined with the fabric of our constructed selves is utter science fiction.

At some level, even Michel Gondry knew it. One incident in Eternal Sunshine is suggestive of how memories might actually be stored. It was after one of the main characters (Joel) had his memories of his ex-girlfriend Clementine erased, and he couldn't remember who Huckleberry Hound was. He had associated the cartoon character and the song "Darling Clementine" with her. That resembles a semantic network, where an overlapping network of neurons and synapses code different but semantically related things. Take out all episodic and semantic memories of Clementine, and knowledge of Huckleberry Hound goes with it.

The latest incarnation of this particular memory erasure meme was provoked by publication of a paper (Kroes et al., 2013) that examined the process of memory reconsolidation in depressed patients administered a course of electroconvulsive therapy (ECT). Here are some of the headlines:
Zapping the brain can help to spot-clean nasty memories

Absolutely shocking: electrocuting brain can wipe unpleasant memories

Unwanted Memories Erased in Electroconvulsive Therapy Experiment

Shocking Memories Away

My companion post at The Neurocomplimenter reviews the literature on memory reconsolidation and describes the experiment of Kroes et al. (2013) in some detail. What I'd like to do here is to point out possible weaknesses in the results that could undermine the authors' conclusions. I'll also discuss a much earlier ECT study which did not support the notion that reactivated memories are especially vulnerable to disruption (Squire et al., 1976).

To briefly reiterate the methods used in the new paper (Kroes et al., 2013), the participants were 39 patients with moderate to severe major depression. They were either at the end of an acute treatment cycle or receiving maintenance ECT. The study used a between-subjects design with three different experimental conditions, with patients randomly assigned to one of the three groups (n=13 in each). The within-subjects factor was whether or not the patients received a reminder of previously learned material before treatment.

All participants learned two different emotionally charged slide stories with audio narration, each consisting of 11 images. In one, a boy is in an accident that severs his feet, which are reattached at the hospital. In the other, two sisters leave their home at night, and one is kidnapped at knife point and attacked by an escaped convict.

Memory for one of the stories was reactivated a week later by presenting part of the first slide, and then giving a test for this slide. Only four minutes later, Groups A and B were anesthetized and received ECT. Group C received their ECT treatment at a later date. The final memory test for Groups A and C was 24 hrs after the reminder, while Group B was tested as soon as they woke up from the procedure (mean = 104 min later). The final test consisted of 40 multiple choice questions about each of the stories.

The basic idea is that reconsolidation of the reactivated story isn't complete within 104 min, so Group B's test performance should be the same for the two stories. In contrast, reconsolidation is complete by 24 hrs, so for Group A the disruptive effect of ECT should selectively impair memory for the transiently reactivated story, which is in a labile state (relative to the "consolidated" story learned 7 days earlier).

Is that what was observed? Statistically speaking, yes. But two patients in Group B (out of 13 total) performed very well on the reactivated story (see purple box in the figure below).

Fig. 1 (modified from Kroes et al. 2013). ECT disrupts reconsolidation. Memory scores on the multiple choice test are expressed as percentage correct (y axis). Memory for the reactivated story shown in solid bars and non-reactivated story in open bars. Each circle is the score for an individual patient. The horizontal dotted line is chance performance. Group A is in red, Group B in blue, and Group C in orange. Edited to add: The purple box highlights 2 outliers in Group B who could be driving the major effect.

If these two individuals are omitted, would the difference between Groups A and B still be significant? This is the key finding of the paper, that memory for the reactivated story is no better than chance if ECT disrupts reconsolidation (a time-dependent process). Hence all the Eternal Sunshine / “memory erasure” headlines.

The purple boxes show that (1) the Reactivation x Group interaction squeaks in at just barely significant (p=.049); and (2) the Group A vs. Group B comparison for the reactivated story is p=.042. Clearly, it would be nice to include twice as many patients in each group. But it took the authors 3.5 years to recruit their final total of n=39.

This type of study is not easy to pull off, which is why I applaud the authors (and the patients) for such an ambitious undertaking. I thought it was a very clever idea as well, but not an original one as it turns out.

In the 1970s and 80s, Dr. Larry Squire and his colleagues published a series of papers on ECT and memory. The one I'll describe here takes a similar approach to Kroes et al. by testing previously learned material after ECT, and by giving a memory reminder just before the treatment (Squire et al., 1976).

Squire et al. (1976) used a completely within-subjects design (n=12) that manipulated the pre-ECT learning interval (14-18 hrs vs. 3-10 min). The third condition presented a memory reminder 3-10 min before ECT for material learned 14-18 hrs previously. Completely different stimuli were used each time, and the order of conditions was counterbalanced. The memory tests were recognition memory for a set of 32 previously learned items (common objects, common words, yearbook photos, and nonsense drawings), and paired associates (producing the correct target for 18 previously learned cue-target pairs). In all conditions, retention was tested 6-10 hrs after ECT (compare to 104 min and 24 hrs in Kroes et al.).

A separate group of patients (n=9) was tested on their remote memories for old TV shows under three conditions: (1) 6-10 hrs after ECT; (2) 14-18 hrs before  ECT and again with the same questions 6-10 hr after ECT; (3) Less than 10 min before ECT and again with the same questions 6-10 hrs after ECT (the reminder procedure).

The critical result is that the memory reactivation procedure did not impair performance (bar graphs A vs. R below). In both of these conditions, material was learned 14-18 hrs before ECT. This is in contrast to the findings of Kroes et al. (2013).

Fig. 1 (modified from Squire et al., 1976). Results from (A) 32-item recognition memory test, and (B) paired-associate learning test, under three conditions in conjunction with the patients' first 3 ECT sessions. Retention was significantly impaired in Condition B (initial learning 3-10 min before ECT). The reminder procedure (Condition R) caused no impairment in performance relative to Condition A.

Squire and colleagues (1976) concluded that “...the results provide no evidence that the presentation of previously learned material just prior to ECT increases its vulnerability to disruption.” Similar results were observed in the patient group tested on their knowledge of old TV shows: “the results clearly indicate that amnesia for remote memory did not occur when remote memory was evoked prior to ECT.”

The final conclusions [clairvoyantly] throw cold water on the study published 37 years later:
The present findings also have important clinical implications. The reactivation phenomenon described in experimental animals has raised the possibility that it might be therapeutically advantageous to evoke depressive ideation just prior to treatment, in order to produce amnesia for this ideation. The results reported here strongly suggest that this procedure would be ineffective.

However, you'll probably notice some differences between the two studies. Kroes et al. pointed out that their effect was observed at a 24 hr retention interval, while Squire et al. only tested at 6-10 hrs (perhaps not long enough to disrupt reconsolidation). The Squire stimuli were neutral in valence, whereas the Kroes stimuli were emotional (and perhaps more susceptible to disruption). There were also differences in the patient groups (Squire's were younger, mean=39 yrs), anesthesia used, electrode locations, and ECT parameters (likely to be way more potent in the earlier study, which would predict worse amnesia). An unfortunate side effect of ECT is memory impairment, although other studies claim the opposite.

Certainly, subjective cognitive complaints after ECT are very common. For a first hand look at some of the more devastating effects, watch the powerful video below. For a lighthearted and critically acclaimed look at fictional memory erasure, watch Eternal Sunshine of the Spotless Mind.


Kroes MC, Tendolkar I, van Wingen GA, van Waarde JA, Strange BA, & Fernández G (2013). An electroconvulsive therapy procedure impairs reconsolidation of episodic memories in humans. Nature neuroscience PMID: 24362759

Squire LR, Slater PC, & Chace PM (1976). Reactivation of recent or remote memory before electroconvulsive therapy does not produce retrograde amnesia. Behavioral biology, 18 (3), 335-43 PMID: 1016174

Liz Spikol (of The Trouble With Spikol fame) tries to explain the confusion and the loss of self she felt after waking up from ECT.

"After the ECT, I did not know how to use a toothbrush. And that lasted for months."
- Liz Spikol (at 9:28)

Neurocrap Funded by the Masses: NeuroOn and No More Woof


Crowdfunders, get a clue! You're throwing your money away on bogus prototypes for impossible technology! Why give your hard-earned cash to the equivalent of modern-day snake oil salesman instead of funding essential projects to bring clean water and hygienic toilets to third world countries?

First we have No More Woof, which was first brought to my attention by Professor Dwayne Godwin. Writing in BrainFacts.org, a blog sponsored by the Society for Neuroscience, he considers whether an EEG-to-speech converter for dogs is plausible [HINT: of course it's not!]:
What is proposed is a gadget that on the basis of a few dry EEG electrodes will do for a creature without known speech centers what we’ve been unable to do for humans (with well-defined speech centers) using the best EEG systems yet developed.

In other words, don't you think you would have heard about a device that could translate the brain waves of a person with speech difficulties due to Broca's aphasia or ALS into fluent sentences? Gizmodo and the New York Times and even Oprah would be all over it!

Here's what the No More Woof developers have to say:
Every mammal creates and transports "thoughts" the same way, as a swarm of electrical signals through a complex neurosystem). It has long been possible to record this activity through Electroencephalogram (EEG) readings. When it comes to humans, the last decade has seen tremendous progress.

However every species uses its unique structure. You could say that all creatures speak the same language only with varying dialects. And as animal brains are less complex than humans their signal patterns are more distinct for feelings of anger, curiosity or tiredness – actually making them easier to distinguish.

There's absolutely no scientific evidence for distinguishing "anger" and "curiosity" brain signals in dogs, especially via a cheap ($65) doggie EEG headset with only one electrode.

What we really need is Professor Schwartzman's canine decoder!

The campaign has already raised $19,152 of their $10,000 goal. And there's 35 days left! So save your money!

But at least the No More Woof developers have issued a caveat. We can't say the same about our next prototype...

NeuroOn: World's first sleep mask for polyphasic sleep

Why waste any time with a trivial and unimportant activity such as sleep? The NeuroOn developers promise their device will deliver a "unique sleep schedule" that will maximizes each user's waking time... up to 22 hours a day! You'll become an efficient and brilliant productivity machine, just like Da Vinci, Tesla, Churchill and even Napoleon!
In conclusion, through great sleep efficiency, Polyphasic sleep can give you an extra 4 hours of free time every day. That’s up to 28 hours (1 day+) a week, 1460 hours a year.

That’s right - Your year now has over 420 working days!

What is polyphasic sleep? It's the division of sleep into several bouts per day, instead of the usual 8 hours or so at night. This schedule is standard in some mammals and may serve a protective purpose, according to Capellini et al. (2008):
The duration of [REM and non-REM] cycles varies extensively across mammalian species. Because the end of a sleep cycle is often followed by brief arousals to waking, a shorter sleep cycle has been proposed to function as an anti-predator strategy. Similarly, higher predation risk could explain why many species exhibit a polyphasic sleep pattern (division of sleep into several bouts per day), as having multiple sleep bouts avoids long periods of unconsciousness, potentially reducing vulnerability.

In humans, "disentrainment" protocols isolate volunteers under strict lab conditions and remove all cues to the time of day. In one study, 50 participants were allowed to eat and sleep at any desired time over a 72 hour period (Campbell & Murphy, 2007). Activity options were limited to a set playlist of recorded music, a deck of cards, and a small anthology of poetry. No strenuous exercise, TV, videos, work, study or hobbies. Why? To look at natural sleep tendencies unencumbered by that Battlestar Galactica marathon you've always wanted.

On average, the participants slept for 27.67 hrs of the 72 hour disentrainment period. That's 9.22 hrs every 24 hours, which was verified by EEG recordings (not based on self-report, as in an earlier study). There was an average of 7.6 sleep episodes per subject (instead of the standard 3 bouts each night). The mean duration of sleep episodes was 3.27 hrs but this varied wildly, with a range of 0.33-13.57 hrs. And the younger subjects (30 and under) slept longer and spent more time in REM than the middle (31-59 yrs) and older (60 and over) subjects.

What is polyphasic sleep according to the NeuroOn team?
It is a term referring to alternate sleep patterns that can reduce the required sleep time to just 2-6 hours daily. It involves breaking up your sleep into smaller parts throughout the day, which allows you to sleep less but feel as refreshed as if you slept for 8 hours or more.

Although I could be wrong, the majority of NeuroOn backers are presumably young and therefore will require more sleep than their older counterparts. Have the developers taken age differences into account?

But but,you say, these techie hipsters spend their lives on more valuable and fulfilling activities than reading poetry and playing solitaire (with an actual deck of cards)!! So of course they don't need as much sleep!

So sure, we can criticize the exaggerated claims that humans have a minimal need for sleep, with wondrous increases in productivity as a result of adopting a proprietary "unique sleep schedule". All without developing a serious psychiatric condition! While ignoring the necessity to medically screen users in the event that such a device would actually work.

The real impetus for writing this post, however, came from Justin Kiggins:

The ensuing discussion on Twitter included debunking of the entire technical premise of the device, which uses a limited number (one? three?) of ill-placed electrodes to purportedly record a wide variety of electrical signals.

Let's take a closer look at the prototype. Is that really only one electrode??* That uses a magical "dedicated and extraordinary biological amplifier" and AI algorithms that can filter and distinguish the differing source generators and frequency bands for EEG, EMG, and EOG? Without a reference electrode connecting to the differential amplifier?

* ADDENDUM Jan 12 2014: No, that is“a part to generate physical vibration.” There are 3 electrodes, as shown in the prototype image further down.

PCB version 2.1

The developers claim:
Thanks to the use of the newest technologies we were able to create a device that will improve your effectiveness and concentration at work to the best possible levels. Measurements of EEG, EOG and EMG, coupled with the usage of artificial intelligence, allows us to create the world's first digital sleep-control system that provides accuracy close to professional polisomnographic clinics.

According to what criteria? Which published studies? Because here's a paper from a group of clinical EEG experts on how difficult it was to reach a consensus on Standardized Computer-based Organized Reporting of EEG (SCORE):
The interobserver agreement in electroencephalography (EEG) interpretation is only moderate (Van Donselaar et al., 1992; Stroink et al., 2006). The EEG signal has a high complexity. It depends on the intricate interplay between the activation of neural networks, localization and orientation (Wong, 1998) of the source (dipole), and its propagation throughout the brain (Lopes da Silva & van Rotterdam, 1993; Scherg et al., 1999; Flemming et al., 2005).

Current prototype (the backside view)

So those three gray squares sitting on your eyebrows are the recording electrodes that will distinguish eye movements like those during REM sleep (very large amplitude signals) from actual brain activity (very tiny signals)? And when the A to D output is transmitted wirelessly via bluetooth to a smartphone application, the app will wake you up precisely at the end of a REM sleep cycle? AND will induce lucid dreaming on demand, so you can literally control your dreams. Really??

No.  Dream on.

And the sad thing is that hundreds of people have pledged $250 to buy a device that will not deliver what's promised.

What is your dream?

Do you need more energy and to feel well - rested?
Do you want to pack even more into your day?
Do you want to have more control over your day?
Do you hate jet lag?
Do you just need that few extra hours every day?
Do you want to be a hero by day and a superhero by night?
Or maybe it's not so sad... people are always susceptible to snake oil and miracle cures, only now in a high tech faux-neuro guise. As of this writing, 1,901 backers have pledged $431,114, far surpassing the $100,000 goal.  Only 15 hours to go!

Don't you think it's more important to expand access to clean water and improved sanitation in poor, rural households in Vietnam? This Kiva microloan has raised 61% of its $4,750 goal, with $1,850 to go before Jan 27, 2014.

Further reading:

Dormivigilia (an actual sleep researcher) on sleep

Gaines on Brains on sleep tracking apps and why their premise is flawed

ADDENDUM #2 (Jan 12 2014): Since a commenter mentioned the Zeo headband (made by the now-defunct company Zeo, Inc.), I thought I'd say a few words about it here. The company published a paper in the Journal of Sleep Research (Shambroom et al., 2012) that examined the performance of their wireless system (WS) to professional polysomnography (PSG; see Gaines on Brains for more on sleep EEG). The Zeo agreed with the simultaneously recorded PSG sleep stages 75% of the time over the course of a night. However, the Zeo did poorly at the detecting onset of the first REM episode:
"The WS significantly and substantially underestimated REML compared to PSG. There were nine nights for which the WS scored REM within the first 6 min of sleep, possibly indicating a tendency for the technology to score REM in the early lightest stage of sleep."
The headband has 3 electrodes on the forehead like NeuroOn and used an Fp1-Fp2 bipolar recording montage (two standard left and right frontopolar sites on the forehead). EEG recorded here is particularly prone to artifacts from eye movements and muscle activity and is thus a mixture of all these signals. Analytic techniques such as independent component analysis (ICA) try to separate the sources. The Zeo group used some sort of training algorithm that used "a combination of time and frequency dependent features derived from the signal to create a best estimate of sleep stage." Interestingly, they had to filter out the very low frequencies (below 2 Hz) that comprise much of the delta wave activity seen during slow wave sleep. This was because of contamination by excessive noise in the low frequency range.

I have no idea of how any of Zeo technology relates to that used by NeuroOn, but the published paper presented some of the challenges involved in developing such a system.

ADDENDUM #3 (Jan 12 2014): While I'm at it, I should mention another neurocrap Kickstarter project -- Aurora: The Dream-Enhancing Headband, which was brought to my attention by Micah Allen. Save your money! If you want to support a worthwhile project, try OpenBCI: An Open Source Brain-Computer Interface For Makers, recommended as legit by Neurobonkers.

ADDENDUM #4 (Jan 13 2014): New post from a sleep researcher: Nonsense neurogadgets: sleep edition, at Taking a cat apart.

BROADEN Trial of DBS for Treatment-Resistant Depression Halted by the FDA

Webpage for the BROADEN™ study formerly run by St. Jude Medical

It's become mainstream these days to say that psychiatric disorders are neural circuit disorders. You can even read all about it in the New York Times! Cognitive training and neuromodulation (“electroceuticals”) are in, and pharmaceuticals are out, as explained by NIMH Director Dr. Tom Insel in a blog post about the Ten Best of 2013:
...if mental disorders are brain circuit disorders, then successful treatments need to tune circuits with precision. Chemicals may be less precise than electrical or cognitive interventions that target specific circuits.

One of the first to champion this position was Dr. Helen Mayberg and her colleagues, who conducted a small trial using deep brain stimulation (DBS) as a treatment for intractable depression (Mayberg et al., 2005). The technique has been heralded as a potential breakthrough in psychiatry, with $70 million in BRAIN Initiative funding going to DBS development. So a recent tweet announcing the failure of a major clinical trial garnered a lot of attention.

The December 13, 2013 issue of the Neurotech Business Report had the scoop:
The news that St. Jude Medical failed a futility analysis of its BROADEN trial of DBS for treatment of depression cast a pall over an otherwise upbeat attendance at the 2013 NANS meeting. Once again, the industry is left to pick up the pieces as a promising new technology gets set back by what could be many years.

It’s too early to assess blame for this failure. It’s tempting to wonder if St. Jude management was too eager to commence this trial, since that has been a culprit in other trial failures. But there’s clearly more involved here, not least the complexity of specifying the precise brain circuits involved with major depression. Indeed, Helen Mayberg’s own thinking on DBS targeting has evolved over the years since the seminal paper she and colleague Andres Lozano published in Neuron in 2005, which implicated Cg25 as a lucrative target for depression. Mayberg now believes that neuronal tracts emanating from Cg25 toward medial frontal areas may be more relevant. Research that she, Cameron McIntyre, and others are conducting on probabilistic tractography to identify the patient-specific brain regions most relevant to the particular form of depression the patient is suffering from will likely prove to be very fruitful in the years ahead.

But it was hard to find any other information about the failed trial. I can't be sure, but I think this is the study in ClinicalTrials.gov A Clinical Evaluation of Subcallosal Cingulate Gyrus Deep Brain Stimulation for Treatment-Resistant Depression. The sponsor is St. Jude Medical. The record hasn't been updated since March 2013.

BROADEN is a tortured acronym for BROdmann Area 25 DEep brain Neuromodulation.

The July 30, 2013 version of the BROADEN website is preserved at archive.org.

The BROADEN (BROdmann Area 25 DEep brain Neuromodulation) study is a study to evaluate the safety and effectiveness of deep brain stimulation in patients with a severe form of depression known as Major Depressive Disorder (MDD) who have not responded to multiple treatments. Stimulation to the brain is provided by a surgically implanted medical device called a deep brain stimulation (DBS) system. The system provides stimulation directly to an area of the brain known as Brodmann Area 25 (sometimes referred to as BA25). The study will build upon the depression work of a research team from the University of Toronto, led by neurologist Helen S. Mayberg, M.D. and neurosurgeon Andres Lozano, M.D., PhD, FRCSC.

On January 10, 2014 an Anonymous commenter at DBS Trial1 said:
Regarding the Broaden Study, I'm not writing it off entirely but things aren't looking good. The FDA has put the brakes on the study so it will not enroll any new participants.
While the study is over a year old, the results so far are not encouraging and the device manufacturer is scaling back on monitoring and programming.
It appears that a possible major misstep was made, by not including fMRI mapping prior to implanting the electrodes. 

As Neurotech Business Report (NBR) mentioned, more precise mapping of the white matter connections of the subgenual cingulate (Brodmann area 25) may be essential (e.g., Johansen-Berg et al., 2008). To determine the anatomical connectivity of the subgenual cingulate region, those authors performed tractography (using diffusion-weighted magnetic resonance imaging) to trace the pathways mediating treatment response with DBS. They compared the connections of the subgenual ACC (sACC, blue/cyan) and the perigenual ACC (pACC, red/yellow).

Fig. 3 (Johansen-Berg et al., 2008). Connectivity-based parcellation of anterior cingulate cortex (ACC) and location of electrode contacts. Effective electrode locations are mainly localized within the sACC subregion.

A July 11, 2011 News Release from St. Jude Medical announced that the FDA had approved an expansion of the BROADEN Trial so that up to 20 different sites could enroll a total of 125 patients. There were only three sites originally Chicago, New York City and Dallas. Perhaps the trial resources were getting stretched too thin.

Another possibility raised by James Cavuoto
, Editor and Publisher of NBR, is that the FDA is too darn stringent in what it considers a treatment response:
Unfortunately, much of the progress in our understanding of DBS mechanisms in depression is potentially wasted without a vibrant installed base of patients and clinicians using and perfecting DBS therapies. ... In our view, the FDA needs to understand the vital importance of getting first-generation devices into the field and move away from arbitrary standards like improving symptoms by 50 percent in 50 percent of the population. The notion that if we can’t help everybody we shouldn’t help anybody has no place in medical science, particularly when you consider that neuromodulation therapies are working with the hardest-case patients who have not responded to other therapies.

Finally, there is the unfortunate possibility that DBS treatment in this patient group doesn't work as well as initially thought...

If anyone has additional information, please leave a comment.


1 This blog is written by an individual who for the past four years has had an implanted device for the treatment of intractible depression.


Johansen-Berg H, Gutman DA, Behrens TE, Matthews PM, Rushworth MF, Katz E, Lozano AM, Mayberg HS. (2008). Anatomical connectivity of the subgenual cingulate region targeted with deep brain stimulation for treatment-resistant depression. Cereb Cortex. 18:1374-83.

Mayberg HS, Lozano AM, Voon V, McNeely HE, Seminowicz D, Hamani C, Schwalb JM, Kennedy SH. (2005). Deep brain stimulation for treatment-resistant depression. Neuron 45:651-60.

Further Reading:

A Depression Switch?

The Sad Cingulate

Sad Cingulate on 60 Minutes and in Rats

...But My Subgenual Cingulate Is Sad

Deep Brain Stimulation for Bipolar Depression

The Brain Radio


The Brain Radio is a long-running French radio program:

THE BRAIN are Eva & Pascal Lebrain aka Puyo puyo, they run this radioshow from 1999, it deals with freaky electro, cheesy vintage, dry rock, movie themes and oddities in general. All is stuffed with absurd aphorisms, written by themselves most of the time.

The fun archive of playlists dates back to 2003 and includes 91 of the 129 radioshows.

The “Brain Radio” is also a deep brain stimulation (DBS) device that “Records and Emits Electrical Pulses,” according to an August 9, 2013 story in the MIT Technology Review:

A new brain implant that can record neural activity while it simultaneously delivers electric current has been implanted into a patient for the first time.

The new device from Medtronic, a Minneapolis-based medical device company, can also adjust its electrical output in response to the changing conditions of the brain. This automated control could one day improve deep-brain stimulation treatment and even enable doctors to use the device to treat more conditions, say experts.

This new generation device seems like what DARPA had in mind for its SUBNETS program, part of the BRAIN Initiative. The MIT Technology Review story continues:
The patient trials launched on Wednesday will test whether Medtronic’s new device can safely record electrical activity in a patient’s brain while also delivering electric currents. These tests will explore how patients’ brains respond to deep brain stimulation therapy. However, according to lab animal tests, the device is capable of not only sensing the electrical activity of the brain tissue it sits in, but of also changing its output accordingly.

The ultimate goal for the device is to provide responsive therapy by detecting brain signals and tweaking its output accordingly, says Lothar Krinke, general manager of the company’s deep brain stimulation division.

The Activa® PC+S Deep Brain Stimulation System was first implanted in a German patient with Parkinson’s disease. But now there's a new clinical trial for treatment-resistant depression (TRD) that will implant the device in the subgenual cingulate (Brodmann area 25):
The experiment described in this application is to use a new DBS device that can record the electrical activity in the brain around the site of stimulation. The electrical activity is known as Latent [sic] Field Potential (LFP) and is a reflection of the activity if the neural network. The new DBS device is an experimental device that has not been approved by the FDA, but allows for simultaneous recording of LFP while stimulation is being delivered. The device is manufactured by Medtronics and is known as Activa Primary Cell + Sensing(PC+S), but because it can be used to record the brain electrical activity it is also known as "the Brain Radio". The Brain Radio is based on an approved device commonly used for DBS for other conditions that has the added sensor capacity. The stimulation system is identical to that in the approved device. The goal of this investigation is to use the Brain Radio to study LFP in the brains of people with TRD before and during active stimulation. 

The device used in the aborted BROADEN Trial of DBS for TRD is manufactured by another company.

As I've mentioned previously, the goal of the SUBNETS program is to develop devices that both stimulate and record neural activity, and provide real-time data that can be decoded as reflecting a particular behavioral state... basically, a futuristic implant that can adjust its own stimulation parameters based on how the patient is doing.

The new DBS trial for intractable depression (which is not yet open for participant recruitment)...
...will recruit 10 patients with advanced TRD and implant them with the Brain Radio system. The recording system will be to record LFP over 3 years, while patients reesceive stimulation. A brief discontinuation study will be conducted after 6 months of stimulation when the device will be turned off and patterns of LFP changes will be recorded. All LFP measures will be correlated with the primary clinical response outcome metric, the Hamilton Depression Rating Scale.

The Journal of Neural Engineering has just published a paper outlining the results of a two year study that tested the Activa® PC+S neurostimulator in a rhesus monkey (Ryapolova-Webb et al., 2014): Chronic cortical and electromyographic recordings from a fully implantable device: preclinical experience in a nonhuman primate.

The senior author on that paper (neurosurgeon Dr. Philip Starr) was one of the first to implant the device in a Parkinson's patient in the US.

Eight Years of Neurocriticism

A Mad Scientist Party Idea, from Party on Purpose.

Eight years ago, I started a blog out of sheer frustration. I decided to call it The Neurocritic. I sent out an anonymous e-mail to some of my friends to describe the project.

subject: unveiling The Neurocritic

I've started a blog to critique the most outrageous claims published in high-profile journals and discussed in the popular press:


Because The Neurocritic is not a member of the all-powerful Editorial Boards at Science, Natute, or Neuron, The Neurocritic is published under an assumed identity.  Your comments are most welcome.

Enjoy the inaugural posting! [we'll see how long it lasts.]

[I had forgotten how surprised I should be that the blog has lasted this long.]

At first, I invited others to join. Two people expressed interest in joining the party, and one was issued an account (but never posted). I soon became very proprietary and revoked that account. I had become The Neurocritic.

I didn't think anyone would read the blog. But then a funny thing happened. Several posts that discussed journal articles drew the attention of the authors, who actually commented.

Meanwhile, I tried my best to stay under the radar and hoped that no one would think of me as a real person.

Pretty colorful brains and simplified explanations of human cognition and emotion and personality had became staples of mainstream newspapers and magazines, first in the dying print media and then in purely online news sources and press release farms. Gradually, a backlash grew against studies on the neural correlates of shopping at Macy's. This blog (and others such as Mind Hacks, Neuroskeptic, and Neurobonkers) was mentioned in the same press outlets that ran outlandish opinion pieces about Loving Your iPhone:

Neuroscience: Under Attack (Nov 23, 2012)

Neuroscience Fiction (Dec 2, 2012)

Why ‘neuroskeptics’ see an epidemic of brain baloney (Apr 13, 2013)

This blog reached the height of its popularity in 2012.  Then we hit 2013... the year of decline.

What happened?? I'll explore some possible reasons in the next post, and take a glimpse into the future.