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Date: Sunday, 31 Aug 2014 22:18

Do I contradict myself?
Very well then I contradict myself,
(I am large, I contain multitudes.)

-Walt Whitman, "Song of Myself" (from Leaves of Grass)


Science is the search for objective truth based on physical laws of the universe. Scientific theories try to explain the consistent and predictable behavior of natural systems. They are generally reductionist, meaning that complex systems are reduced to simpler and more fundamental elements. The principles of physics, for instance, are expressed in the form of beautiful equations that are the envy of the softer sciences.


xkcd: Purity


The enterprise of explaining how human brains produce complex thought (or how any nervous system produces observable behavior, for that matter) is notably lacking in the realm of grand unifying theories, a topic of discussion recently in the New York Times: “What would a good theory of the brain actually look like?”

But the “search for a general ‘bridging theory’ may be a fruitless one” – like Awaiting a theory of neural weather. The “bridge, some way of connecting two separate scientific languages — those of neuroscience and psychology” may not exist.

I'm not sure why the question, “What would a good theory of the brain actually look like?” was even posed in the first place (or posed in that fashion, like a single theory should be expected to explain “the brain”). Adam Calhoun asked what I think is a more productive question:  Are these the equations of the brain?




English theoretical physicist Paul Dirac said, “A physical law must possess mathematical beauty.” Are these equations beautiful? 1

I cannot say. I am neither physicist nor mathematician. I traffic in matters less sublime. All I can do here is to include this citation from neuroaesthetician Semir Zeki and colleagues (2014), who reported that the neural correlates of perceiving mathematical beauty are the same as those that appreciate fine visual art. To be more precise, ratings of mathematical beauty were parametrically related to BOLD signal in field A1 of the medial orbitofrontal cortex, a part of the brain involved in  emotion, reward, and decision making.

At the phenomenological level of subjective experience, this knowledge of brain activity does no more to explain what it's like to behold Dirac’s wave equation than the Temporal Difference Learning equation describes what it's like to feel this emotionally rewarding experience — the Nagelian conundrum of qualia.

We sail the arctic sea, it is plenty light enough,
Through the clear atmosphere I stretch around on the wonderful beauty,
The enormous masses of ice pass me and I pass them, the scenery is plain in all directions,

-Whitman, ibid


What does any of this have to do with Walt Whitman? Yesterday I saw a pair of articles that encapsulate Whitman's principle of “I am large, I contain multitudes” when applied to neuroimaging studies of unclear psychological phenomena.

“The results obtained suggest that dysfunctional [lower] activation of the SMA [supplementary motor area] for response inhibition is one of the candidate mechanisms of IGD [internet gaming disorder].”

“...adults with IGD have ... greater activation of the fronto-striatal network in order to maintain their response inhibition performance.”

The first study claimed that reduced recruitment of the SMA (a motor control area) could be responsible for the impulsivity seen in individuals with internet gaming disorder (an actual “Condition for Further Study” in the DSM-5). The second study suggested that enhanced activity in the fronto-striatal network (implicated in motor control as well, but also in reward) was necessary for IGD participants to maintain the same restrained behavior as control participants.

So which is it?

These results are not consistent. They contradict themselves. This is not unusual. The greater problem is that the discrepant results were reported by the same lab, each without any reference to the other study.

Do I contradict myself?
Very well then I contradict myself


This world view makes for profound and transcendent poetry, but unacknowledged internal contradiction should not be adopted as the optimum path to scientific enlightenment.

Empirical falsification, on the other hand, is a staple of the scientific method.

I don't mean to single out this particular lab (which is why I did not include in-line citations), but this is a pet peeve of mine, along with a refusal to acknowledge any and all evidence that refutes one's signature theory. There's no shame in obtaining inconsistent results (or at least, there shouldn't be). But at least say so, try to come up with a plausible explanation, and do more experiments.


Clear and sweet is my soul, and clear and sweet is all that is not my soul.

Lack one lacks both, and the unseen is proved by the seen,
Till that becomes unseen and receives proof in its turn.

-Whitman, ibid



Additional Reading

Awaiting a theory of neural weather

Song of Myself

The Beauty of Brain Science

The Trouble With Brain Science


Footnote

1 Do the equations of the brain give insights into its fundamental structure and function? Do they have the power to describe the brain? In the 1993 Dirac Lecture (Freeman, 1994), physicist Daniel Z. Freeman said:
Many quotations remind us of Dirac’s ideas about the beauty of fundamental physical laws. For example, on a blackboard at the University of Moscow where visitors are asked to write a short statement for posterity, Dirac wrote: “A physical law must possess mathematical beauty.” Elsewhere he wrote: “A great deal of my work is just playing with equations and seeing what they give.”. And finally there is the famous statement: “It is more important for our equations to be beautiful than to have them fit experiment.” This last statement is more extreme than I can accept. Nevertheless, as theoretical physicists we have been privileged to encounter in our education and in our research equations which have simplicity and beauty and also the power to describe the real world. It is this privilege that makes scientific life worth living, and it is this and its close association with Dirac that suggested the title for this talk [SOME BEAUTIFUL EQUATIONS OF MATHEMATICAL PHYSICS].


References

Chen, C., Huang, M., Yen, J., Chen, C., Liu, G., Yen, C., & Ko, C. (2014). Brain correlates of response inhibition in Internet gaming disorder. Psychiatry and Clinical Neurosciences DOI: 10.1111/pcn.12224

Daniel Z. Freedman (1994). Some beautiful equations of mathematical physics. CERN-TH.7367/94 arXiv: hep-th/9408175v1

Ko, C., Hsieh, T., Chen, C., Yen, C., Chen, C., Yen, J., Wang, P., & Liu, G. (2014). Altered brain activation during response inhibition and error processing in subjects with Internet gaming disorder: a functional magnetic imaging study. European Archives of Psychiatry and Clinical Neuroscience DOI: 10.1007/s00406-013-0483-3

Zeki, S., Romaya, J., Benincasa, D., & Atiyah, M. (2014). The experience of mathematical beauty and its neural correlates. Frontiers in Human Neuroscience, 8 DOI: 10.3389/fnhum.2014.00068



I bequeath myself to the dirt to grow from the grass I love,
If you want me again look for me under your boot-soles.

You will hardly know who I am or what I mean,
But I shall be good health to you nevertheless,
And filter and fibre your blood.

Failing to fetch me at first keep encouraged,
Missing me one place search another,
I stop somewhere waiting for you

-Whitman, ibid
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 25 Aug 2014 06:04

“My attention shifts to the fact that the comforting engine hum is eerily gone. Where has the comforting hum of the engines gone. Something has gone very, very wrong, the plane continued to shake.”

-Daniel Goncalves, recalling the terror of Air Transat Flight 236


I'm sitting here in an airport, reading a harrowing first person account of Air Transat Flight 236, which fell out of the sky when it lost all power on Aug. 24, 2001.

The plane was bound from Toronto, Ontario to Lisbon, Portugal when a fuel leak in the right engine began 3 hrs and 46 min after takeoff (at 04:38 UTC). The leak went undetected by the flight crew for over an hour, when it finally became apparent that the remaining fuel was insufficient to reach their destination in Lisbon. At 05:45 UTC, the pilot diverted the flight to Lajes Field on Terceira Island in the Azores, a cluster of islands about 850 miles west of Portugal.



Image: Humberta Augusto/AP – via The Globe and Mail

Air Transat Flight 236 with its emergency slides deployed, sitting on the tarmac of Lajes Field in the Azores island of Terceira, after an emergency landing on Friday, Aug, 24, 2001.



Here, Mr. Goncalves' gripping narrative should speak for itself.

“All lights turn off, TV's off, P.A. system off, emergency lights light up the floors marking the emergency exit door. What the hell is going on? Is this a joke? Another clearly tense voice takes over and tried to address the 300+ passengers without the aid of a P.A. system. "Everyone put on their life vest and prepare for emergency ditching at sea." Huh? What the hell does that mean? Are you kidding me? Disbelief. "The captain has informed us that we are two hours away from Lisbon and we will not make it. We are preparing for an emergency ditch at sea. When you hear BRACE, BRACE, BRACE, lean against the seat in front of you, fold your arms and brace yourself."

WHAT WHAT WHAT WHAT????? Oh my God, what is happening. We're going into the cold and black Atlantic? Now? Why? Is this a Joke? Are we part of that Just for Laughs show? Stop playing, come on. No joke. I was in denial. This fully loaded Airbus A330 was going into the ocean and all I knew was that my poor family were there with me. It hit me. This wasn't going to go away. This was it. This really was it. The end. Unimaginable death by catastrophe.”

-Daniel Goncalves, My Air Transat flight 236 story


I'm reading this story because of a very unique paper published recently in Clinical Psychological Science (McKinnon et al. 2014), a study of  post-traumatic stress disorder (PTSD) and memory in survivors of the near-fatal Air Transat flight. Fifteen of the individuals WHO WERE ACTUALLY ON THAT FLIGHT participated in an experiment of autobiographical memory for the event, a shared horror of impending death. The comparison events were the terrorist attacks of September 11, 2001 (9/11) and a neutral event from around the same time.1

Seven of the survivors had been diagnosed with PTSD, six did not have PTSD, and the status of the remaining two was unknown. This immediately raises the caveat of very small comparison groups, further complicated by the fact that some of the assessment instruments were missing from various participants (e.g., the NEO-Five Factor Inventory of personality was missing from four).

The study was conducted in the lab of Dr. Brian Levine, a well-known memory researcher at the Rotman Research Institute in Toronto. Adding another unexpected twist, the first author of the paper, Dr. Margaret C. McKinnon, was a passenger on Flight AT236!




Now I'm flying in an Airbus 319, returning home. The setting sun to my right is blinding across the aisle.



Here is the series of events on AT236 as recounted by Goncalves:

Timeline:

4:38am-fuel started leaking
5:45am- diverted to Lages Air Base in Azores
5:48am- emergency declared
6:13am- engine no 2 flamed out 217 km from Lages Air Base, full thrust to engine #1 on left wing and plane descended 6,000 feet (this was scary and when when the passengers first found out something was very wrong).
6:23am- Mayday declared
6:26am- engine no 1 flamed out 120 km from Lages Air Base
6:45am- plane touched down hard on runway 33



Then a flight attendant came over the PA system on my flight:

“Ladies and gentlemen, we are experiencing a little turbulence, please return to your seats and fasten your seat belts.”

OK, there's the turbulence, good thing I took an anti-emetic...



But the bumpiness was quite short-lived, so back to our main story.




Image via International Aviation Safety Association


McKinnon et al. (2014) administered the Autobiographical Interview (AI) and a number of other questionnaires to the AT236 survivors. A group of control participants (n=15) were queried about 9/11, a neutral event, and a personally negative event. The AI distinguishes between episodic and non-episodic details (e.g., facts you might hear on the news), and has been used to probe autobiographical memory in number of different patient populations, including those with dementia, mild cognitive impairment, medial temporal lobe amnesia, and epilepsy (Levine et al., 2002).

The results of the study indicated that the passengers recalled vivid details of the flight, which was not surprising. Neither the number of details recalled, nor the accuracy of memories (their veridicality in relation to actual events) was associated with PTSD. Instead, it was recall of extraneous details, repetition of events in the retelling of their stories, and additional commentary or editorializing about the events that was associated with PTSD. This pattern held for all three of the autobiographical events, although some of the statistical results were rather weak.


Fig. 1 (adapted from McKinnon et al., 2014). Mean number of details recalled across all events for passengers (with and without PTSD) and healthy controls (HCs) for the Autobiographical Interview. 
[NOTE: Internal = episodic and External = non-episodic (semantic, repetitions, metacognitive statements, external events).]



Cognitive Control Deficits Were Associated With PTSD

The authors suggested that greater difficulty in constraining and editing the content of one's autobiographical narratives, whether recalling the Air Transat flight or a neutral event, was associated with a PTSD diagnosis in this small sample of trauma survivors. This could reflect a more general deficit in cognitive control, i.e. the ability to regulate complex cognitive processes to achieve goal-directed behavior (Lenartowicz et al., 2010).

While a unique and important study, we must keep in mind the limited and perhaps self-selected nature of the population (7 with PTSD, 6 without PTSD). The experiment required recalling the most frightening and horrific 30 min imaginable, and many survivors may have declined to sign up for that.

The authors acknowledged these and other weaknesses:
The participants in this study reflect only a small percentage of the 306 passengers aboard AT Flight 236; we did not have access to the passenger manifest, and individuals with more significant psychopathology may have avoided participation for fear of retraumatization. Thus, the current study was limited to a small number of participants. Moreover, as passengers’ memory was assessed several years after the traumatic incident (approximately 3.5 years later), it remains unknown how trauma might have impacted memory in the more acute stages of trauma exposure among this sample. 

NBC News also addressed these issues in a quote from Mr. Goncalves, who wrote about his ordeal in a blog post to avoid having to retell it over and over:
“Just reading something about it, I’ll lose myself in thought, catch myself visualizing it and get sweaty fingers,” said study subject Daniel Goncalves, who was 24 while traveling with his family on Flight 236 to see a dying uncle in Portugal. He was never formally diagnosed with PTSD. “I’m getting goose bumps now, talking about it.” 2

Today, working as a photographer in Dallas, Goncalves, has sometimes shied away from discussing the event. To help friends understand, he wrote a blog post about those the 32 minutes so “I can send them over there instead of going through the whole ordeal and avoid getting emotional.”


Daniel Goncalves, My Air Transat flight 236 story:
“Later on we found out that those white knuckle, torturous last few seconds which were filled with terrible thoughts waiting for impact stretched to fill an unbearable 32 minutes of misery. I still can't explain how terrible it was waiting, expecting it to be any second now and that going on for 32 mins. It felt like an eternity of waiting for a very bad thing to happen. During these 32 minutes the plane never stopped shaking. You could hear the plane cut through the air, no engine noise, muttering of prayers, crys, pleads. The whole time.”

In the end, Captain Robert Piché, the heroic pilot, was able to glide the powerless plane to a safe landing at Lajes Field. None of the 306 passengers died, and there were only 18 minor injuries. Many thought of this feat as a miracle, or at least “a moment of miraculous relief.”  Daniel Goncalves considered this the day he was reborn.


Footnotes

1 The neutral event was uniquely generated by each participant prior to the start of the autobiographical memory interviews, I believe.

2 These symptoms are all highly consistent with a PTSD diagnosis.


Reference

McKinnon, M., Palombo, D., Nazarov, A., Kumar, N., Khuu, W., & Levine, B. (2014). Threat of Death and Autobiographical Memory: A Study of Passengers From Flight AT236. Clinical Psychological Science DOI: 10.1177/2167702614542280


Link to Daniel Goncalves' blog via NBC News.


Author: "noreply@blogger.com (The Neurocritic)"
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Date: Thursday, 14 Aug 2014 09:56

NEUROTECH LIGHT AND DARK »

Tweet length visions of our DARPA-funded future


The Neurocritic has recently blogged about The Neuroscience of the Future:
Neural prosthetics, brain-computer interfaces (BCI), “closed-loop” deep brain stimulation (DBS) devices, and a world without human brain disorders. The first three of these are already here... is the last one possible?


Here’s a sample of Neurotech Light and Dark, a sci fi collection of 16 very short stories about neuroscience and technology, by S. Kay.
A brain-computer interface controls her robotic arm. As easily as not thinking, she uses it to drink another shot of tequila.

Analyzing data from an EEG experiment on reaction times and impulse control disorders, the neuroscientist finds a link to Twitter usage.

Read the rest at Science Creative Quarterly.


And read more about the neurotech of the present, including DARPA's SUBNETS program, the Brain Radio, and other new DBS devices.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 10 Aug 2014 10:13


Today I'm chatting with Dr. Jan Kabitzer, a Physician and Leader of the Neurochemistry Research Group at Charité - Universitätsmedizin Berlin.

Dr. Kabitzer is first author of the “Twitter Psychosis” article that made international news and took social media by storm on August 6, 2014. His provocatively titled paper, “Twitter Psychosis: A Rare Variation or a Distinct Syndrome?” (Kalbitzer et al., 2014), appeared online a week earlier in The Journal of Nervous and Mental Disease. I was struck by the title, of course, and an abstract claiming that “Twitter may have a high potential to induce psychosis in predisposed users.”

I wrote a critical blog post on July 31, 2014 (Twitter Psychosis as a Cultural Artifact) arguing that Twitter resembles other technologies and cultural artifacts that can potentially influence the phenomenology of delusions, citing the work of Vaughan Bell and colleagues (Bell et al., 2005).

It is now August 10, and the media huff has died down a bit. The overarching narrative of this story is very meta —  social media about social media. It is in this spirit that I present the interview. 1





Q: Could you tell me a little about your clinical work and your research?

Since my Ph.D. in Copenhagen at the Neurobiology Research Unit from 2007 to 2009 I have been working clinically at the psychiatric department of the Charité Berlin to specialize in psychiatry. Most of the time I worked on an acute psychiatric ward. We do have some time for research but I did mainly see patients. We are responsible for larger Berlin-Mitte which includes Berlin-Tiergarten and Berlin-Wedding so we see a lot of patients with severe mental disorders who are often in a precarious social situation. My research was initially with PET (positron emission tomography) but over the last year I have changed direction because I became very interested in recovery concepts and right now we are planning a project where we want to study which effect it has to abstain from using diagnostic classifications systems on different measures of mental health and well being. But since February my time as a resident is over and I am actually on paternity leave since then. The reviewing process of this case just took some time.


Q: The first question on everyone's mind is, why did you choose to include the term “Twitter Psychosis” in the title?

We observed the symptoms that we describe only in a few cases but it really disturbed us how these spam bots [Twitter bots] messed with our patients’ perception. We had the impression that abbreviations were intentionally used to create confusion and curiosity to follow the link in the tweet. We saw that this method that was used for commercial purposes can have a destructive effect. So we wanted to spark a discussion about what Twitter does to our minds and chose a provocative title to bring this subject up. But I see now that the main effect was that some news sites, like the Daily Dot, profited insanely from repetitively tweeting their exaggerated headlines. So I would not choose to be that provocative again outside of a closed scientific context. That is sad because I hate ivory towers - but being provocative as a researcher just doesn’t work well with the mass media.


Q: How do you compare the coverage you've seen on blogs vs. mass media?

I have seen both horrible blogs and great blogs. My impression is that in the case of blogs there is more often someone who feels responsible for it which is not always the case with the media (even though there are of course also great journalists).

You would have thought that I was a coveted interviewee during the last week. But I was only contacted by three journalists from NBCNews, betanews and Wired (UK). The NBC guy was great, I told him that I want the article to put things into perspective and he was fine with that. He quoted me exactly how I wrote it and I particularly insisted that he put in the sentence that this is not “real”, what he did. Just the headline wasn't that great. betanews I had never heard of, I just saw all these ads on their page, but I thought I’d rather reply to influence what they write and I think they covered it ok. And I asked them to take down the unbearable picture of a “crazy man” which they used first and they did. And, finally, Wired UK where Liat Clark offered to write against the panic. She interviewed me, but the article isn’t out yet and I am wondering if they will still cover it because the main wave on Twitter and in the news seems to have passed and the interview was Friday evening.

But I did contact some of the newspapers/magazines with the worst headlines myself. The funny thing is that none of them were really interested in an interview with the first author of the study they were writing about. After a while I realized that this is not about me and our article.

Bloggers like you and “Dr. Shock” warned early on and in this case we contacted you and you felt responsible for following up on the story.


Q: The tone of the article was confusing to many people. It wasn't clear if you were being completely serious, somewhat sensationalistic, partially joking, or if it was a joke paper. Your comment gave a brief answer, but could you elaborate here?

The case study had a small political flavor by citing Ben Goldacre (as a homage because I like his critical work about the pharmaceutical industry) but besides that it was completely serious. It would be preposterous to say that we aren’t sensationalistic at all. Every researcher who likes to publish also likes to be read and to be mentioned. But the fact is that our department is strongly influenced by the ideas of the recovery movement. So we focus on treating our patients according to their individual needs and not according to their diagnoses. So, yes, a ‘Morbus Kalbitzer’ [Kalbitzer's Syndrome] and being famous would be great. But would I get to use it? No. And even if ‘Twitter Psychosis’ entered Wikipedia with us describing it first, it would not have been worth it that all these people all over the world became even more insecure about how they should feel about modern media.

Besides that I think there are two things that contributed to the fact that the paper had such a provocative tone:

1. I love Paul Feyerabend2 [a philosopher of science] and I believe that you should always challenge existing research theories with new, provocative hypotheses. I learned during the last week that this holds true if you are among reasonable people but in the context of globalized digital mass media you probably can’t do that with scientific publications.

2. Although we do often complain about the quality of our media in Germany, we are actually quite spoiled, so I was naive. News channels went mad in the US and the UK but it didn’t cross over to Germany. Even though I am sure that German journalists do follow these news channels, nothing went viral here. People in Germany are always a bit intimidated by the intensity of North American News.

But at the core of our paper is clearly a scientific question: is that what we observe on Twitter a new, unique feature that has a distinct effect on the development and course of delusions? While you and Vaughan seem to disagree with this, I believe that it makes a difference whether you are watching TV and believe the talk show host is talking to you or watching something that actually does react to what you do like the stream on Twitter. For example, you watch a morning show and still run around naked and suddenly the guy on TV says that running around naked in the morning can cause athlete's foot. That is what spam bots do on Twitter. This is what we meant by “Twitter communication responds to changes in communication style.” When you don’t use Twitter for a while you get emails that you are missed. And then you log in again and might see a spam tweet that links to a book about loneliness by some social guru. Isn’t that different to seeing a telephone post?


Q: One of the most puzzling things to me was the Twitter “experiment”. The purpose was unclear, the details were sparse, and it was difficult to follow what happened. Can you explain?

This partially got messed up by being reviewed for more than one journal. This one-page case study had probably more reviewers contributing to it than authors. We created several experimental accounts which are all deleted now and wrote tweets to more or less famous people on Twitter to see what kind of spam tweets we get in response to our tweets. We tried out different concepts but it was quite difficult for us to simulate what our patients described. So in the end we just used an example for the features of Twitter we described.

But it doesn’t say anywhere that we did a ‘Twitter experiment’ or a ‘Ben Goldacre experiment’, we just say that we used an experimental account. Instead of writing that we ‘test’ something we could have written something like: here is an example of such a tweet to illustrate the features we are talking about. It was more like psychiatrists who treat a patient who took a new designer drug and then, for the case study, the authors take the drug themselves and describe what they’ve experienced. The funny thing is, though, that we had a hard time simulating what most patients described as losing control, in this case that “it would not stop”. Today I know exactly what they are talking about. I surely had a Twitter overdose. Sometimes I used the live search function and watched the stream of tweets on ‘twitter’ and ‘psychosis’. It was a bit like the 'Listening Post' in the Science Museum in London,  just much more disturbing. And after this experience, when thousands of people on Twitter just oafishly retweeted the “news” without looking up the source, and some of these people were psychologists and doctors, I can say that “to twitter” is the right term for what they do. It’s not my cup of tea.


Q: Usually journal articles have a formal Methods section where the authors describe the procedures (hopefully in enough detail so others can try to replicate). In retrospect, would you change the word Experiment to something else, like Demonstration?

As I said, we presented an example of a tweet that we received when we used an experimental Twitter account. I think what added to the confusion is that this was published as a 'Brief Report'. The Journal of Mental and Nervous Disease doesn’t have a section for case studies so we first submitted the case study as a letter to the editor but were asked to re-submit it as a 'Brief report'. But it is still a regular case report with no experiment, just an experimental Twitter account that we created in order to receive spam messages to, well, yes: demonstrate the features we are talking about.


Q: How do you think scientific articles should be communicated to the public?

I believe that most researchers in social neuroscience are to some degree lay people. Both the PET people who talk about ’the mind’ and the philosophers who want to find the voxel of morality. So I think experiments should be as simple as possible and then be published with absolute transparency and open access (even though I am a bit disturbed by the commercial approach of some open access journals). Then many other 'lay' people will understand what is going on.

I do also believe that you should use scientific data to provoke. In my Ph.D. I wrote in a small paragraph that the whole serotonin - depression story may just be based on mis-interpreting changes in motor activity and vigilance. George Ashcroft already questioned the serotonin story in a similar way. But I guess nobody except my opponents ever read my Ph.D. and they didn’t seem so provoked. It is difficult to find the golden mean.


Now I would like to ask you something! Q: Neurocritic, in your posts you can be fun and ironic but being in contact with you over the last week I realized that you are very serious about your work on this blog. You have been writing extensive and well researched posts for eight years. What is your motivation to do this? Is fighting sensationalistic research your 'Raison d’être‘? And why?

Although it may not be obvious, I am a serious person in real life. I started this blog out of sheer frustration with peer review, during a time when I was facing many rejections. When deeply flawed papers were routinely appearing in top journals, I wondered why all my hard work did not pay off. 3 Since I wanted to critique outrageous claims published in high-profile journals and discussed in the popular press, fighting sensationalistic research is largely my 'Raison d’être.

I saw this as cathartic at the time (since I never expected many readers), but my reasons over the years have evolved to include educating the public and providing a service to the field. I've remained anonymous because the vast majority of peer review is anonymous, which allows reviewers to be rude and insulting. I never want to do that.

However, the humorous and sometimes snarky nature of the blog may have unintended consequences on occasion, and I think that was true in the case of your paper. I try to think about the potential impact of my posts on the authors involved, and in this case I did not anticipate such a media circus. In fact, one of my parting thoughts was, "Hopefully we will not see “Twitter causes psychosis” headlines any time soon."  

So overall I'm sorry about this whole ordeal.



And thank you, Jan, for taking the time to answer these questions.


ADDENDUM (August 11 2014) - This new article at Wired UK has the clearest coverage: Twitter spam may 'aggravate psychosis' in the vulnerable


Footnotes

1 Jan's answers were very lightly edited by me for English language smoothness and formatting.

2 Paul Feyerabend was an Austrian philosopher of science who...
...became famous for his purportedly anarchistic view of science and his rejection of the existence of universal methodological rules. He is an influential figure in the philosophy of science, and also in the sociology of scientific knowledge. ... His major works include Against Method (published in 1975).
According to the Stanford Encyclopedia of Philosophy, Feyerabend:
made a name for himself both as an expositor and (later) as a critic of Karl Popper's “critical rationalism”, and went on to become one of the twentieth century's most famous philosophers of science. An imaginative maverick, he became a critic of philosophy of science itself, particularly of “rationalist” attempts to lay down or discover rules of scientific method.

3 This was in stark opposition to the "All your hard work will soon pay off" fortune taped to my monitor.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Thursday, 31 Jul 2014 22:36
UPDATE (Aug 6 2014): This story has spun entirely out of control, with breathless coverage at The Daily Dot and Jezebel. Today the hapless first author told NBC News: "No, at this point Twitter psychosis is not 'real.'" 

And no, a woman was not committed to psychiatric hospital with ‛Twitter psychosis’! However, the general confusion created by the ensuing media circus might be what the authors were trying to get at...


The original post resumes below.



The creation of the category “Twitter Psychosis" tells us more about the culture of contemporary psychiatry than it does about the purported dangers of social media overuse. Can Twitter really “cause” psychotic symptoms in predisposed individuals? Or is Twitter merely the latest technical innovation that influences “the form, origin and content of delusional beliefs” (Bell et al., 2005)? Twitter as the new telephone tower, radio waves, microchip implant or personal TV show, if you will.

Via Twitter (@DrShock, @vaughanbell), of course, comes news of a one page paper entitled, Twitter Psychosis: A Rare Variation or a Distinct Syndrome? (Kalbitzer et al., 2014):
The authors report the development of psychosis in a young woman coinciding with excessive use of the online communication system Twitter and the results of an experimental account to argue that Twitter may have a high potential to induce psychosis in predisposed users.

The authors presented the case of a 31 year old woman who was hospitalized for intensive suicidal thoughts and compulsions. She had no previous history of psychiatric illness and denied current hallucinations.1 Her friends and family said the symptoms began about 8 months earlier. Approximately 4 months prior to that she started using Twitter “excessively” (defined as “several hours a day reading and writing messages, neglecting her social relationships and, sometimes, even meals and regular sleeping hours”).2 At some point she came to believe that a famous actor was communicating to her personally (a common delusion), and to see hidden symbolic messages in Tweets:
During the next couple of weeks, Mrs. C increasingly felt that the messages of other users were “meant in a symbolic way” and that she had to react to these “tasks” in a certain manner. After approximately 2 months, she started to discover the same symbols in her real-world environment. She then started to feel that there “must be some organization behind these tasks” and started to suspect a sect, pointing to the development of systematized paranoid delusion.

None of this really seems like a Distinct Syndrome, and I doubt it's even a Rare Variation any more. The authors wanted to discuss (with the larger medical community) “whether they already have to speak of a distinct syndrome of social media-induced psychosis.”

And in fact, Dr. Vaughan Bell is one of the top experts to discuss this issue, and I imagine he will address the authors over at Mind Hacks.

But then the Brief Report completely derails with an “experiment” reported in the remaining paragraphs...


The Ben Goldacre Experiment


Someone (it's not clear who) created a fake account to address whether “Twitter communication responds to changes in communication style.” [NOTE: I'm not sure what this means.]

To test this, a test person created an account and responded to the messages of Ben Goldacre, the maker of the blog http://badscience.net. Our test person responded to a message of Mr. Goldacre about the pope, but Mr. Goldacre did not reply. However, the authors received an answer from an unknown participant, writing "<our username> Cold blooded RT. XXX: I am in the church: <link>." The link led to different Web pages with commercials.

...when the authors followed the link, they were confused about a flood of useless information (commercials). The authors understood that this was a spam message, but this might not be the case for a person who is predisposed to psychosis and, in addition, in a stressful psychosocial situation.

So from this ill-defined, bizarre and staged interaction with a test person, the authors concluded that “Twitter might combine several aspects that could induce or further aggravate psychosis.” In a presumably peer-reviewed publication.3

This is preposterous. Hopefully we will not see “Twitter causes psychosis” headlines any time soon.

 Vaughan should have the last Tweet here:



Further Reading

Returning to the title of the post, here's more on Twitter and cultural artifacts:

Twitter as a Cultural Artifact

Tools for Tech Thinking: McLuhan on Twitter


ADDENDUM Aug 6 2014: The authors have commented on this post to clarify that they were being deliberately provocative with their title and approach to the topic, but serious about the possibility that the interactive social media aspects of Twitter might have unique qualities in how it could affect those with (or predisposed to) psychosis. Furthermore, the authors are not inclined to generate a new host of DSM-5 diagnoses; in fact, Heinz and Friedel (2014) stated: "The inclusion of non-substance, behavioral addictions poses the danger of pathologizing a wide range of human behavior in future revisions of the classification."


Footnotes

1 However, Bell et al. (2008) showed that individuals with delusions do not always have anomalous perceptual experiences.

2 I imagine “several hours a day” could apply to many individuals without a formal diagnosis of mental illness. I will not deny that Twitter and other forms of social media can have an addictive quality for some people, but the “Twitter addiction” construct is not very useful.

3 Can I put this blog post on my CV?? Here we learn about academic publishing in psychiatry and the propensity to categorize.


Reference

Kalbitzer J, Mell T, Bermpohl F, Rapp MA, & Heinz A (2014). Twitter Psychosis: A Rare Variation or a Distinct Syndrome? The Journal of nervous and mental disease, 202 (8) PMID: 25075647
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 21 Jul 2014 09:46
I wanted to submit a paper for the Frontiers in Human Neuroscience Research Topic on Critical Neuroscience: The context and implications of human brain research, but I couldn't decide what I should write about.

Could I just submit a blog post like Professor of Literary Neuroimaging that critiqued the entrée of fMRI into Literature Departments?
“So literature is abandoning Marxism and psychoanalysis in favor of neuroimaging!! Meanwhile, key neuroimagers have taken up psychoanalysis (Carhart-Harris & Friston, 2010) and socialism (Tricomi et al., 2010).

Would they accept short humorous pieces like this...

Tenure-Track Position in Neuroetiquette and Gender Theory

Department of Critical Socioneurobiology.

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

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

NDSFSR is an Equal Opportunity Employer.



...accompanied by a [somewhat] more serious meditation on Neuroetiquette and Neuroculture, which explained that neuroscientists are not taking jobs away from philosophers, sociologists and gender theorists:
I think the neuro-panic among social scientists is overblown. How many philosophers, sociologists, and gender theorists are unemployed because their respective departments have decided to hire neuroscientists instead? How many developmental neurobiologists have applied for this Instructor of Philosophy position at Rochester Community and Technical College? Will a cognitive neuroscientst be able to teach transnational feminism or postcolonial feminism, queer theory, and critical race theory in the Women's and Gender Studies Program at Illinois State University?

Could I have converted all of the above content into a coherent scholarly manuscript that addressed firstly, the pestilent neuro-ization of the academy (and the kitchen),1 and secondly, the reactionary anti-neuro manifesto pushback? Did I even want to? There was certainly no time (or money) for such a project...

Or how about something on The Mainstreaming of Neurocriticism (followed by its inevitable decline)? That would have been a lot easier for me.


But Is Neurocriticism the same as Critical Neuroscience

The call for papers said:
Critical neuroscience is an approach that addresses these contested issues surrounding the field of cognitive neuroscience from multiple viewpoints. The aim is to engage neuroscientists with researchers in the humanities and social sciences who deal with the implications of brain-based approaches to fields such as education, law, medicine, social policy, business and with the expansion of neuroscience in the University more broadly. Critical neuroscience encourages collaborative approaches to careful assessments of the status quo, longer-term impacts, potentials and problems of cognitive neuroscience within the laboratory and in the various areas of application. The project has been analyzing methods, technologies and theoretical paradigms, while also drawing on history and philosophy of science, anthropology, sociology and cultural studies, and reaching out to include practitioners from medicine, social policy, counseling and science journalism in order to better understand whether and how neuroscience could have value for these other domains.

Presciently,2 the Editors wanted to “address the visions and challenges surrounding new grand-scale initiatives in neuroscience — including the EU-funded Human Brain Project and a comparable initiative planned in the U.S.”

As it so happens, a mere two weeks ago, the €1-billion HBP was roundly criticized in an open letter signed by 156 neuroscientists (the list of signatories and supporters is now over 700):
...the HBP has been controversial and divisive within the European neuroscience community from the beginning. Many laboratories refused to join the project when it was first submitted because of its focus on an overly narrow approach, leading to a significant risk that it would fail to meet its goals. Further attrition of members during the ramp-up phase added to this narrowing ....  including the removal of an entire neuroscience subproject and the consequent deletion of 18 additional laboratories...
. . .

In this context, we wish to express the view that the HBP is not on course and that the European Commission must take a very careful look at both the science and the management of the HBP before it is renewed. We strongly question whether the goals and implementation of the HBP are adequate to form the nucleus of the collaborative effort in Europe that will further our understanding of the brain.

A flurry of press and blog coverage ensued, followed by a bigwig defense in New Scientist and an official statement [PDF] from the HBP. Although it's clear there are fundamental differences of opinion about a massively optimistic and expensive attempt to model the human brain, organizational issues of power and control are key as well:
The nixed subproject, called Cognitive Architectures and headed by French neuroscientist Stanislas Dehaene, represented all the neuroscience in Europe that isn't working on a molecular or synaptic level, says Zachary Mainen of the Champalimaud Centre for the Unknown in Lisbon, one of the authors of the letter. HBP “is not a democracy, it’s Henry’s game, and you can either be convinced by his arguments or else you can leave,” Mainen says.
link via Neuroecology


You might think that the current HBP dispute has drifted outside the realm of the “Critical Neuroscience” Research Topic.3 But you'd be wrong, because Extending the mind: a review of ethnographies of neuroscience practice (Mahfoud, 2014) appeared online only one month before the brouhaha:
Ethnographic studies of neuroscience knowledge can potentially offer insight into the relationship between the everyday of scientific practice and reasoning on the one hand and the political and moral economy of science on the other, as well as encouraging conversation between the social and biological sciences, as this special issue aims to do. 

So what do I think about the Critical Neuroscience enterprise? The 18 articles are pretty diverse and include fMRI methods papers on Machine Learning Classifiers and deficient approaches to neuroimaging.

I already blogged about one paper in the special issue, on the fun topic of Empirical Neuroenchantment: From Reading Minds to Thinking Critically (Ali et al., 2014). So see The Seductive Allure of Spintronics™ Neuroimaging mock mind reading scanner for that.

Another article is basically a sociocultural mega-thrashing of the NIMH RDoC framework for mental health research. Worth quoting:
In this article we consider the rationale of the RDoC and what it reveals about implicit models of mental disorders. As an overall framework for understanding mental disorders, RDoC is impoverished and conceptually flawed. These limitations are not accidental but stem from disciplinary commitments and interests that are at odds with the larger concerns of psychiatry. 

There are also contributions from “historians of science, STS scholars and philosophers.” The acronym highlights a language gap between disciplines, because I had to look up STS scholars — they're not experts in the superior temporal sulcus, they study science, technology and society.4 On that note, I'm not sure how many readers will devour a support vector machine classifier using a linear kernel and a critical philosophical investigation of the brain qua image.

But that's the problem with a multiplicity of specialized viewpoints in academic publishing. Maybe someone (the Editors?) can host a series of interdisciplinary blog posts that are comprehensible to a broader audience?


Footnotes

1 Who can forget Neurokitchen Design? Or The Neuroscience of Kitchen Cabinetry?

2 The call for papers went out over a year ago.

3 Unless, perhaps, you want to critique the growing literature on whether Neurocoaching could improve the Neuroleadership skills of HBP oligarch Henry Markram....

4ADDENDUM (July 21 2014) - Neuroskeptic has informed me that STS also stands for Science and Technologies Studies. Cornell, Berkeley, Wisconsin, RPI, and UC Davis, for instance, call their programs Science and Technology Studies. Harvard, Stanford and NC State call it Science, Technology, and Society (but Harvard hedges their bets and uses both terms).
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 14 Jul 2014 03:25
via @mallelis


At the literary/pop culture/feminist/humor blog known as The Toast, the hilarious Mallory Ortberg has skewered those ubiquitous ads from brain training behemoth Lumosity.

The Five Stages Of Lumosity

Stage I – Initiation

. . .
Friend, are you troubled by persistent waking blackouts? Do you tremble and shudder and flicker out of consciousness when asked to recall basic facts about your acquaintances? Does your right eye fill with blood whenever you have to try to remember your PIN? Let Lumosity patch over those mysterious missing blank spots in your sick and addled mind.


“Lumosity: Improving your brain through the science of neuroplasticity, but in a way that just feels like games.”

Lumosity: you can trust us. It doesn’t hurt. It’s normal. It feels normal. Good and normal. Just like a game. Won’t feel a thing. It’s normal, and you’re normal, and your brain is working better now than it was before. Before was bad. Now is good.

Then the user progresses to Stage II – The Audit,  Stage III - Saturation,  Stage IV – Synergy/Assimilation, and finally to...

Stage V – Full Compliance

The Golden Age of Tech II


Stage V features a series of screenshots taken from a flabbergasting Scientology promotional video (discussed on Reddit).

Ortberg's post is really quite brilliant the cult-like following, the testimonials from humans ascended to a higher plane, the suspiciously vague ad campaigns that use suspiciously vague terms like "neuroplasticity".

In reality, though, it's hard to imagine two world views more completely out of step than Neuroscience and the bizarre set of beliefs known as Scientology.  {floating tone arms, anyone??}




In fact, Scientology is quite vehemently anti-psychiatry and anti-neuroscience. Many of you might remember Tom Cruise's condemnation of Brooke Shields for taking antidepressants to treat her postpartum depression, to which Shields replied: “Tom should stick to saving the world from aliens and let women who are experiencing postpartum depression decide what treatment options are best for them.”

The stance against psychiatric medication goes much further than that: they would like to eliminate NIMH, the major U.S. funding body for biological psychiatry and mental health research. The Secrets of Scientology site maintained by Carnegie Mellon Computer Science Professor David S. Touretzky has covered the sect's excesses for many years, including in a poster presented at the 1998 Society for Neuroscience meeting:
Opposition to Mental Health Research

Scientology demonizes the mental health professions in part because psychology and psychiatry are Scientology's main competitors. But another reason is that all cult groups need an external enemy to rally against. Scientologists are taught that modern psychiatrists still use lobotomy and electroshock treatments to dominate and control their patients.

Despite this, Scientology started out with a materialist model of the mind before it was derailed (perhaps by founder L. Ron Hubbard's alcohol and drug addiction). As Prof. Touretzky explains:
In 1950 Dianetics presented a purely materialistic view of the mind as a simple computer, with frequent references to "memory banks", "circuits", and data recording. The mind was implemented by the brain, and memory was a product of a cellular recording mechanism. Hubbard did not rule out the possibility that psychic phenomena such as ESP or telepathy might some day be demonstrated, but they played no role in Dianetics.

With the introduction of past lives, Hubbard switched from a materialist to a dualist conception of mind. In Dianetics, the "I" that looked at mental image pictures was the analyzer. In Scientology the "I" is the thetan, a spirit, that moves from one body to the next, carrying its reactive mind along with it. And in advanced Scientology auditing, subjects are instructed to communicate with their body thetans "telepathically", not verbally.

The E-Meter

Touretzky's SFN poster again:
The scientific trappings of Scientology extend even to instrumentation: a skin galvanometer called an E-meter (electropsychometer) is said to allow an auditor (therapist) to observe the creation or destruction of "mental mass'' by reading the needle movement.

 
Mark Super VII Quantum E-meter (Wikimedia Commons)


The E-meter (known variously as the Electropsychometer or the Electroencephaloneuromentimograph)1 provides a crude measure of skin conductance. How crude? The original model used a pair of tin cans as electrodes. To learn more, you can surf the Internet's most extensive E-Meter site hosted by (you guessed it!) Prof. Touretzky.

According the Church of Scientology's own materials, however, the E-meter is used by auditors to locate areas of spiritual distress or travail:
The E-Meter measures the mental state or change of state of a person and thus is of enormous benefit to the auditor in helping the preclear locate areas to be handled. The reactive mind’s hidden nature requires utilization of a device capable of registering its effects – a function the E-Meter does accurately. 
. . .

When the person holding the E-Meter electrodes thinks a thought, looks at a picture, reexperiences an incident or shifts some part of the reactive mind, he is moving and changing actual mental mass and energy. These changes in the mind influence the tiny flow of electrical energy generated by the E-Meter, causing the needle on its dial to move. The needle reactions on the E-Meter tell the auditor where the charge lies, and that it should be addressed by a process.

Different needle movements have exact meanings and the skill of an auditor includes a complete understanding of all meter reactions.

Wow, that is true scientific precision. Impressive, now isn't it? Even the most computationally sophisticated cognitive neuroscientists don't claim to read the hidden mind's reactive nature using multivoxel pattern analysis (MVPA) of fMRI data. Or do they?


‘Neural Valence Meter’

I know the authors of a recent Nature Neuroscience paper that used MVPA to classify subjective affective states2 (Chikazoe, Lee, Kriegeskorte, & Anderson, 2014) would be utterly horrified with the analogy, but I thought of the e-meter when I read this quote in a press release:
“It appears that the human brain generates a special code for the entire valence spectrum of pleasant-to-unpleasant, good-to-bad feelings, which can be read like a ‘neural valence meter’ in which the leaning of a population of neurons in one direction equals positive feeling and the leaning in the other direction equals negative feeling,” Anderson explains.

Call it priming by Ortberg if you will, but terminology like 'special code', 'entire valence spectrum', 'leaning in one direction/the other direction', and 'neural valence meter' sounded a little cult-like to me...


E-Meter Controls and Indicators

{imagine that the needle leaning in one direction = 'good' (clear), and in the other direction = 'bad'}


Footnotes

1 A Gizmodo article that called the device an electroencephaloneuromentimograph is most notable for posting the lengthy complaining e-mail sent by the Church of Scientology.

2 Let's call them 'neuroqualia' perhaps - “The entire valence spectrum was represented as a collective pattern in regional neural activity as sensory-specific and abstract codes, whereby the subjective quality of affect can be objectively quantified across stimuli, modalities and people.” (Chikazoe et al., 2014).


Reference

Chikazoe J, Lee DH, Kriegeskorte N, Anderson AK. (2014). Population coding of affect across stimuli, modalities and individuals. Nat Neurosci. Jun 22. doi: 10.1038/nn.3749. [Epub ahead of print]
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Thursday, 10 Jul 2014 10:58


In the 2000s, enthusiasm was high that a novel class of drugs would reach the market as blockbuster treatments for psychiatric disorders. These drugs act on receptors for a group of neuropeptides known as tachykinins (or neurokinins). These peptides — substance P (SP), neurokinin A (NkA), and neurokinin B (NkB) — function as neurotransmitters or neuromodulators in the central nervous system, but are quite different from the usual monoamines targeted by current psychotropic medications prescribed for schizophrenia, depression, and other mental illnesses.

The tachykinin receptors (NK1, NK2, NK3) have varying affinities for the different peptides, being greatest for SP, NkA, and NkB respectively. A series of clinical trials with NK1 antagonist compounds (i.e., SP blockers) was conducted as potential treatments for major depression, generalized anxiety disorder, alcohol craving, and post-traumatic stress disorder (PTSD). Substance P is released during times of increased stress and localized in brain regions implicated in the stress response (Ebner et al., 2009), so the idea was that dampening the effects of SP would lead to symptom amelioration in these disorders.  However, except for some mildly promising results in stressed alcoholics, the trials were disappointing in patients with generalized anxiety and PTSD. Results were mixed in major depression. But those trials, with a GSK compound called orvepitant, were terminated to due serious adverse events (seizures) in several patients.

In contrast, the most promising target for schizophrenia seemed to be the neurokinin 3 (NK3) receptor. This was because of prominent expression on the midbrain dopamine (DA) cells implicated in the pathophysiology of schizophrenia, and because selective NK3 antagonists can block NkB-induced excitation of dopamine neurons (Spooren et al., 2005). The original “typical” antipsychotic medications are DA antagonists, which can have untoward side effects with chronic use. Because NK3 antagonists lack the major extrapyramidal and metabolic side effects of typical and atypical antipsychotics, they were heralded as “the next generation of antipsychotics” in 2005.

How well have they fared since then?

(1) The NK3 antagonist osanetant was under development by Sanofi-Synthélabo as a potential treatment for schizophrenia:
In October 1999, Lehman Brothers predicted that the probability of the product reaching the market was 10%, with a possible launch in 2003 and potential peak sales of US $200 million in 2011.
However, Sanofi-Aventis stopped any further development of osanetant in 2005.


(2) The NK3 antagonist talnetant was under development by GlaxoSmithKline, with several clinical trials conducted between 2002 and 2005. But it too was discontinued (in 2007).

In other words, these drugs have not lived up to their original promise as novel treatments for schizophrenia.


“Repurposing” of Drugs

“We should continue to repurpose treatments and to recognise the role of serendipity,” said Geddes and Miklowitz (2013) in a recent review on new treatments for bipolar disorder. Although the article did not hint at any impending pharmacological breakthroughs, the idea that existing drugs can find new indications is especially pertinent in this era of shrinking investment in neuro/psych drug development.

Sometimes the serendipity and repurposing comes from mechanistic preclinical studies that can then be retranslated back to the clinic. Jumping ahead to that possibility, a press release from Emory declares:
Potential drug target for PTSD prevention

Scientists at Yerkes National Primate Research Center, Emory University have identified a drug that appears to make memories of fearsome events less durable in mice.

The finding may accelerate the development of treatments for preventing PTSD. The drug, called osanetant, targets a distinct group of brain cells in a region of the brain that controls the formation and consolidation of fear memories.
. . .

“Potentially, drugs that act on this group of cells could be used to block fear memory consolidation shortly after exposure to a trauma, which would aid in preventing PTSD,” says Kerry Ressler, MD, PhD, professor of psychiatry and behavioral sciences... “PTSD is unique among psychiatric disorders in that we know when it starts – at the time of the trauma. Finding ways to prevent its development in the first place – in the emergency department or the battlefield - is an important and exciting avenue of research in this area.”

NkB and the Consolidation of Fear Memories 

A new study in mice found that osanetant could block the consolidation of fear memories when administered within a narrow time window (Andero et al., 2014):
Notably, when osanetant is dosed from 30 min before auditory FC [fear conditioning] up to 1 hr after training, it does not affect fear acquisition but impairs fear memory consolidation as shown by decreased freezing in the fear expression test. 

Furthermore, mice previously traumatized by 2 hours of immobilization (a rodent model of PTSD-like behaviors that include impaired fear extinction) also showed reductions in fear memory consolidation when given osanetant (IMO-Osa), compared to placebo (IMO-Veh).


Modified from Fig. 4 (Andero et al., 2014). G: Osanetant given immediately after FC impaired fear memory consolidation in mice that had been previously exposed to a traumatic stress as shown by reduced freezing in the fear expression test, ∗p ≤ 0.05. n = 8 per group.


The starting point of this study, however, was not to test the effects of osanetant on the formation of fear memories. Rather, Andero et al. (2014) began by casting a wide net in search of genes that are regulated during fear conditioning. They found that the Tac2 gene (TACR3 gene in humans) is regulated during fear memory consolidation, specifically in the central nucleus of the amygdala (a “fear learning central” of sorts).
Furthermore, increased expression of the Tac2 gene, NkB peptide, and activation of Nk3R may be involved in stress sensitization and overconsolidation of fear. In contrast, genetic silencing of Tac2-expressing neurons impairs fear consolidation. Blockade of this pathway may provide for a novel therapeutic approach for disorders with altered fear learning such as PTSD.

The clinical potential of this finding is not lost on the authors. If given shortly after a traumatic event (e.g., in an emergency room or combat situation), it's possible that osanetant could reduce the emotional potency of trauma memories:
Finally, one of the most interesting aspects of our data is the potential use of the Nk3R antagonist osanetant as a pharmacological agent to block fear memory consolidation shortly after exposure to a trauma. Additionally, we found that osanetant prevented the upregulation of the Adcyap1r1 gene, which encodes the PAC1 receptor. The PACAP-PAC1R pathway is involved in PTSD, fear conditioning, amygdala excitatory neurotransmission, and stress. All this could be relevant in PTSD prevention since it has previously been found that osanetant is safe in humans, although additional preclinical studies, such as those described herein, are needed first to establish the mechanisms involved. This gives our findings an exciting potential approach to translation to human patients.

This study also provides a perfect example of NIMH's new mandate for specifying a hypothesized mechanism of action for interventions that will be tested in funded clinical trials. Does peri-trauma osanetant (vs. placebo) reduce later development of PTSD symptoms and attenuate amygdala activation to trauma script-driven imagery in fMRI? Is TAC3 gene expression altered in primate models? [The distribution of Nk3R likely differs between mice and primates.] Are there declines in PACAP blood levels in traumatized individuals given osanetant (vs. placebo)? Are there longer-term effects on methylation of ADCYAP1R1 in peripheral blood? These latter measures are biomarkers of an abnormal stress response in PTSD that are currently studied by the Ressler Lab.

At any rate, NIMH Director Insel might as well hand over the money right now...


References

Andero, R., Dias, B., & Ressler, K. (2014). A Role for Tac2, NkB, and Nk3 Receptor in Normal and Dysregulated Fear Memory Consolidation Neuron DOI: 10.1016/j.neuron.2014.05.028

Ebner K, Sartori SB, Singewald N. (2009). Tachykinin receptors as therapeutic targets in stress-related disorders. Curr Pharm Des. 15:1647-74.

Maggi CA. (2000). The troubled story of tachykinins and neurokinins. Trends Pharmacol Sci. 21(5):173-5.

Spooren, W., Riemer, C., & Meltzer, H. (2005). NK3 receptor antagonists: the next generation of antipsychotics? Nature Reviews Drug Discovery, 4 (12), 967-975 DOI: 10.1038/nrd1905



Spooren et al. (2005)
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 22 Jun 2014 20:36


A retrospective of an artist's work gives the viewer insight into their creative process over an extended period of time. In some cases, a retrospective seems to allow access into the artist's mind.

Canadian artist and writer Douglas Coupland adopted this stance more literally by creating a room filled with 5,000 objects he collected over 20 years and carefully arranged in a masterwork called The Brain. Coupland is best known (to Americans at least) as the author of Generation X: Tales for an Accelerated Culture, but his prolific artistic output “over the past 12 years addresses the singularity of Canadian culture, the power of language, as well as the ever-pervasive presence of technology in everyday life.”


Douglas Coupland
everywhere is anywhere is anything is everything
May 31 — Sept 1, 2014
#CouplandVan


NOTE: the artist encouraged photography and tagging of his work.
This exhibition brings together works made since the early 2000s as well as major new installations created specifically for this presentation. It sheds light on subjects as varied as the distinct nature of Canadian identity, the rise of utopian ideas, the power of words, the ubiquitous presence of digital technologies, the emerging culture of fear and the unshakeable nature of one’s own constitution—ideas that Coupland examines with both optimism and some trepidation.

The retrospective at the Vancouver Art Gallery is divided into six parts, culminating in The Brain. Its impact as a work of art is more effective in the context of what came before it, including a meditation on the distinctiveness of Canadian Identity. Another section examined youth and the optimism of an earlier era: Growing Up Utopian as depicted in Lego blocks.


100 identical Lego houses


The highlight of Words Into Objects is a room of slogans and aphorisms on colorful posters, reminiscent of Jenny Holzer or Barbara Kruger but with a distinctive focus on the internet and technology.

Douglas Coupland, Slogans for the 21st Century (2011-2014).


Returning to The Brain, the massive collection of objects from thrift stores, garage sales, and eBay appeared mighty close to hoarding, in my view. But where is the border between collecting and hoarding objects (e.g., televisions)? Is there a difference if you're hoarding for artistic purposes?


Materials used in the The Brain, 2000–2014, mixed-media installation with readymade objects [NOTE: prior to arrangement]. Courtesy of the Artist and Daniel Faria Gallery. Photo: Trevor Mills, Vancouver Art Gallery.


These questions were quite salient for me because I attended another exhibition at the same gallery in 2010, called Waste Not (by artist Song Dong). This one examined hoarding overtly in the context of culture, scarcity, and loss:
Waste Not—or wu jin qi gong in Chinese—describes the philosophy of life for a generation of people in China, of which Song Dong’s mother was a part, who grew up during the Cultural Revolution with the experience of displacement, poverty and the constant shortage of goods. The installation stands as a record of his mother’s life, as well as a tribute to his father’s death.

After the artist's father died, his mother's compulsive hoarding intensified, which is not uncommon. Over 10,000 objects were on display. The exhibit was quite moving and sad:
...Carefully sorted, arranged, and displayed in the gallery, along with the wooden frame of one of the rooms of her house, these objects include everything from cracked wash basins, chipped tea cups, old radiators, and burnt-out light bulbs to flattened toothpaste tubes, yellowing newspapers, ripped nylon stockings, and empty containers of every description. And all in startling multiples.

The purpose and impact of The Brain was quite different, however. Much of the collection was whimsical and idiosyncratic, with the metaphorical layout designed to represent the contents and organization of Coupland's physical brain, incomprehensible to all but the artist. Without reading the gallery notes, the viewer struggles to find meaning in the chaos, and would miss out on pieces like the amusing Seat of Consciousness (“the elusive site of self-reflexive awareness that scientists have yet to pinpoint”).


The Seat of Consciousness, part of The Brain (by Douglas Coupland)




Highways and byways of The Brain.


The “corpus callosum” divides the installation into left and right hemispheres, which is clearly an overarching metaphor not intended to be accurate [presumably].1  So we can excuse the artist for placing Language in the Right Brain, because his purpose here isn't a veridical (or even stylized) rendition of the brain destined to win the Brain Art Competition 2014.  It's more like the struggle for an external representation of memories, an exploration of why he is who he is. And for this reason it's deeply personal, and at the same time a reflection of a specific culture and era.




COLOUR MEMORY BANK: “a visual representation of the artist's recollections, attractions, and repulsions.”

This is not a pipe or a road sign in Chinese or a bunch of old cans...

Note the aqua-colored Stroop banana.


WHITE MEMORY BANK: “This white structure, built in a Brutalist style, is an archival collection of white objects, including scale models of seminal 20th and 21st century buildings, as well as numerous corporate mascots painted white.  ...  The fact that the objects are white also tinkers with the brain's need to classify and make sense of structure, the need to interpolate a narrative, not unlike looking for shapes in clouds.”




In total, the effect on the viewer is overwhelming and disorienting, and yet exhilarating (particularly in hindsight).

Objects from Coupland's memory bank here bleed into the signage structures, awaiting information as to where they will be routed. The overall effect is surrealistic and can be interpreted as a snapshot of Coupland's thinking.

Coupland asks, “What is consciousness? Is it a park [sic] that dances through the brain at any given time? A spark that, while it exists, can never be visualized on its own?”

And here he captures the challenge of the “hard problem” of consciousness that has confounded scientists and philosophers alike.


Footnote

1 It's possible that Coupland is left handed and had a Wada test to demonstrate right hemisphere dominance for language, but this is highly unlikely.



Coupland wall

Douglas Coupland, Slogans for the 21st Century (2011-2014) at the Vancouver Art Gallery
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 16 Jun 2014 10:07

Neural prosthetics, brain-computer interfaces (BCI), “closed-loop” deep brain stimulation (DBS) devices, and a world without human brain disorders. The first three of these are already here... is the last one possible?

In the utopian world of The Hedonistic Imperative, an ambitious, admirable (and unlikely) 1995 manifesto by philosopher David Pearce, the goal is to “eradicate suffering in all sentient life” through paradise engineering —  which involves sophisticated applications of nanotechnology, genetic engineering, and psychopharmacology. And going beyond the eradication of suffering, “Life-long happiness of an intensity now physiologically unimaginable can become the heritable norm of mental health.” 1

Lest you think such speculation is limited to those wacky transhumanists, respected neuroscientists Kent Berridge and Morten Kringelbach have written seven reviews on the neuroscience of happiness and pleasure and well-being. In contrast to the vegan and animal rights supporter Pearce, however, Berridge & Kringelbach (e.g., 2012) see animal research as the key to unlocking the brain mechanisms of human pleasures.

Sure, we have BRAIN 2025 and the DARPA deep brain stimulation awards. But we're getting ahead ourselves here, aren't we? Using neuroscience to alleviate human suffering takes precedence over the attainment of  “a sublime and all-pervasive happiness” in wealthy Western post-industrial societies (doesn't it)? Doesn't it??


Neurofutures that aren't mine

There used to be a blog called Neurofuture (“Brain Science and Neofuturism”), written by Sandra K. It covered topics like HedWeb and neuroscience nanotechnology and NeuroArm and the Blue Brain Project back in 2006-2007.

Since February 2012, there's been an unrelated NeuroFuture twitter feed @NeuroFutureNews (“Mind-blowing tweets! Follow me if you are interested in brain, bionics, BCI, robotics and mind-controlled news”). A guy named wolfgang berke has had the @neurofuture account since March 2010, but he hasn't tweeted once.


And now, there's NeuroFutures 2014, a conference in Seattle starting tomorrow:

NeuroFutures Conference: June 17 - 18, 2014

Thought leaders in research, engineering, industry, and clinical domains will explore how the intersection of neurotechnology innovations in neuromodulation, brain mapping, neuroimaging, big data analytics, and brain computer interfaces will transform our understanding of neural systems and enable life-changing medical treatments.

If you're already in Seattle, you can attend a public lecture by a prominent DBS neurosurgeon today at 7 PM:

NeuroFutures Public Lecture: 7:00 PM, June 16

Dr. Andres Lozano from the University of Toronto will kick off the NeuroFutures summit with a talk on “The Future of Brain Stimulation: Parkinson’s, Depression, Alzheimer’s and beyond" (see his related TED Talk here). Afterwards, he will discuss his work with science educator and author David Heil, and field questions from the audience.

Organizational and industry sponsors include Center for Sensorimotor Neural Engineering, Allen Institute for Brain Science, Cyberonics, and Neurotech Business Report,3 among others.

Why NeuroFutures?

Problem: One in four U.S. adults suffer from a diagnosable neurological disorder and a quarter of these are seriously disabled as a result. These patients endure immense physical and emotional suffering, and their family members and caregivers bear a heavy emotional and financial burden. From a scientific standpoint, the human brain is the most sophisticated computing system in the known universe, and we are only starting to understand how it works.
. . .

Plan: To accelerate the pace and impact of innovation we will bring together neurotechnology thought leaders from different disciplines to exchange ideas and forge collaborations at the two-day NeuroFutures Conference on June 17 and 18, 2014 in Seattle, Washington. We will highlight people and resources in the Northwest that position the region to play a leading role in our NeuroFuture...


So what will it be... better living through chemistry (pharmaceuticals), biotechnology, or engineering? With conference sessions on BCI and Neuromodulation Innovations, Learning, Plasticity, and Adaptation in Neural Interfaces, and The Past, Present, and Future of Closed-loop Neuromodulation, one might think it's a great time to be a Neuroengineer at places like the Center for Sensorimotor Neural Engineering, the Brain-Machine Interface Systems Laboratory, and the Neural Prosthetic Systems Laboratory.


Footnotes

1 The HedWeb manifesto has been online in its entirety since 1995, I believe. For many years, the labyrinth of links and early-acquisition domain names such as biopsychiatry.com, huxley.net, mdma.net, opioids.com, cannabis.net, and general-anaesthesia.com were entirely unattributed, except for affiliation with an organization known as BLTC RESEARCH. But be careful, or you could fall down the rabbit hole of supercentenarian.com or reproductive-revolution.com or oxytocin.org or sensualism.com or nootropics.com or.....2

2 OMFG! There are 2,244 PARADISE-ENGINEERING BLTC WEBSITES as of JUNE 2014:
Paradise-engineering websites (2014)
Good domains for a better world?

3 Neurotech Business Report was the first to break the news about the failed BROADEN clinical trial for treatment-resistant depression, and they've continued their close coverage of the neuromodulation market.


top image via Alternative Media News



Figure 1. Pleasure Cycles (Berridge & Kringelbach, 2012), from Building a neuroscience of pleasure and well-being.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 08 Jun 2014 21:48


...UCSF and MGH!

Work on DARPA’s Systems-Based Neurotechnology for Emerging Therapies (SUBNETS) program is set to begin with teams led by UC San Francisco (UCSF), and Massachusetts General Hospital (MGH). The SUBNETS program seeks to reduce the severity of neuropsychological illness in service members and veterans by developing closed-loop therapies that incorporate recording and analysis of brain activity with near-real-time neural stimulation. The program, which will use next-generation devices inspired by current Deep Brain Stimulation (DBS) technology, was launched in support of President Obama’s brain initiative.

UCSF and MGH will oversee teams of physicians, engineers, and neuroscientists who are working together to develop advanced brain interfaces, computational models of neural activity, and clinical therapies for treating networks of the brain. The teams will collaborate with commercial industry and government, including researchers from Lawrence Livermore National Laboratory and Medtronic, to apply a broad range of perspectives to the technological challenges involved. 

Our Tale of Two BRAINS (#BRAINI and DARPA's SUBNETS) continues...

Image: DARPA
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 08 Jun 2014 16:57

“We believe this to be a moment in the science of the brain where our knowledge base, our new technical capabilities, and our dedicated and coordinated efforts can generate great leaps forward in just a few years or decades. Like other great leaps in the history of science—the development of atomic and nuclear physics, the unraveling of the genetic code—this one will change human society forever. Through deepened knowledge of how our brains actually work, we will understand ourselves differently, treat disease more incisively, educate our children more effectively, practice law and governance with greater insight, and develop more understanding of others whose brains have been molded in different circumstances.”

- BRAIN 2025: A Scientific Vision

That modest quote jumped out from the Preamble to the BRAIN Working Group Report to the Advisory Committee of the NIH Director.  A decade-long $4.5 billion project that focuses on technology development and neural circuits in model systems will change government, society, and human interactions forever.

It's a manifesto, so why not aim big?

There's no doubt about it, systems neuroscience takes the BRAIN prize:
The Roads Not Taken

In any project, decisions must be made about where to focus. Neuroscience addresses brain function from the level of molecules to the level of psychology, and at many levels in between. This plan for the BRAIN Initiative proposes a concerted attack on brain activity at the level of circuits and systems, rather than suggesting incremental advances in every area. All areas of neuroscience are important, however, and the BRAIN Initiative should therefore supplement, not replace, existing efforts in basic, translational, and clinical neuroscience.

The report is 146 pages long. More to follow...
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 01 Jun 2014 11:36

I went on this trip once, back to my hometown after a long absence. Have you ever felt that your surroundings seem odd and distant, and that you're completely detached from them? That the things and places around you aren't real? This can happen to me, on occasion.

It did on this trip, perhaps because I've dreamed about those places so many times that the real places and the dream places are blurred in memory.




Of course time marches on. The stores in the strip mall have changed, and you go to Starbucks with your father. But sometimes new and surprising things appear in the landscape.




Or maybe old and unexpected things pop up in the background, renewing a long-standing confusion between rural and suburban.




These nostalgic travel vignettes illustrate the phenomenon of derealization, a subjective alteration in one's perception or experience of the outside world. The pervasive unreality of the external environment is a key feature, along with emotional blunting. The world loses its vividness, coloring, and tone. Some even report seeing things as if they're looking through a fog or a haze. Or a pane of blurry glass.




Derealization is often (but not always) associated with depersonalization, a feeling of detachment from oneself, as if you yourself are unreal or even outside your body. Both of these phenomena can be mild and transient, or the symptoms can be chronic and disturbing in Depersonalization Disorder, which is considered a dissociative disorder.

Not surprisingly, these dissociative states can be induced by drugs such as ketamine (a dissociative anesthetic) and hallucinogens (e.g., LSD, psilocybin). The symptoms can also be induced by stress and anxiety, or by trauma, or by sleep deprivation. Not all instances of derealization and depersonalization qualify as a disorder, however.

The DSM-5 diagnostic criteria for Depersonalization/Derealization Disorder are as follows:
A. An individual consistently has a feeling of both or either depersonalization or derealization.
  1. Depersonalization: Experiences of unreality, detachment, or being an outside observer with respect to one's thoughts, feelings, sensations, body, or actions (e.g.,perceptual alterations, distorted sense of time, unreal or absent self, emotional and/or physical numbing.)"
  2. Derealization: "Experiences of unreality or detachment with respect to surroundings (e.g., individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, or visually distorted."
B. "During the depersonalization or derealization experiences, reality testing remains intact."
C. "The disturbance is not attributable to the physiological effects of a substance (e.g., a drug of abuse, medication or other medical condition (e.g., seizures)."
D. "The disturbance is not better explained by another mental disorder."

What other mental disorders can manifest as derealization (included as one of a core set of symptoms)? Among the most curious of these is an unusual neurological disorder called Kleine-Levin syndrome (KLS).


Kleine-Levin Syndrome

Imagine sleeping 20 hours a days for days end, with your limited waking hours spent confused, disoriented, cognitively impaired, and voraciously hungry. Sometimes referred to as “Sleeping Beauty” syndrome in the media, KLS is a very rare sleep disorder (1-2 cases per million) characterized by intermittent bouts of hypersomnia (Arnulf et al., 2012). Other symptoms can include hyperphagia (compulsive overeating), hypersexuality, apathy, behavioral disturbances, depression, delusions, and derealization.1

Considered a relapsing/remitting disease that typically onsets during adolescence, there is no known cause, no objective laboratory findings, and no cure. In the review by Arnulf et al. (2012), episodes lasted 10-12 days on average, followed by almost 6 months of normal sleep, cognition, and behavior. The disease can resolve spontaneously once the patient reaches their 30s. Those with childhood or adult onset can show a different disease course.

The review suggested that confusion, apathy, and/or derealization are the best diagnostic indicators, when coupled with recurrent hypersomnia.


The Phenomenology of Derealization in KLS

Since derealization is such a prominent symptom of KLS, Arnulf et al. (2012) provided examples reported by patients during Kleine-Levin episodes:
  • Patients feel as though they are in a dream or a bubble
  • They claim sight, sound, smell, taste, and perception of cold, hot, and pain feel wrong
  • The environment feels flat and two-dimensional
  • In the shower, patients might see the water flowing on their bodies, but not feel its temperature
  • Patients who injure themselves might not understand when or how the injury happened or that it has happened at all
  • Actions do not have consequences
  • Patients might do something to test for a normal action, such as breaking an object (eg, a cup)
  • Patients might ask whether they are dead or alive

Are there any changes in brain activity during symptomatic periods in KLS? A Paris-based research group led by Dr. Isabelle Arnulf recently reported on a functional imaging study in 41 asymptomatic patients (Kas et al., 2014), 11 of whom were also scanned during an episode. The authors used SPECT (single photon emission computed tomography) to measure blood perfusion in the brain. SPECT is a relatively inexpensive cousin of PET scanning, albeit with lower spatial resolution. Although there is a place for SPECT in nuclear medicine, it is not accepted as a method to diagnose psychiatric disorders, and Kas et al. did not treat it as such.

I found it remarkable that 11 patients were scanned during an episode, a phenomenal number considering the rarity of the disease and the nature of the presenting symptoms. In fact, two additional patients could not be scanned because they were so agitated and delusional. The patients completed questionnaires related to KLS symptoms, sleep disturbances, apathy, depression, and the Depersonalization/ Derealization Inventory (Cox and Swinson, 2002).

One major finding was reduced perfusion in the general region of the temporal-parietal junction (TPJ), which was associated with more severe symptoms of derealization. The TPJ has been related to multimodal sensory integration the integration of information from the somatosensory system (body knowledge) and the external world (visual, auditory) among other things (like theory of mind, attention, and language). Damage or dysfunction of the TPJ can result in out-of-body experiences (Blanke & Arzy, 2005).



Modified from Fig. 6 (Kas et al., 2014). Correlation between middle temporal perfusion and Derealization/Depersonalization Inventory scores during symptomatic periods. Plots show normalized brain perfusion values in (A) left TPJ region (x = 46, y = 66, z = 11, filled circles) and (B) right TPJ region (x = 38, y = 55, z = 25, open circles).


Changes in perfusion between episodes were also observed (relative to controls). KLS patients showed hypoperfusion in the hypothalamus, thalamus, caudate nucleus, and some cortical association areas that persisted during asymptomatic periods.

Although we must issue the appropriate caveats (small patient group, imprecise localization, limitations of the methodology etc.), the current results are suggestive of a neurological correlate of derealization. I'll keep this in mind the next time I visit my hometown after a long absence...


Footnote

1 The KLS Foundation describes the following symptoms (for informational purposes only):
KLS patients would have symptom A, one or more of the B symptoms, and the pattern described in C.
A. Recurrent episodes of severe hypersomnia (2-31 days)
B. Plus one or more of the associated features:
  1. Cognitive abnormalities such as feeling of unreality, confusion, hallucinations.
  2. Abnormal behavior such as irritability, aggression, odd behavior
  3. Binge eating
  4. Hyper-sexuality
C. Interspersed with long periods of normal sleep, cognition, behavior, mood

References

Arnulf, I., Rico, T., & Mignot, E. (2012). Diagnosis, disease course, and management of patients with Kleine-Levin syndrome. The Lancet Neurology, 11 (10), 918-928 DOI: 10.1016/S1474-4422(12)70187-4

Blanke O, Arzy S. (2005). The out-of-body experience: disturbed self-processing at thetemporo-parietal junction. Neuroscientist 11:16-24.

Kas, A., Lavault, S., Habert, M., & Arnulf, I. (2014). Feeling unreal: a functional imaging study in patients with Kleine-Levin syndrome. Brain DOI: 10.1093/brain/awu112




A few years ago I went on a trip back to my hometown after a long absence....

All images by the author, unless otherwise stated (CC BY-NC-ND 3.0).
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 26 May 2014 20:27

Modified from Fig. 2 (Ponseti et al., 2014). Brain areas that selectively respond to faces of the sexually preferred age.


Just when we thought it was safe to bury the dead salmon of uncorrected statistical thresholds in neuroimaging studies, a new and incendiary study on face processing in pedophiles emerges (Ponseti et al., 2014). Even if it were surprising and informative that “Human face processing is tuned to sexual age preferences” (Ponseti et al., 2014), the fMRI data analyses failed to correct for multiple statistical comparisons, which is standard in the field. Therefore, by using a very liberal statistical threshold of p < 0.01 uncorrected for the large number of tests, the results could be a series of untrustworthy false positives.1

Importantly, the basic pattern of findings, that visual parts of the brain are more responsive to pictures of faces that fall within the broad category of “sexual attractiveness”, does not tell us why someone has a particular sexual orientation, nor does it tell us if this preference is “hard wired” (i.e., innate).

The participants in the study were 56 men, 11 of whom were heterosexual pedophiles (prefer young girls), 13 homosexual pedophiles (prefer young boys), 18 heterosexual teleiophiles (prefer adult women) and 14 homosexual teleiophiles (prefer adult men). These are small groups, but to complicate matters, half of the pedophiles had committed sexual offenses and the other half had not. This is a critical difference, as one might expect differences between men who could refrain from acting on their impulses and those who could not. Yet, activation in the dorsal striatum was interpreted as a potential indicator of “efforts in withholding actions”.

Furthermore, the results presented here were part of a larger study that aimed to classify pedophiles solely on the basis of their brain responses to nude photos showing whole-body frontal views or genitals only (Ponseti et al., 2012). The authors claimed an astounding 95% accuracy in distinguishing between pedophiles and non-pedophiles.2

Overall, the participants viewed 14 different categories of visual stimuli in these two papers, so you can see that the number of potential statistical comparisons is astronomical.

The take-home message is that the participants' subjective attractiveness ratings of each face (completed after the fMRI study) were much more reliable at identifying their sexual preferences (p < 0.001) than the brain imaging data. Neuroscientists working with such controversial populations need to be especially careful in analyzing their data, and aware of how their work may be used in a broader social context.


Footnotes

1 Thanks to commenter Com__Truise on reddit who alerted me to this paper and who noted:
Published cognitive Neuroscientist here. This should not have gotten through peer review. The fMRI analysis is invalid. The study uses an uncorrected threshold (not corrected for multiple comparisons) of p< 0.01 (considered very liberal!) and all the results are probably false positives. This is not to say that the theory is not correct - however, the statistics are invalid and meaningless. You can read more here: http://neurocritic.blogspot.de/2012/03/how-much-of-neuroimaging-literature.html http://www.danielbor.com/dilemma-weak-neuroimaging/

Here is another cautionary note from Professor James Ogloff, Director of the Centre for Forensic Behavioural Science and Legal Studies at Swinburne University of Technology, Victoria.

2 Critical and ethical evaluation of this study is beyond the scope of the present post.


References

Ponseti J, Granert O, Jansen O, Wolff S, Beier K, Neutze J, Deuschl G, Mehdorn H, Siebner H, Bosinski H. (2012). Assessment of pedophilia using hemodynamic brainresponse to sexual stimuli. Arch Gen Psychiatry 69(2):187-94.

Ponseti, J., Granert, O., van Eimeren, T., Jansen, O., Wolff, S., Beier, K., Deuschl, G., Bosinski, H., & Siebner, H. (2014). Human face processing is tuned to sexual age preferences Biology Letters, 10 (5), 20140200-20140200 DOI: 10.1098/rsbl.2014.0200
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 19 May 2014 02:18
Dream scene from Inception


DIY brain stimulation geeks were supercharged last week by the finding that dream awareness could be enhanced by transcranial alternating current stimulation (tACS)1 at frequencies of 25 and 40 Hz (Voss et al., 2014). Headlines were abuzz with zingers like Brain Zaps Can Trigger Lucid Dreams and A Jolt to the Brain Triggers Lucid Dreams and Brain Zap Could Help You Control Your Dreams. Visualize all the incipient Kickstarter campaigns ready to capitalize on the lucid dreaming market...

Except did the stimulation really induce lucid dreaming? The only critical evaluation of this claim (that I'm aware of) came from Christian Jarrett in his post, Psychologists Give People Control of Their Dreams Using Brain Stimulation. Really? He closely examined the Lucidity and Consciousness in Dreams scale (LuCiD) used by the experimenters (Voss et al., 2013) and saw that the participants' self-ratings weren't actually indicative of lucid dreaming.

Although the scores on some LuCiD factors were indeed significantly higher after frontal stimulation at 25 Hz (beta, actually) and/or 40 Hz (gamma) frequencies (relative to sham or other frequencies), this did not mean the dreams were technically “lucid”.


Fig. 3 (Voss et al., 2014). Mean scores for three LuCiD factors [NOTE: each self-rating scale goes from 0: strongly disagree to 5: strongly agree].


The LuCiD scale consists of 28 statements, each followed by a 6-point rating scale (0: strongly disagree, 5: strongly agree). Insight is the awareness that one is currently dreaming, Dissociation is taking a third-person perspective, and Control is control over the dream plot.

Of the eight LuCiD factors, Insight is the single most important criterion for lucid dreaming (Voss et al., 2013).  However, the mean Insight score in the current study is well below that reported for lucid dreams in the earlier study used to construct the scale.


modified from Fig. 5 (Voss et al., 2013). Mean scores for LuCiD scales for non-lucid vs. lucid dream reports [NOTE: each scale goes from 0: strongly disagree to 5: strongly agree. The yellow bars indicate means after 25 or 40 Hz tACS in Voss et al. 2014].


In other words, the 25 Hz and 40 Hz brain stimulation significantly increased Insight and Control, but not to the levels reported in lucid dreams (according the authors' previous definition). The definition in the present study was less stringent: “Lucidity was assumed when subjects reported elevated ratings (>mean + 2 s.e.) on either or both of the LuCiD scale factors insight and dissociation.”

Nonetheless, induced gamma band oscillations did result in a heightened perception of self-awareness during REM sleep, in particular the ability to view the ongoing dream activities as a detached observer. But don't waste your money investing in the latest neurocrap that claims to induce lucid dreaming... As Seen On Nature Neuroscience.


Further Reading

Psychologists Give People Control of Their Dreams Using Brain Stimulation. Really?

Neurocrap Funded by the Masses: NeuroOn and No More Woof


Footnote

1 Note that tACS is different from the usual DIY tDCS (transcranial direct current stimulation). tACS is thought to modulate and entrain brain oscillations in a frequency-specific manner, although others are much more cautious in their interpretation.


References

Voss, U., Holzmann, R., Hobson, A., Paulus, W., Koppehele-Gossel, J., Klimke, A., & Nitsche, M. (2014). Induction of self awareness in dreams through frontal low current stimulation of gamma activity. Nature Neuroscience DOI: 10.1038/nn.3719

Voss, U., Schermelleh-Engel, K., Windt, J., Frenzel, C., & Hobson, A. (2013). Measuring consciousness in dreams: The lucidity and consciousness in dreams scale. Consciousness and Cognition, 22 (1), 8-21 DOI: 10.1016/j.concog.2012.11.001



“Shared Dreaming” scene from Inception
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Sunday, 18 May 2014 03:19


Neuroscience Information May Provide an Illusion of Explanatory Depth

In our continuing twilight saga on the seductive allure of all things neuroscientific comes this new entry by Rhodes et al. (2014). The paper isn't available yet so the abstract will have to do for now:

Rhodes RE, Rodriguez F, Shah P. Explaining the alluring influence of neuroscience information on scientific reasoning. J Exp Psychol Learn Mem Cogn. 2014 May 12. [Epub ahead of print]. PMID: 24820673

Abstract

Previous studies have investigated the influence of neuroscience information or images on ratings of scientific evidence quality but have yielded mixed results. We examined the influence of neuroscience information on evaluations of flawed scientific studies after taking into account individual differences in scientific reasoning skills, thinking dispositions, and prior beliefs about a claim. We found that neuroscience information, even though irrelevant, made people believe they had a better understanding of the mechanism underlying a behavioral phenomenon. Neuroscience information had a smaller effect on ratings of article quality and scientist quality. Our study suggests that neuroscience information may provide an illusion of explanatory depth. (PsycINFO Database Record (c) 2014 APA, all rights reserved).

Do colorful brain images and neuroscientific information hold powerful sway over the unsuspecting reader's logic, leading them to overlook shoddy science coverage? From what I can gather, the seductive allure of neuroimages has not replicated (Farah & Hook, 2013; Michael et al., 2013; Schweitzer et al., 2013), but the appeal of neuroscience information (à la Weisberg et al., 2008) has yet to lose all its luster.1



Credit for the "smouldering glance" terminology goes to Vaughan Bell.


Footnote

1 This is debatable, however:
Farah and Hook also debunked the study of Weisberg et al., (2008), which didn't use images at all but added neuroscience-y explanations to 18 actual psychological phenomenon. The problem was that the neuroscience-y paragraphs were longer than the no-neuroscience paragraphs. The author of the excellent but now-defunct Brain In A Vat blog had a similar objection, as explained in I Was a Subject in Deena Weisberg's Study...

Neuroskeptic also raised this point in his otherwise [mostly] positive evaluation of the study, Critiquing a Classic: "The Seductive Allure of Neuroscience Explanations"...



Photo Credits:
Kristen Stewart by Inez & Vinoodh for V Magazine (Spring Preview 2013)
Ian Somerhalder by Angelo Kritikos



fyeahbiancadelrio

ADDENDUM May 20 2014: Bianca del Rio is 
America's Next Drag Superstar!
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 12 May 2014 04:42
Spintronics™ Neuroimaging mock scanner used in experiment by Ali, Lifshitz & Raz (2014)


A new study has tricked undergraduates into believing that “Spintronics,” a whimsical new “mind reading” technology constructed using an old hair dryer, was able to accurately read their thoughts  (Ali et al., 2014). This held even for students enrolled in a class on the pros and cons of neuroimaging methods taught by the senior author (McGill Professor Amir Raz). The paper coined the phrase “empirical neuroenchantment” to explain why a highly dubious experimental setup would lead to such a deficit in critical thinking.

The participants were 58 McGill students, 26 of whom were upper-level psychology, neuroscience or cognitive science majors enrolled in a skeptical neuroimaging course that warned them about overblown claims. Furthermore, the professor had lectured about his experience as a “mind reading” magician who fools audiences into believing he has paranormal abilities:
The professor in the course (AR) repeatedly harped on the present impossibility of mind-reading and tested this information on the final examination verifying that students internalized these points. He also spoke about his background as a mentalist – a magician who performs psychological tricks, such as mind-reading – and led class demonstrations to exemplify why the public often misinterprets these effects and takes them for genuine paranormal powers.

And in fact, sleight of hand was used to further the ruse that the hair dryer contraption was able to read their minds. Subjects were told they were participating in a study on “The Neural Correlates of Thought” (amusingly described in the Methods) where they...
...encountered a rickety mock brain scanner built from discarded medical scraps from the 1960s and adorned with an old-fashioned hair-dryer dome [shown in the figure above]. We told participants that scientists at the Montreal Neurological Institute had developed new experimental technology to decode resting state brain activity and read the human mind. We labeled the technology Spintronics and displayed warning signs around the scanning equipment similar to those found in MRI environments.

The participants were told to think of a two-digit number, a three-digit number, a color, and a country and to write down their answers on a piece of paper. The first author cleverly pocketed their answers,1 then participants were told to think about their choices while their brains were faux scanned. During this time, “a pre-recorded video displayed rotating three-dimensional brain slices with accompanying scanner-like audio, lending the appearance of collecting and analyzing patterns of brain activity.”

Afterwards, the subjects were shown the results of the scan. Lo and behold, the machine could read their minds! A brief questionnaire rated their level of belief on a 0 to 6 point scale (from “not at all” to “extremely”).

How did the informed students fare against the non-Neuro controls? The Neuro students found the results significantly less believable (3.96 vs. 4.96), and they rated themselves as more skeptical (3.42 vs, 1.94) than the controls. However, they were not immune to ascribing even greater mind-reading capabilities to Spintronics© after being shown that the contraption successfully “read” their thoughts.

Can we conclude from the present study that neuroimaging is special in the annals of scientific technology in its ability to dupe even those who should know better? No, and the authors acknowledge as much. We don't know whether the dual phenomena of deferring to experts in a professional laboratory, and overriding scientific knowledge on the basis of one compelling experience, would occur in other fields of study. We could potentially see meteoroenchantment or roboenchantment in the realms of weather prediction and artificial intelligence, respectively.

Nonetheless, the Spintronics study ups the ante in the Brainwashed sweepstakes on The Seductive Appeal of Mindless Neuroscience, which maintains that the media can easily dupe an unsuspecting public into believing nearly anything couched in the guise of neuroscience.


The Seductive Allure of Neuroscience Explanations




Remember the “seductive allure” of colorful brain images? This was the idea that college undergraduates could be swayed to believe implausible explanations for psychological phenomena if accompanied by brain images (McCabe & Castell, 2008). For example, a fictitious news article explaining that ‘Watching TV is Related to Math Ability’ since watching television and completing math problems both lead to activation in the temporal lobe, watching TV will of course improve math skills was more believable when accompanied by a brain scan than by a bar graph.


The Not So Seductive Allure of Colorful Brain Images



However, this finding was not replicated in more recent studies (Farah & Hook, 2013; Michael et al., 2013; Schweitzer et al., 2013). Is this because participants in psychology experiments have gotten more sophisticated in the past five years? 2  Or is it because the results weren't that strong to begin with?

It'll be much more difficult for other labs to replicate the present results of Ali and colleagues (2014), namely because (1) most Principal Investigators aren't magicians, and (2) recruiting 1,068 participants via the online marketplace Mechanical Turk just won't work here...


Further Reading

Are Brain Scans Really So Persuasive?

The Not So Seductive Allure of Colorful Brain Images


Footnotes

1 I should add here that the first author, Sabrina Ali, was an undergraduate researcher at the time, and thus the participants may have had fewer suspicions that she would try to dupe them (as opposed to the magician, Dr. Raz). The present experiment was a portion of Ali's Master's Thesis at McGill.

2 More sophisticated, say, from reading critical neuroscience blogs?  Or much more likely, reading critical coverage in places like the New York Times?  Or am I living in a bubble which assumes way too much public interest in these topics?


References

Sabrina Ali, Michael Lifshitz, and Amir Raz (2014). Empirical Neuroenchantment: From Reading Minds to Thinking Critically. Frontiers in Human Neuroscience doi: 10.3389/fnhum.2014.00357

Farah MJ, Hook CJ (2013). The seductive allure of "seductive allure". Perspectives in Psychological Science 8:88-90.

McCabe DP, Castel AD. (2008). Seeing is believing: the effect of brain images on judgments of scientific reasoning. Cognition 107:343-52.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 05 May 2014 03:11


We now have definitive proof that the propensity of womankind to postpone sex due to a headache is of evolutionary origin! This annoying habit has been traced back directly to a strain of ovariectomized CD-1® IGS mice supplied by Charles River.

In a naturalistic design that precisely mimics the mating habits of humans, sexual receptivity was induced in the female mice with subcutaneous injections of estradiol. Then the female mice and their preferred male partners were injected in various body parts with two different compounds to induce inflammatory pain. Lo and behold, the mounting behaviors of male mice were hardly deterred by these painful treatments, but the females declined sexual congress and hid from the males.

“These findings suggest that the well known context sensitivity of the human female libido can be explained by evolutionary rather than sociocultural factors, as female mice can be similarly affected,” concluded the authors (Farmer et al., 2014).


Of Mice and Women

This study was published in the Journal of Neuroscience, and the strongly worded quote above is how the authors chose to conclude their abstract. They go to great lengths to “prove” that the loss of libido was due to lack of sexual motivation in the female mice, rather than a direct consequence of pain. The authors also stretch the clinical applicability (and evolutionary validity) of their work a bit beyond belief, in my view. Why? Perhaps because promoting a viable animal model of low sexual motivation in women will ultimately serve drug development purposes (Farmer et al., 2014):
The link between pain and sexual motivation is evident in human sexual relations. The widespread aphorism, “Not tonight, dear, I have a headache” refers to a lack of sexual motivation due to pain. No clinical data exist on the direct impact of pain on sexual motivation, yet high prevalence of reduced sexual desire in chronic pain populations (Basson et al., 2010; Fine, 2011) suggest that pain may adversely influence sexual motivation.

It's not exactly true that “No clinical data exist on the direct impact of pain on sexual motivation...” (as we'll see later), but first let's take a look at the actual study.1

Pairs of vigorously mating mice were assigned to either male “open field” or female “paced mating” situations, which mimics their respective natural preferences. One member of each pair was injected with a pain-inducing inflammatory compound (zymosan A or λ-carrageenan) into their genital or nongenital (hind paw, tail, cheek) regions. Sexual behavior was measured by mounting in open field (for males) or in paced mating (for females) conditions. In the latter situation, the smaller females could run into their safe room to avoid the males. 

The results generally indicated that the females hid from the males when injected with painful substances (Fig. 1A), but the males were not bothered (based on the total number of mounts) with the exception of a non-significant decline when the penis was injected with zymosan (Fig. 1C).



Fig. 1 (modified from Farmer et al., 2014). Reduction of sexual behavior in female but not male mice by inflammatory pain. A. Decreased mounting behavior in a paced mating paradigm when female mice receive zymosan (ZYM) or carrageenan (CARR) injections to the vulva, hind paw, tail, or cheek, compared with uninjected female mice (No Inj.). Bars represent mean ± SEM mounts with (shaded) or without (open) intromissions. C. No decreases in mounting behavior in an open field when male mice are treated in a similar fashion. *p < 0.05, **p < 0.01 compared with vehicle [NOTE: using uncorrected t-tests].


[As an aside, one could imagine that the mating behavior of human males might be more greatly affected by penile injections of any sort, and by inflammogen injections into the hand or cheek than what we're seeing here in the male mice.]

In addition to mounts, Table 1 in Farmer et al. lists 8 other behaviors × 2 treatments. Of these 16 comparisons to the vehicle control, five indicated reductions and one indicated an increase in activity of some sort, meaning that certain behaviors (number of ejaculations, latency to first mount, number of crossings to the male side, latency to return to the male side) were unaffected by one or both treatments [NOTE: using Dunnett's post-hoc comparisons that do correct for multiple comparisons]. Make of that what you will.

However, the pained females did indeed spend significantly less time in their male partner's side of the apparatus.

Next, some of the pained female mice were given pregabalin (Lyrica), an anticonvulsant drug used to treat neuropathic pain (kindly provided by one of the study sponsors, Pfizer). You'll be comforted to hear that analgesic administration and concomitant pain relief will lead to increased sexual activity in injured female mice (and probably in injured creatures of any sort).

On the other hand, administration of the non-selective dopamine agonist apomorphine, which is “pro-sexual” in mice but strongly emetic in humans, is unlikely to be welcomed by women as an antidote to a pain-quashed libido. Apomorphine (not related to morphine) is sometimes given to Parkinson's patients, but always in conjunction with other drugs to prevent vomiting. In fact, apomorphine is so unpleasant to humans that it has been used for aversion therapy in gay people (an “anti-sexual” agent if there ever was one).

Anyway, it was interesting to learn that rodents do not vomit, and that apomorphine reverses the pain-induced reduction in sexual behavior exhibited by female mice. This was interpreted to mean that sexual motivation was enhanced. But since apomorphine also increases locomotion in rodents, I wonder if other appetitive behaviors were enhanced as well.

The other pro-sexual drug used in the current study was melanotan-II, which is converted to the melanocortin-3/melanocortin-4 receptor agonist, bremelanotide (formerly known as PT-141, developed by Palatin Technologies). Intranasal bremelanotide underwent clinical testing to treat sexual dysfunction in humans (male and female), but trials were halted in 2008 because of untoward elevations of blood pressure in some individuals.

When given to injured female mice, melanotan-II reversed the reduction in sexual behavior. Unlike apomorphine, however, melanotan-II: (1) does not increase locomotion, and (2) is undergoing further testing in humans via a subcutaneous route of administration that doesn't increase blood pressure. Moreover, the authors are highly aware of their potential animal model:
Thus, the reversal of pain-induced reductions in female-paced sexual behavior likely reflects an enhanced incentive value of the paced mating context, indicating that motivational mechanisms can overcome the effects of pain. We suggest that restoration of pain-induced loss of libido may provide a more sensitive test of prosexual drugs than current paradigms. 2

According to the highly reputable Men's Journal, a co-author on the current paper, Dr. Jim Pfaus, is “arguably the world's preeminent expert on bremelanotide.” The 2009 magazine article states:
...Originally developed as a self-tanning agent, the drug had been repurposed when male study subjects reported a surprising side effect: erections.   ...

Pfaus showed me stunning testimonials from human test subjects. "On the five-point scale, I would rate the erection I had as a six," said one of the 1,300 anonymous testers. "You get this humming feeling," said another. "You're ready to take your pants off and go."

The drug worked equally well on women, who chronicled "an intense arousal" that lasted from six to 72 hours. "I was focused on sex," said one of the women.

However, the pesky side effects of increased blood pressure (in some men) and nausea (in one third of the women) were still an issue. That didn't stop the black market bremelanotide distributors.
But was it safe? "Well," says Pfaus, "we never resolved that blood pressure thing. There's no guarantee of purity. The FDA won't regulate it."

Five years later, Palatin has its subcutaneous version of bremelanotide in Phase 2B clinical trials for Hypoactive Sexual Desire Disorder (poster PDF) and other Female Sexual Dysfunctions (poster PDF). HSDD is a controversial diagnosis, discussion of which is beyond the scope of this post. 3

The media furor over the “not tonight, dear, I have a headache” evolutionary interpretation of sexual behavior in mice has completely overshadowed the potential drug marketing angle.


The Media Frenzy

Pain can kill ‘women’s sex drive’ but not men’s screams one headline. Not tonight dear, I have a headache: science behind the excuse: “Chronic pain diminishes a woman's sexual desire but has no impact on a man's, according to a study published in the journal of Neuroscience,” claims The Telegraph. 4

Quite obviously, no humans were tested by Farmer et al., 2014 and yet even the McGill press release plays up that angle, assisted by helpful quotes from the senior author:
“Not tonight, dear, I have a headache.” Generally speaking, that line is attributed to the wife in a couple, implying that women’s sexual desire is more affected by pain than men’s.

Now, researchers from McGill University and Concordia University in Montreal have investigated, possibly for the first time in any species, the direct impact of pain on sexual behaviour in mice.  ...

“We know from other studies that women’s sexual desire is far more dependent on context than men’s – but whether this is due to biological or social/cultural factors, such as upbringing and media influence, isn’t known,” says Jeffrey Mogil, a psychology professor at McGill and corresponding author of the new study. “Our finding that female mice, too, show pain-inhibited sexual desire suggests there may be an evolutionary biology explanation for these effects in humans – and not simply a sociocultural one.”

I've written at length about whether animal models of sexual problems are appropriate stand-ins for the human condition:
Which brings us to animal models for what we typically regard as profoundly human states: longing, angst, futility.  Or Desire, Dread, and Despair. The words don't easily lend themselves to rodent analogues, because they remind us of an unrequited crush or an existential crisis...

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

Does the model of pain-induced reduction of sexual behavior in female mice hold up in humans? The claim is that a lack of sexual motivation (or libido, if you will) is the inhibiting factor, rather than the pain itself.


Real Pain in Real Humans

How does chronic pain affect human sexual behavior? Is there a pronounced difference between men and women in terms of responsiveness? Is it true that this topic has never been studied?

One survey of 327 chronic pain patients (Ambler et al., 2001) found few differences between men and women:
Seventy-three percent of respondents had pain-related difficulty with sexual activity; most had several, in various combinations of problems with arousal, position, exacerbating pain, low confidence, performance worries, and relationship problems. ... There were few differences between men and women, and only weak relations emerged between specific problems and mood and disability.

Furthermore, it wasn't easy to attribute the problems to reduced libido or to physical limitations, as there wasn't a simple relationship between primarily physical and primarily psychological issues and overall physical, psychological, and emotional health.

Several other studies have examined sexual function specifically in patients with arthritis, a chronic pain condition. van Berlo et al. (2006) analyzed surveys from 271 patients with rheumatoid arthritis and found that men felt less sexual desire, while women masturbated and fantasized less often than controls. However, the patients did not report a difference in sexual satisfaction (although we don't know about the 77% who did not return the questionnaire).

An earlier study examined the effects of osteoarthritis of the hip joint on sexual activity (Currey, 1970). The author mailed a questionnaire to 235 potential patients and received replies from 121. He found that sexual problems were more commonly reported in women, but this was literally caused by stiffness and pain. A decline in sexual motivation was not the primary factor. In fact, the causes of sexual difficulty (i.e., interfering with heterosexual intercourse) did not differ between men and women. For women, it was pain in 49%, stiffness in 76% and loss of libido in only 20%. For men, those numbers were 50%, 75% and 27%.

So much for bremelanotide in female patients with chronic pain...

You may complain about demand characteristics and biased samples among those who complete and return surveys about sexual behavior, even when anonymous. Mice are so much simpler, they're not embarrassed to talk about it, they're not influenced by how their partner or doctor may react. Male mice are not less inclined to report sexual problems because they might be perceived as less macho. And female mice don't become sexually disinterested if their husbands are inconsiderate at any number of levels.

Oh wait, those are all sociocultural factors, which simply cannot explain the flighty female libido.


Further Reading

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

Lybrido for Low Libido?

How to Measure Female Desire

Underwear Models and Low Libido

Media HSDD: "Hyperactive Sexual Disorder Detection"

The Joy of Melanocortin Receptors


Footnotes

1 DISCLAIMER: Note that I am not an expert in mouse sexual behavior, so I am not qualified to critique the study on those grounds. I recognize that the present experiments represent a huge amount of work that builds upon a body of research by established investigators.

2 “The authors declare no competing financial interests.”

3 As I've written previously:
Hypoactive Sexual Desire Disorder (HSDD) is a controversial diagnosis given to women who have a low (or nonexistent) libido and are distressed about it. Dr. Petra Boynton has written extensively about the problematic aspects of the HSDD diagnosis and the screening tools used to assess it, as well as the medicalization of sexuality for pharmaceutical marketing purposes.
4 But Were the Experimenters Male or Female? Another study by the same research team received even more press coverage: the finding that male experimenters stress out laboratory rodents to a much greater extent than female experimenters. However, we don't know whether the animal handlers in the present study were male, female, or both.

ADDENDUM May 5 2014: Bethany Brookshire has a fantastic summary of that study, You smell, and mice can tell. A closer examination of the author contributions on the Farmer et al. paper suggests that the majority of investigators handling the mice (perhaps 10 out of 11) were female.


References

Ambler N, Williams AC, Hill P, Gunary R, & Cratchley G (2001). Sexual difficulties of chronic pain patients. Clinical Journal of Pain, 17 (2), 138-45 PMID: 11444715

Currey HL. (1970). Osteoarthrosis of the hip joint and sexual activity. Ann Rheum Dis. 29:488-93

Farmer, M., Leja, A., Foxen-Craft, E., Chan, L., MacIntyre, L., Niaki, T., Chen, M., Mapplebeck, J., Tabry, V., Topham, L., Sukosd, M., Binik, Y., Pfaus, J., & Mogil, J. (2014). Pain Reduces Sexual Motivation in Female But Not Male Mice Journal of Neuroscience, 34 (17), 5747-5753 DOI: 10.1523/JNEUROSCI.5337-13.2014

van Berlo WT, van de Wiel HB, Taal E, Rasker JJ, Weijmar Schultz WC, van Rijswijk MH. (2007). Sexual functioning of people with rheumatoid arthritis: a multicenter study. Clin Rheumatol. 26:30-8.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Wednesday, 23 Apr 2014 10:03

The "Guess the Developmental Cognitive Neuroscience Speaker" contest yielded two correct guesses (both Martha Farah for #4) and six incorrect guesses. Basically, the entire exercise was an excuse to feature the eminently quotable soundbytes of Dr. Martha Farah. A leader in the growing field of neuroethics, she directs the Center for Neuroscience & Society at the University of Pennsylvania.

But all our speakers are winners really... The symposium was a smashing success.


Invited Symposium Session 1
The Broader Applicability of Insights from Developmental Cognitive Neuroscience

Chair: Silvia Bunge, UC Berkeley
Speakers: John D. E. Gabrieli, Margaret Sheridan, Martha J. Farah, Helen J. Neville



Finally, here are the answers.......




(1) Martha Farah - “I am not a neurochauvinist”

(2) Sylvia Bunge - “U.S. Prison Experiment”

(3) Helen Neville - “evidence-based politics”

(4) Martha Farah - “IMHO still premature to dictate policy based on neuro”

(5) Martha Farah - “Here's where going ‘neuro’ earns its keep”

(6) Martha Farah - ‘descriptive’ often considered derogatory in science

(7) John Gabrieli - SCHOOLS MATTER!


Dr. Gabrieli's soundbyte was in the context of discussing charter schools, which have a positive impact on standardized test scores (crystallized intelligence) but no effect on fluid intelligence. Another large-scale study identified structural differences in the brains of pre-literate kindergartners that predicted later reading ability. The CNS 2014 Blog covered his talk in much greater detail. Another Gabrieli soundbyte: “Children are born into a neurodevelopmental lottery.”

Dr. Sheridan spoke about the effects of profound deprivation in institutionalized Romanian orphans and the results of the Bucharest Early Intervention Project. This is a very depressing topic, not one that inspires witty quips or quotable soundbytes. As her abstract put it, “Many aspects of postnatal brain development depend critically on experience for development to proceed normally. In this talk we will discuss what happens to children whose postnatal experience violates what we have come to expect as a species.”

Dr. Farah's talk was about socioeconomic status and the developing brain. Low SES affects some cognitive domains more than others: language, executive function, and declarative memory are the most heavily impacted. For language development, environmental stimulation is the sole factor (other than age). For declarative memory, parental nurturance is the sole factor. “Here's where going ‘neuro’ earns its keep”  e.g., it's been shown that the deleterious effects of stress on the hippocampi of rat pups is buffered by maternal care. Farah believes it's “still premature to dictate policy based on neuro” but acknowledged the tactical advantages of using neuroscience for framing/spin e.g., “science speaks with authority” and appeals to government technocrats. “We're not sentimental old fluffs” for promoting social justice (now in the clever guise of brain plasticity). The negative neural consequences of “toxic” environments can replace social justice frames on the Left and “poverty as a moral failing” frames on the Right. Neuroscience for the bipartisan win!

Dr. Neville spoke about specific training programs designed to narrow the socioeconomic gap in achievement. She was less circumspect about policy implications than Farah, arguing in favor of “evidence-based politics” e.g., publicly proclaiming [in the U.S.] that social equality will improve school performance “up to the levels of Cuba and Sweden,” she said in a deadpan manner. Partnering with Head Start school programs in Oregon, she and her colleagues have implemented an attentional training program in low SES children (the Brain Train) and their parents. She said we should convince the public and policy makers to be guided by evidence from brain research. Again, see the CNS 2014 Blog for more details on her talk.


Neuroscience and Education

I'll end with a collection of links that opine on whether neuroscience really has much to say about “evidence-based” education. Teachers in the UK think it does, according to this article:
Teachers demand training in neuroscien​ce to improve classroom practice

Thousands of teachers are set to receive training in neuroscience after union members called for guidance on how the subject could be applied in the classroom.

Members of the Association of Teachers and Lecturers (ATL) at the union’s annual conference narrowly voted for a motion calling for training materials and policies on applying neuroscience to education and for further research on how technology can be used to develop better teaching.

. . .

“It is true that the emerging world of neuroscience presents opportunities as well as challenges for education, and it’s important that we bridge the gulf between educators, psychologists and neuroscientists.”

Neuroscience could also help teachers tailor their lessons for creative “right brain thinkers”, who tend to struggle with conventional lessons but often have more advanced entrepreneurial skills, Ms Neal said.

If nothing else, perhaps the teachers could learn there's no such thing as “right brain thinkers.”

A more cynical take is at Mind Hacks: It’s your own time you’re wasting.

Professor Dorothy Bishop has been critical as well (see comments):
I really don't want to seem like a Cassandra who rubbishes every attempt at doing neuroscientific studies of development or developmental disorders. ... But my concern is that we are prioritising neuroscience approaches to developmental problems, and this is happening in part because researchers are offering the promise of educational relevance. In contrast, clinical trials of behavioural interventions, which have more potential for helping children, are much harder to fund, and are deemed far less exciting.

Prof. Bishop also asks What is educational neuroscience? 

Here's what Wikipedia has to say about Educational Neuroscience.

Professor Daniel Willingham has covered both sides of the issue in his Science and Education Blog:
Teachers shouldn't need to learn neuroscience

Neuroscience Applied to Education: Mostly Unimpressive

When educational neuroscience works! The case of reading disability.

The University of Oregon is Changing Brains.

Tools of the Mind.

Neuroscience and Education at Columbia.

Centre for Neuroscience in Education at Cambridge.

Mind, Brain, and Education at Harvard.

Trends in Neuroscience and Education journal.

Finally, we have The Brain/Education Barrier and The Santiago Declaration about what science can tell us about early education.
Author: "noreply@blogger.com (The Neurocritic)"
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Date: Monday, 21 Apr 2014 08:03


Dr. Suzanne Corkin on H.M.

One of the highlights of this year's Cognitive Neuroscience Society Meeting was Dr. Corkin's keynote address about Henry Molaison the person and his lasting contribution to the neurobiology of memory. In her more timely recap of the meeting, Daisy Yuhas included this moving quote from H.M., who could not remember meeting Corkin even after decades of testing:
Corkin also discussed the man behind the initials, describing his gentle and remarkably upbeat disposition, given that he was repeatedly confronting a confusing, context-free present. Her talk included a poignant and powerful audio recording of Corkin and H.M. chatting in 1992. In the excerpt, H.M. professes to “not mind” all of the tests and studies, saying simply, “I figure what’s wrong about me helps you help others.”

Henry Molaison died on December 6, 2008. Corkin described the post-mortem handling of H.M.'s brain, which was first scanned before autopsy. Then the brain was removed and preserved in formaldehyde for 10 weeks, and later scanned in a 7T magnet (see Annese et al., 2014 for details).1


H.M.'s brain flew Jet Blue


H.M.'s brain was transported across the country, where it underwent lengthy processing prior to sectioning into 2,401 slices on a heavy duty frozen microtome (Annese et al., 2014).2 This event was webcast live at the Brain Observatory, which she said was “like watching paint dry.”  I beg to differ.  I thought the live coverage was like the Stanley Cup of Neuroscience, as mesmerizing as watching the Zamboni clean the ice at a hockey game.



At the time, I noted that “H.M.'s ventricles are quite enlarged. Then again, he was 82 when he died (so that's not unexpected).”

H.M. was, in fact, demented when he died. His cerebellum was severely atrophied after years on the anticonvulsant drug Dilantin. Cerebellar dysfunction on its own can be associated with explicit memory deficits (Baillieux et al., 2008). And finally, his amygdalae were gone bilaterally (Annese et al., 2014): 
The excision of the anterior hippocampus, together with the bulk of the amygdala, may explain H.M.’s dampened expression of emotions, poor motivation and lack of initiative19. The fact that he was impaired in reporting internal states such as pain, hunger and thirst and his apparent lack of initiative was ascribed to the almost complete removal of the amygdala...

Dr. Corkin has long said that “H.M.'s amnesia was pure.” But these additional issues, along with some reports that his language production and visual cognition were not entirely normal, raise questions about his status as the definitive hippocampal amnesic. Nonetheless, there's no denying the immense importance of what H.M. so generously taught us about memory. “It’s a funny thing,” he said, “you live and learn. I’m living and you’re learning.”


Footnotes

1 H.M's brain was...
...fixed in standard buffered formalin (4% formaldehyde; postmortem interval of ∼14 h). The brain was fixed for 10 weeks at 4 °C with three changes of fixative during that time; it was suspended upside down, hung by the basilar artery. When the tissue was firm enough, the brain was immersed in fixative laying on a cushion of hydrophilic cotton. Subsequently, multiple series of MRI scans of the fixed specimen were acquired in 3T and 7T scanners.

2 Annese et al., 2014:
The results of our examination are based on 2,401 digital anatomical images and selected corresponding histological sections that were collected at an interval of 70 μm over the course of an uninterrupted 53-hour procedure. The series of digital images of the block’s surface was obtained using a digital camera mounted directly above the microtome stage. Volumetric reconstruction from these images was the basis for subsequent visualization and 3D measurements along arbitrary planes. The dissection of the brain was video-recorded and streamed live on the web to permit scientific scrutiny and to foster public engagement in the study.


References  [added 4/27/14]

Annese, J., Schenker-Ahmed, N., Bartsch, H., Maechler, P., Sheh, C., Thomas, N., Kayano, J., Ghatan, A., Bresler, N., Frosch, M., Klaming, R., & Corkin, S. (2014). Postmortem examination of patient H.M.’s brain based on histological sectioning and digital 3D reconstruction Nature Communications, 5.  DOI: 10.1038/ncomms4122

Baillieux H, De Smet HJ, Paquier PF, De Deyn PP, Mariën P. (2008). Cerebellar neurocognition: insights into the bottom of the brain. Clin Neurol Neurosurg. 110(8):763-73.
Author: "noreply@blogger.com (The Neurocritic)"
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