Tuesday, September 16, 2014

Should Policy Makers and Financial Institutions Have Access to Billions of Brain Scans?


"Individual risk attitudes are correlated with the grey matter volume in the posterior parietal cortex suggesting existence of an anatomical biomarker for financial risk-attitude," said Dr Tymula.

This means tolerance of risk "could potentially be measured in billions of existing medical brain scans." 1

-Gray matter matters when measuring risk tolerance

Let's pretend that scientists have discovered a neural biomarker that could accurately predict a person's propensity to take financial risks in a lottery. Would it be ethical to release this information to policy makers? That seems to be the conclusion of a new paper published in the Journal of Neuroscience (Gilaie-Dotan et al., 2014):
The results will also provide a simple measurement of risk attitudes that could be easily extracted from abundance of existing medical brain scans, and could potentially provide a characteristic distribution of these attitudes for policy makers.

If we accept this line of thinking, it's not much of a stretch to imagine that financial institutions, employers, consumer reporting agencies, and dating services could use this information in a discriminatory, preemptive fashion to screen out potentially risky applicants. Or perhaps casinos, lotteries, and predatory lending companies could target these individuals with personalized ads.

Conversely, investment firms could vie for traders with the largest right posterior parietal cortices, since they would have the highest tolerance for risk.

Or am I being alarmist about the breach of ethics involved in releasing protected medical information to outside entities? Although the authors subtly deter extrapolation to this invasive scenario by using phrases like "characteristic distribution" and "risk attitudes of populations" (as opposed to risk attitudes of individuals), they're pretty clear about the promise of their gray matter measure to inform policy (Gilaie-Dotan et al., 2014):
Our finding suggests the existence of a simple biomarker for risk attitude, at least in the midlife [sic] population we examined in the northeastern United States. ...  If generalized to other groups, this finding will also imply that individual risk attitudes could, at least to some extent, be measured in many existing medical brain scans, potentially offering a tool for policy makers seeking to characterize the risk attitudes of populations.

Now let's all take a step back and evaluate whether this is currently feasible. The short answer is no (in my view, at least).1A

First, we have to be somewhat skeptical of the study's major conclusion. Voxel-based morphometry (VBM) was to quantify cortical volume from structural MRIs.2 Gray matter volume in a small chunk of the right posterior parietal cortex (PPC) was the only place in the entire cerebral cortex that correlated with individual attitudes toward financial risk. In humans, right lateralized PPC has been strongly implicated in visuospatial attention.

Doesn't it seem more plausible that a region like the orbitofrontal cortex (OFC), which has been activated in numerous functional neuroimaging studies of decision making and risk, would show such an association? Studies in primates have demonstrated that economic risk is coded by single neurons in the OFC (O'Neill & Schultz, 2014), and in rats risk preference can be differentiated by OFC neuronal responses (Roitman & Roitman, 2010).

The authors do cite an extensive literature on the role of parietal neurons in decision making, but fMRI studies have observed effects of risk preference in left PPC, and uncertainty in bilateral PPC (Huettel et al., 2005, 2006).

But what is the purpose of having a larger gray matter volume in PPC in relation to financial risk attitude? Does it allow for a higher "computational capacity" that can accommodate greater risk tolerance? We don't actually know, as Gilaie-Dotan et al. (2014) explain:
We do not know precisely how GM volume translates to the neural level. It is possible that volume differences reflect synaptogenesis and dendritic arborization (Kanai and Rees, 2011), but to-date there is no clear evidence of correlation between GM volume measured by VBM and any histological measure, including neuronal density (Eriksson et al., 2009).

In contrast to the neural correlate of risk attitude, a participant's attitude toward ambiguity was not associated with structural differences anywhere in the cortex (Gilaie-Dotan et al., 2014). How were these attitudes (or preferences) measured? Experimental economics methods were used to estimate individual preferences for risk (uncertainty with known probabilities) and ambiguity (uncertainty with unknown probabilities).

Participants played a game where they could choose between lotteries that varied in monetary value and in the degree of either risk or ambiguity. In the example trial below, the participant chooses either this option, where they stand a 38% chance of winning $18, or the reference option that offers a 50% chance of winning $5.



Modified from Fig. 1A (Gilaie-Dotan et al., 2014).


There were five reward levels ($5, $9.50, $18, $34, and $65), each fully crossed with three probabilities of winning and three levels of ambiguity around the winning probability, as shown below.


Figure 1 (Levy et al., 2012). Risky and ambiguous stimuli. A) In risky stimuli the red and blue areas of each image are proportional to the number of red and blue chips. Three outcome probabilities were used: 13, 25 and 38%. B) In ambiguous stimuli the central part of the image is obscured with a gray occluder. In the gray area the number of chips of each color is unknown, and thus the probability of drawing a chip of a certain color is not precisely known. Three levels of ambiguity were used, where 25, 50 or 75% of the image is occluded.


Using a maximum likelihood procedure, the choice data of each participant was fit to a logistic function. Fitting the choice data with a choice function provided estimates for the risk attitude (α) and ambiguity attitude (β) for each person. These were included in multiple regression analyses to determine the neuroanatomical correlates of risk and ambiguity based on the model estimates.3

Two populations of subjects were tested. The first was a group of 21 individuals who participated in the fMRI study of Levy et al. (2010) at NYU; thus the first analysis was entirely post hoc, and 7 more people were added later to make the total n=28 (mean age = 25).4

The second group, which served as a validation sample, consisted of 33 healthy subjects from the University of Pennsylvania (mean age = 21.34).5 A region of interest (ROI) analysis created spheres of six different sizes around the right PPC peak that were compared to control ROI spheres in primary motor/primary somatosensory areas. The right PPC finding replicated at p<.05 or p<.01, whereas there was no correlation between risk attitudes and gray matter volume in the M1/S1 control area.

If you're wondering, like me, whether any other part of the cortex showed a relationship to either risk or ambiguity in Group #2, one sentence in the Results assures us that no other regions were implicated in risk with a standard VBM whole-brain analysis.

Unlike the sweeping conclusions about the policy implications of their results (which were mentioned three times), the authors were appropriately cautious about causality, saying it's not possible to determine whether a big PPC causes higher risk tolerance, or having a higher risk tolerance leads to an increase in PPC gray matter volume. They also warn against assuming any relationship between genetics and risk attitudes. Finally, they acknowledge that the results may not generalize beyond their populations of students at Northeastern universities who are in their early to mid 20s, a time when the prefrontal cortex isn't fully developed.

I suspect we'll soon see studies that examine risk attitude and gray matter volume across the life span, given the interest of these researchers in Separating Risk and Ambiguity Preferences
Across the Life Span: Novel Findings and Implications for Policy (PDF).


Footnotes

1 It's impossible that there are "billions of existing medical brain scans" because the entire world population is currently 7.19 billion. Dr. Tymula could have been quoted in error, but this exact phrase appeared in both ScienceDaily and the original University of Sydney press release. In the Yale press release on the study, the number was downgraded to millions:
"Based on our findings, we could, in principle, use millions of existing medical brains scans to assess risk attitudes in populations," said Levy. "It could also help us explain differences in risk attitudes based in part on structural brain differences."
It's commendable that the title of the Yale press release (Brain structure could predict risky behavior) was more circumspect than the one given to the J Neurosci article itself.

1A ADDENDUM (Sept 16 2014): The billions [i.e. millions] of existing medical brain scans are not all high-resolution T1-weighted anatomical images (1 × 1 × 1 mm3) acquired using a 3T Siemens Allegra scanner equipped with a custom RF coil. In other words, most may not have the anatomical resolution to measure such a small brain area.

2 Gray matter volume in the whole cerebral cortex was quantified, but you'll notice that no subcortical structures (e.g., striatum, nucleus accumbens, cerebellum) were measured.

3 More methodological details:
The age and gender of the participants and global GM volume (following ANCOVA normalization) were included in the design matrix as covariates of no interest, and were thus regressed out. F contrasts were applied first with p < 0.001 uncorrected as the criterion to detect voxels with significant correlation to individual’s risk attitudes. Whole-brain correction procedures were then applied...

4 The authors stated that this did not affect the outcome.

5 Oddly, these two groups of young people (mean ages of 25 and 21 yrs) were called "midlife" adults three times in the paper.


References

Gilaie-Dotan, S., Tymula, A., Cooper, N., Kable, J., Glimcher, P., & Levy, I. (2014). Neuroanatomy Predicts Individual Risk Attitudes. Journal of Neuroscience, 34 (37), 12394-12401 DOI: 10.1523/JNEUROSCI.1600-14.2014

Huettel SA, Song AW, McCarthy G. (2005). Decisions under uncertainty: probabilistic context influences activation of prefrontal and parietal cortices. J Neurosci. 25(13):3304-11.

Huettel SA, Stowe CJ, Gordon EM, Warner BT, Platt ML. (2006). Neural signatures of economic preferences for risk and ambiguity. Neuron 49(5):765-75.

Levy, I., Rosenberg Belmaker, L., Manson, K., Tymula, A., & Glimcher, P. (2012). Measuring the Subjective Value of Risky and Ambiguous Options using Experimental Economics and Functional MRI Methods. Journal of Visualized Experiments (67) DOI: 10.3791/3724

Levy I, Snell J, Nelson AJ, Rustichini A, Glimcher PW. (2010). Neural representation of subjective value under risk and ambiguity. J Neurophysiol. 103(2):1036-47.

O'Neill M, Schultz W. (2014). Economic risk coding by single neurons in the orbitofrontal cortex. J Physiol Paris. Jun 19. pii: S0928-4257(14)00025-4.

Roitman JD, Roitman MF. (2010). Risk-preference differentiates orbitofrontal cortex responses to freely chosen reward outcomes. Eur J Neurosci. 31(8):1492-500.





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Sunday, September 07, 2014

A Dangerous New Dish


Bibimbop Brugmansia *

* Do NOT try this at home.


Edible flowers can make for a beautiful garnish on salads and trendy Brooklyn cocktails, but these decorative flourishes can be a disaster for the oblivious amateur. An unusual case report in BMC Research Notes summarizes what happens when you sprinkle toxic flower petals on your bibimbop (Kim et al., 2014).

A 64 year old Korean woman came to the emergency room with incoherent speech and fluctuations in attention, orientation and comprehension. She had called her daughter for help but couldn't remember why. (Hint: that's because she ingested flowers containing scopolamine and atropine, two potent anticholinergic compounds that can cause amnesia).

In contrast to these alterations in her mental state, she did not show dilated pupils, dry mouth, increased heart rate, or other changes to the autonomic nervous system typically observed with anticholinergics [which seems odd to me]. After 10 hours had elapsed, she became fully conscious and remembered that she had added a few flowers to her bowl of bibimbop, a traditional Korean dish. Twenty-four hours later, her memory for the entire episode was hazy.




Angel's Trumpet (Brugmansia), a popular ornamental shrub, has a long history in ethnobotany and toxicology as a deliriant, differentiated from the psychedelic and dissociative hallucinogens. There are numerous case reports of presumed Angel's Trumpet poisoning in the literature. A 2003 review reported on 33 patients, 31 of whom deliberately consumed a brewed tea (Isbister et al., 2003). Dilation of the pupils (mydriasis) was seen in 100% of the patients, which is why it's odd that Kim et al. did not observe this.

In fact, one paper reported on accidental unilateral mydriasis in a 11 year old girl who touched “a nice pink flower, similar to a trumpet” and then rubbed her eye (Andreola et al., 2008).

But the most infamous case of deliberate Angel's Trumpet abuse is the young man who severed his own penis and tongue after drinking a tea, “illustrating that consuming this beautiful flower with the name of an angel and the poison of the devil can be very dangerous” (Marneros et al., 2006).

Scopolamine blocks M1 muscarinic acetylcholine receptors that are prominently distributed in the cerebral cortex, amygdala, and hippocampus. The septo-hippocampal cholinergic system plays an important role in learning and memory, accounting for the oft-observed amnesia.

Brugmansia was (and is) used by Native groups in South America for religious ceremonies. According to Lockwood (1979), the Jivaro in eastern Ecuador used Brugmansia in a boyhood rite of passage. The adults understood the potential danger of the delirious and hallucinatory state and closely supervised the child:
When a Jivaro reaches the age of six he seeks an arutam wakani, an acquired soul. ... To acquire an arutam soul, the boy, usually accompanied by his father, makes a pilgrimage to a sacred waterfall where he bathes, fasts, and drinks infusions of fresh tobacco water. If no vision or apparition appears, recourse may be to drink maikua, the juice of Brugmansia...
. . .

The arutam seeker is watched over by men not taking the maikua, in order to protect him from accidents or self-inflicted harm that might occur during the initial violent stages when the drug is taking effect. If the boy is fortunate, the arutam will appear to him, usually in the form of a pair of large creatures, often animals such as jaguars or anacondas.

In more recent times, the street drug 'burundanga' has been used by criminals to incapacitate potential victims, as Vaughan Bell has explained.

So the question arises, with such a long and distinguished literature, why was a new case study of Brugmansia poisoning published? Obviously, there are vast cultural differences between indigenous South American peoples, curious German and Australian youth, and elderly Korean women.



Heungmi kkotjeon (Pan-fried Sweet Black Rice Cake with Flower Petals)


The beautiful Korean dish above is made with non-toxic edible flowers. Another (similar?) dish is hwajeon, or "flower cake". Might this lead to a greater danger in accidentally eating toxic flowers? Kim et al. conclude:
This case is unique in that AT was ingested as an ingredient of a traditional Korean dish.  ...  Considering the fact that one can purchase it from virtually any florist without much difficulty, and that the number of adolescent recreational drug users is increasing, AT could be misused in the near future. The flowers of AT are occasionally used to garnish foods, so raising the awareness of the toxicities of this plant to the general public is important.


Further Reading

The tree of drunkeness

Hallucinations and hospitalizations: Angel’s Trumpet

The plant of human puppets

Cultural Chemistry - the plant that robs you of your free will?

Is free will spent by a knock-out drug?

Mind controller: What is the 'burundanga' drug?

If you must, 23 Recipes That Will Feed Your Inner Flower Child at Buzzfeed





References

Andreola B, Piovan A, Da Dalt L, Filippini R, Cappelletti E. (2008). Unilateral mydriasis due to Angel's trumpet. Clin Toxicol (Phila). 46(4):329-31.

Isbister, G., Oakley, P., Dawson, A., & Whyte, I. (2003). Presumed Angel's trumpet (Brugmansia) poisoning: Clinical effects and epidemiology. Emergency Medicine Australasia, 15 (4), 376-382 DOI: 10.1046/j.1442-2026.2003.00477.x

Kim, Y., Kim, J., Kim, O., & Kim, W. (2014). Intoxication by angel’s trumpet: case report and literature review. BMC Research Notes, 7 (1) DOI: 10.1186/1756-0500-7-553

Tommie Lee Lockwood, summarized by Evans Schultes, R., & Plowman, T. (1979). The ethnobotany of Brugmansia. Journal of Ethnopharmacology, 1 (2), 147-164 DOI: 10.1016/0378-8741(79)90004-7

Marneros A, Gutmann P, Uhlmann F. (2006). Self-amputation of penis and tongue after use of Angel's Trumpet. Eur Arch Psychiatry Clin Neurosci. 256(7):458-9.






More Photo credits: Bibimbop by Agnes Ly, via Wikimedia Commons and Brugmansia (angel’s trumpet) by Asit K. Ghosh Thaumaturgist, via Wikimedia Commons. Neurocritic Remix CC BY-SA 3.0.

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Sunday, August 31, 2014

Whitman Was Not a Neuroscientist


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.




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

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Sunday, August 24, 2014

Autobiographical Memory for a Life-Threatening Airline Disaster


“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.






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.



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Thursday, August 14, 2014

The Neuro Sci-Fi of the Near Future

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.

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Sunday, August 10, 2014

Interview with Dr. Jan Kalbitzer, author of the "Twitter Psychosis" article



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.

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Thursday, July 31, 2014

Twitter Psychosis as a Cultural Artifact

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

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