Monday, July 21, 2014

The Neurocritic Critiques Critical Neuroscience

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).

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Sunday, July 13, 2014

Scientology Tropes Enter Mainstream Neuroscience?



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 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...



{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]

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Thursday, July 10, 2014

Can a Failed Schizophrenia Drug Prevent PTSD?



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





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Sunday, June 22, 2014

Welcome to Douglas Coupland's Brain



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

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Monday, June 16, 2014

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?

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 . 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.

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Sunday, June 08, 2014

And the DARPA deep brain stimulation awards go to...



...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

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Humble BRAIN 2025


“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...

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Sunday, June 01, 2014

Feeling Mighty Unreal: Derealization in Kleine-Levin Syndrome


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).

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