Sunday, January 22, 2017

Why Do Political Figures Lie So Blatantly?

Are They Pathological Liars? Narcissists? Psychopaths? “Masterful Manipulators”? 

Trump Spokesman’s Lecture on Media Accuracy Is Peppered With Lies

Nearly all American politicians lie, but few as blatantly as those affiliated with the present administration. How do they do it? Are they lacking a conscience? Do they believe their own lies? Do they start with small falsehoods, stretch the truth, reinterpret events, and finally graduate to verifiably false statements?

“This was the largest audience to ever witness an inauguration, period,” Spicer said, contradicting all available data.

Crowds on the National Mall just before Donald Trump’s inauguration in 2017 (left) and Barack Obama’s in 2009.
Photograph: Reuters.

Here are three major points from an astute analysis of why the first press conference of the Trump administration was such a bizarre sham:
1. Establishing a norm with the press: they will be told things that are obviously wrong and they will have no opportunity to ask questions.  ...

2. Increasing the separation between Trump's base (1/3 of the population) from everybody else (the remaining 2/3).  ...

3. Creating a sense of uncertainty about whether facts are knowable, among a certain chunk of the population...   ...

I recommend you read the entire statement, it's very insightful.

How Do People Reach the State of Shameless Lying?

Is there a “slippery slope”? The notorious academic fraudster Diederik Stapel describes his descent from respectable social psychologist to data fabricator:
After years of balancing on the outer limits, the grey became darker and darker until it was black, and I fell off the edge into the abyss. I’d been having trouble with my experiments for some time. Even with my various “grey” methods for “improving” the data, I wasn’t able to get the results the way I wanted them. I couldn’t resist the temptation to go a step further. I wanted it so badly. I wanted to belong, to be part of the action, to score.
. . .

I opened the file with the data that I had entered and changed an unexpected 2 into a 4; then, a little further along, I changed a 3 into a 5. It didn’t feel right. I looked around me nervously. The data danced in front of my eyes.
. . .

No. I clicked on “Undo Typing.” And again. I felt very alone. I didn’t want this. I’d worked so hard. I’d done everything I could and it just hadn’t quite worked out the way I’d expected. It just wasn’t quite how everyone could see that it logically had to be. I looked at the door of my office. It was still closed. I looked out the window. It was dark outside. “Redo Typing.”

Most of us never reach the abyss of Diederik Stapel or Sean Spicer. Or the average politician:
"People want their politicians to lie to them. The reason that people want their politicians to lie them is that people care about politics," said Dan Ariely, a professor of psychology and behavioral economics at Duke University. "You understand that Washington is a dirty place and that lying is actually very helpful to get your policies implemented." 

But we all lie to some extent. “Why yes, that outfit looks great on you” when we really mean to say, “Well, it's not the most flattering ensemble.” White lies like these are meant to spare another person's feelings, and can be considered a norm of politeness. But do small lies desensitize us to any negative feelings that may ensue, and make it easier to tell more substantial lies in the future?

Lying may be your brain's fault, honestly

Of course it is...

A recent neuroimaging study tracked brain activity while participants were given repeated opportunities to lie for financial gain (Garrett et al., 2016). The goal was to follow the escalation of dishonest behavior over time, and to determine its neural correlates. One of the authors of this paper was Dan Ariely, who is famous for his popular books and his TED talks and his work in behavioral economics. He runs the Center for Advanced Hindsight, the (Dis)Honesty Project, and wrote The (Honest) Truth About Dishonesty: How We Lie to EveryoneEspecially Ourselves. If there's anyone who understands lying, it's Ariely.

In the study, the subjects viewed pictures of jars filled with pennies. The experimental set-up involved the subjects in the role of 'Advisor' and confederates in the role of 'Estimator'. The Advisors got a better and longer look at the jars and relayed their estimated count to the confederates, who in turn guessed the number of pennies in each jar. The players were told that at the end of the experiment, one trial would be randomly selected and both parties would be paid according to how accurate the Estimator had been on that trial. Then the Advisor was privately told that the final payment did not depend on accuracy, but the Estimator didn't know this.

The Advisor was also told that the incentive structure would be manipulated, but the Estimator didn't know this, either. Dishonesty about the amount of money in the jar (overestimation) could benefit the participant at the expense of their partner (self-serving/other-harming), benefit both (self-serving/other-serving), benefit the partner at the expense of the participant (self-harming/other-serving), or a baseline condition where it would benefit neither. There were 60 trials of each, in four separate blocks, to track any changes in dishonesty over time.

A total of 55 volunteers performed the task, with 25 of them participating in the fMRI portion of the study. The behavioral results were collapsed across all 55 participants and were not reported separately for the fMRI subjects. As expected, dishonesty escalated across the course of the blocks that were self-serving, to a greater extent for self-serving/other-harming (green) than for self-serving/other-serving (purple).

But in general, this wasn't an overly selfish bunch of people. The participants started at a dishonesty level of £4 when out for only themselves, compared to £12 when it benefited them as well as their partners. Altruistic dishonesty, you might say.

Fig. 1 (Garrett et al., 2016). (ce) Averaging mean dishonesty across participants on every trial and correlating with trial number (N = 60 trials) in each condition revealed significant escalation when dishonesty was self-serving but not otherwise (Self-serving–Other-harming: r58 = 0.66, P < 0.001; Self-serving–Other-serving: r58 = 0.83, P < 0.001; Self-harming–Other-serving: r58 = −0.23, P = 0.08).

What about the neuroimaging results? Were there brain regions that tracked the subtle increase in dishonesty? The authors selected their regions of interest (ROI) via Neurosynth, an online meta-analytic framework based on words that appear in a huge database of articles. The search term they used was “emotion”, which is rather general now isn't it. The rationale for this choice was that (1) people show increased emotional arousal when dishonest; and (2) responses to emotional stimuli diminish with repeated presentation (variously known as habituation, repetition suppression, or adaptation).

It wasn't clear to me why the authors didn't conduct a whole-brain analysis in the first place; they treated it as an “exploratory analysis”.1 And the emotion ROI was basically the amygdala.
My Cousin Amygdala had an opinion about this.

One of the authors explained the results in a press release:
"When we lie for personal gain, our amygdala produces a negative feeling that limits the extent to which we are prepared to lie," explains senior author Dr Tali Sharot (UCL Experimental Psychology). "However, this response fades as we continue to lie, and the more it falls the bigger our lies become. This may lead to a 'slippery slope' where small acts of dishonesty escalate into more significant lies."

Would I Lie to You About Lie Adaptation?

But it's not that simple. Amygdala activity negative feeling. The senior author certainly knows this, since her previous work linked amygdala activity to optimism, of all things (Sharot et al., 2007). 2  The CNN report on the study had a silly eye-rolling title, but they did interview an independent expert, to their credit.
[Lisa Feldman Barrett] says focusing on the amygdala as the brain's source of emotion may be misguided.

Hand-selected, meta-analyses of brain mapping data, as opposed to results spit out by Neurosynth, she says, have shown that the amygdala is not necessarily critical for emotion.
. . .

Barrett said she also wonders if the research results would hold outside a laboratory's doors.

"They did not reward or punish for lying, whereas there is always a payoff or risk in real life," she said. "That might cause the amygdala to maintain its engagement."

All of this said, Barrett said she doesn't doubt that habituation plays a part in lying. She just isn't sure this new research, pointing to the amygdala as the source of emotion, focuses on the correct cause.

A very high-stakes real life experiment would put the most egregious public liars in a scanner during a simulated press conference or a late night bout of tweeting to see what happens when the falsehoods get more and more preposterous.

There is no such thing as “alternative facts.” Do not become desensitized to bald-faced lies.

White House press secretary attacks media for accurately reporting inauguration crowds
. . .

"This was the largest audience to ever witness an inauguration, period," Spicer said, contradicting all available data.


1 This wasn't always the case, apparently.

2 I was quite critical of that study at the time:

My Amygdala Is Very Optimistic Today...

...But My Subgenual Cingulate Is Sad


Garrett, N., Lazzaro, S., Ariely, D., & Sharot, T. (2016). The brain adapts to dishonesty. Nature Neuroscience DOI: 10.1038/nn.4426

Sharot T, Riccardi AM, Raio CM, Phelps EA. (2007). Neural mechanisms mediating optimism bias. Nature 450(7166):102-5.

A Good Piece in Politico

Trump's Lies vs. Your Brain

The Neurocritic Archives of Lie Detection

Would I Lie to You?

More Lies... Damn Lies...

Would I Lie To You Yet Again?

Lie To Me on the Autobiographical Implicit Association Test

Brain Scans and Lie Detection: True or False?

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Sunday, January 15, 2017

Neuroscience Can't Heal a Divided Nation

Brain activation during challenges to political vs. non-political beliefs (Figure modified from Kaplan et al., 2016).

Lately I've been despairing about the state of America.

I'm not sure how denying access to affordable health care, opposing scientific facts like global warming and the benefits of vaccines, alienating our allies, banning Muslims, building a wall, endorsing torture, and reviving nuclear proliferation are supposed to “make American great again” (as if the U.S. is a backward, put-upon, and defeated nation).

Cancer survivor (and former Republican Jeff Jeans) 1

Why do so many Americans believe that a corrupt, lying billionaire will improve their economic standing?

This way of thinking is alien to me. Is there anything that could change my mind about even one of these issues? What happens when you challenge an opponent's strongly held political views?  Typically, he will double down and affirm his closely held beliefs even more strongly. Why?

As a general slogan, The Personal Is Political is not limited to white radical feminists of the 1960s.2 Much to the dismay of fundamentalist Christians and male white supremacists in the alt-right, their respective personal identities are also closely entwined with their political views. And in turn the “political” is based on a religious/moral/ethical mindset (or an anti-religious/amoral/unethical worldview, as the case may be).

Although Trump supporters (and privileged Liberals gnashing their teeth) would like you to believe that the term “identity politics” is divisive and limited to groups like the LGBT community, the Black Lives Matter movement, Tumblr feminists, SJWs, hard-working undocumented immigrants, and 1.6 billion Muslims who live in hundreds of different countries, they too cling to their groups' identity politics. Across the political spectrum, then, an attack on your core beliefs is taken an attack on you personally. All this arguing about politics with someone on the internet is pointless, because the opponents hold an unimaginably different worldview, or else they delight in outrage.

Appealing to an ideological opponent using an argument based on one's own moral framework is doomed to failure. To briefly generalize, conservatives value in-group loyalty, respect for authority, and purity. Liberals, on the other hand, favor fairness and reciprocity, caring, and protection from harm. Talking to the other camp in terms of your own values is ineffective. But that's what we always do anyway. According to Feinberg and Willer (2015):
(a) political advocates spontaneously make arguments grounded in their own moral values, not the values of those targeted for persuasion, and (b) political arguments reframed to appeal to the moral values of those holding the opposing political position are typically more effective.

In one study, conservatives were slightly more likely to support the Affordable Care Act (ObamaCare) when the arguments in favor were framed in a “purity” context compared to a “fairness” context (Feinberg & Willer, 2015):

Purity.The absence of universal healthcare in the United States practically ensures that we will have unclean, infected, and diseased Americans walking among us.

Fairness.In its current state healthcare in the U.S. is inherently unfair and unjust.”

The purity argument went to outrageous lengths, however:

Purity.  “These diseases [of poverty] are disgusting infestations that invade the human body and leech out needed nutrients to survive. Many of these diseases have grotesque symptoms like yellowing of the skin and eyes, coughing up bloody mucus, itchy rashes, and lesions. These diseases are contagious and spread through the population infecting many, including those who are not poor.”

Other arguments included Gay Americans are Proud and Patriotic Americans (to promote conservative support for gay marriage) and The Military Provides a Fair Chance for Minorities and the Poor (to promote liberal support for military spending). Are there specific areas of the brain associated with greater (or lesser) willingness to change one's beliefs when presented with persuasive opposing evidence? This is one aim of the newly emerging field of political neuroscience.

Can Neuroimaging Heal a Divided Country?

Press Release: When political beliefs are challenged, a person’s brain becomes active in areas that govern personal identity and emotional responses to threats, USC researchers find

This study examined what happened in the brain when the political views of 40 liberals were challenged (Kaplan et al., 2016). What can we learn from this fMRI study, beyond what we already know from political psychology? Jumping ahead, the major conclusions were...
  • The political is personal.
  • When political beliefs are challenged, people get emotional.
...which we already knew. And this quote from the first author strengthened my bias against the study:
“...Kaplan says a good way to make facts matter is to remind people that who they are and what they believe are two separate things.”

Identity politics be damned! Good luck with that! But then I read another quote from Kaplan:
“Political beliefs are like religious beliefs in the respect that both are part of who you are and important for the social circle to which you belong ... To consider an alternative view, you would have to consider an alternative version of yourself.”

This seemed much more insightful, so I took a closer look at the paper. From the outset, one notable limitation is that no conservatives were included in the study. The only participants were politically avid young people who identified as strong liberals. They read eight political statements and eight non-political statements they strongly agreed with (as rated in a pre-scan questionnaire). Each statement was followed by five “challenges” that presented a counter-argument. Then they rated their belief in each statement on a scale of 1 (strongly disbelieve) to 7 (strongly believe).

Fig S1 (Kaplan et al., 2016).

Here are some examples.

Political statements

The U.S. should reduce its military budget.

The laws regulating gun ownership in the United States should be made more restrictive.

Welfare and food stamp programs offer necessary help to the poor.

Nonpolitical statements

Long term exposure to second-hand smoke is a significant health concern.

Lowering one's consumption of foods that are high in cholesterol is a good way to prevent heart disease.

People tend to feel the most trust for those who are most like them racially, culturally, economically, etc.

To be as compelling as possible, the challenges were often exaggerations or distortions of the truth. For the military budget example, one of the challenges was “Russia has nearly twice as many active nuclear weapons as the United States” (which is untrue; the number is 1,740 vs. 2,150 for the US). We can ask, is it really fair to lie to persuade someone to change their opinions? Then again, this is a mild distortion compared to some of the whoppers thrown out during the 2016 Presidential Race (and beyond).

Alas, the challenges weren't all that successful in persuading participants to change their minds about political statements. Ratings dropped by only .3, going from 6.8 to 6.5. And there was virtually no variability across subjects. Belief strength in non-political statements showed greater flexibility, dropping by 1.3 (with slightly more variability across subjects). This becomes important when we look at the brain-behavior correlations below.

For the fMRI data, three task periods were modeled (Statement, Challenge, and Rating) and compared for political vs. non-political trials. Activation maps were reported for the Challenge phase (Fig. 2 below). However, the statistical analysis used a cluster threshold that was overly liberal (see Cluster Failure), which raises the possibility of inflated false positive findings.3

Fig. 2 (Kaplan et al., 2016). In red/yellow, brain regions that showed increased signal while processing challenges to political beliefs (P > NP). In blue/green, brain regions that showed increased signal during challenges to non-political beliefs (NP > P).

At any rate, the authors argued that the big yellow blobs in the default mode network (precuneus, posterior cingulate, medial prefrontal cortex, inferior parietal lobe, and anterior temporal lobe) indicate that participants were accessing their self-identity during challenges to political beliefs: “Given the personal importance of political beliefs for the subjects enrolled in this study, we expected our stimuli to evoke cognition related to social identity.” But just as easily, they could have been disengaging from the task of reading the challenges (mind wandering), which is also associated with the DMN.4 Perhaps the participants found the political challenges more far-fetched than the non-political challenges.

Since it was impossible to correlate brain activity with political belief change across individuals (due to low variance), belief change in the impersonal, non-political condition was examined. But here, in contrast to the other whole-brain analyses, regions of interest (ROIs) in the amygdala and the insula were selected because of their status as “emotion” areas. The finding was that...
...participants who changed their minds more showed less BOLD signal in the insula and the amygdala when evaluating counterevidence. These results highlight the role of emotion in belief-change resistance and offer insight into the neural systems involved in belief maintenance, motivated reasoning, and related phenomena.

But this result has no direct relationship to emotional responses or belief change in the political condition, which is what some pop neuro articles claimed.

Overall, the fMRI data can be interpreted to fit a known narrative. The authors are quite correct that “the inability to change another person’s mind through evidence and argument, or to have one’s own mind changed in turn, stands out as a problem of great societal importance.” But they haven't persuaded me that neuroimaging can further our knowledge of how to go about this. Our collective well-being and survival may depend on the ability to change others' minds, now more than ever.

Further Reading: these two Vox pieces are pretty good.

A new brain study sheds light on why it can be so hard to change someone's political beliefs

Most people are bad at arguing. These 2 techniques will make you better.


1 In one night, the GOP voted to take away these 6 essential health benefits
  1. Protect people with pre-existing conditions
  2. Let young adults stay on their parents’ plan
  3. Maintain access to contraceptive coverage
  4. Ensure Medicaid expansion stays in place
  5. Protect children on Medicaid or CHIP
  6. Protect veterans’ health care
2 Did you know the core argument of this radical manifesto by Carol Hanisch? I didn't either. It's that women are really neat people!! How outrageous, how scandalous and offensive!
This is part of one of the most important theories we are beginning to articulate. We call it “the pro-woman line.” What it says basically is that women are really neat people. The bad things that are said about us as women are either myths (women are stupid), tactics women use to struggle individually (women are bitches), or are actually things that we want to carry into the new society and want men to share too (women are sensitive, emotional).

3 Kaplan et al. used a Z threshold of 2.3 and a cluster size probability threshold of p < 0.05. Although they used FSL FLAME1, which fared well in the Cluster Failure paper (Eklund et al., 2016), a post in the OHBM blog questioned whether this was true for task activation data:
The resting state data have a low true between-subject variance, leading to lower FWE than we might see with task data where systematic differences in task performance might indeed yield the predicted large between-subject differences. This is supported by a secondary simulation using task fMRI data with randomly assigned groups that found FLAME1 to have error rates comparable to FSL’s OLS [which were high].

4 Although the relationship between DMN activity and mind wandering isn't as straightforward anymore (Kucyi et al., 2016; Mittner et al., 2016)...


Feinberg, M., & Willer, R. (2015). From Gulf to Bridge: When Do Moral Arguments Facilitate Political Influence? Personality and Social Psychology Bulletin, 41 (12), 1665-1681 DOI: 10.1177/0146167215607842

Kaplan, J., Gimbel, S., & Harris, S. (2016). Neural correlates of maintaining one’s political beliefs in the face of counterevidence. Scientific Reports, 6. DOI: 10.1038/srep39589

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Monday, December 26, 2016

Penn's Restoring Active Memory dataset freely available

Image from an earlier DARPA news story

Restoring Active Memory (RAM) is a DARPA research program that aims to enhance memory in military personnel who have suffered traumatic brain injuries. The goal is to design an implant, or “memory prosthesis,” that will treat memory loss via electrical stimulation.

Although the failure to replicate a previous study that showed a beneficial effect of entorhinal stimulation was considered “Bad News” by The Neurocritic, among the pieces of good news is the public release of an extensive human intracranial recording dataset.

Penn’s Restoring Active Memory Project Releases Extensive Human Brain Dataset

. . .
Two years into the DARPA-funded Restoring Active Memory or RAM program, lead researcher Daniel Rizzuto, director of cognitive neuromodulation, and Michael Kahana, Penn psychology professor and RAM principal investigator, along with colleagues, have enrolled more than 200 patients and collected more than 1,000 hours of data from patients performing memory tasks. They have now released the largest human intracranial brain recording and stimulation dataset to date, and it’s available for public use, for free.

This data release (from 149 subjects collected during Phase I of RAM) includes:
  • Electrocorticographic (ECoG) recordings
  • Individual electrode contact atlas location and coordinates for localization
  • Session notes, behavioral event data, and iEEG recording data (split by channel) for the following RAM Phase 1 experiments:
    • FR1/2: Verbal Free Recall
    • CatFR1/2: Categorized Verbal Free Recall
    • PAL1/2: Verbal Paired Associates Learning
    • YC1/2: Yellow Cab Spatial Navigation

see RAM Public Data for more.

Also of interest are at least 10 posters that were presented at the 2016 meeting of the Society of Neuroscience. The abstracts for these include:

Targeted brain stimulation to modulate memory in humans (and poster).

Large-scale assessment of the effects of direct electrical stimulation on brain network activity (and poster).

Studying the effects of direct subdural electrical stimulation in human subjects during a verbal associative memory task.

Human memory enhancement through stimulation of middle temporal gyrus
In total, 40 patients implanted with intracranial electrodes for seizure monitoring were stimulated during encoding of word lists for subsequent recall in two verbal memory tasks.  ...  50Hz continuous bipolar stimulation was delivered during epochs of word presentation...

We report memory enhancement in two out of two cases of stimulation in the left posterior middle temporal gyrus, which resulted in significantly increased number of remembered words on stimulated versus non-stimulated lists (p<0.05, permutation test) with subjective experience of improved remembering of words in one of the patients. The effect of stimulation was correlated with univariate changes in spectral power, coherence and phase synchrony, as well as by a multi-variate classifier analysis of spectral power changes characterizing successful word recall. There was no positive effect found in any other of the structures tested in this study, which included areas of the prefrontal cortex, hippocampus and the associated medial temporal neocortex.

The Computational Memory Lab at Penn has been a commendable model for the Open Science movement.

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Friday, December 23, 2016

Bad news for DARPA's RAM program: Electrical Stimulation of Entorhinal Region Impairs Memory

The neural machinery that forms new memories is fragile and vulnerable to insults arising from brain injuries, cerebral anoxia, and neurodegenerative diseases such as Alzheimer's. Unlike language, which shows a great deal of plasticity after strokes and other injuries, episodic memory memory for autobiographical events and contextual details of past experiences doesn't recover after permanent damage to the hippocampus and surrounding structures.1 Is it possible to improve memory by directly stimulating specific regions in the medial temporal lobes (MTL), even in damaged or diseased brains?

Restoring Active Memory (RAM) is a DARPA research program that aims to enhance memory encoding and retrieval in military service members who have suffered traumatic brain injuries. The approach is to design an implant, or “memory prosthesis,” that will treat memory loss via electrical stimulation.
The end goal of RAM is to develop and test a wireless, fully implantable neural-interface medical device for human clinical use ... DARPA will support the development of multi-scale computational models with high spatial and temporal resolution that describe how neurons code declarative memories—those well-defined parcels of knowledge that can be consciously recalled and described in words, such as events, times, and places. Researchers will also explore new methods for analysis and decoding of neural signals to understand how targeted stimulation might be applied to help the brain reestablish an ability to encode new memories following brain injury.

Initial Funding

The first RAM awards went to teams led by investigators at University of California Los Angeles (Dr. Itzhak Fried, PI) and University of Pennsylvania (Dr. Michael Kahana, PI). DAPRA's contributions to the White House BRAIN Initiative are known for their ambitious overreach.2  The modest call for proposals requested the following:
Proposers should develop a computational model of human neural and behavioral function underlying declarative memories that can be explicitly recalled.  [sure, no problem!]
. . .

Researchers must propose a method for validating their model by demonstrating that the model can be used to restore declarative memories through neural stimulation (i.e., electrical, optical, chemical, etc). ... Efficacy of the model must be validated by demonstrating that human patients can explicitly retrieve the restored memories after at least 14 days.
Piece of cake, right?

from Fig 1A (Jacobs et al., 2016). Stimulation in the left entorhinal region did not improve memory in this patient.

Maybe not...

Initial Findings

The first step in this noble quest has been to stimulate the MTL in epilepsy patients who have electrodes implanted for another clinical reason: to monitor the location of their seizures. The UCLA group reported that stimulation of the entorhinal region improved spatial memory (Suthana et al., 2012), a finding that predated the RAM program. Let's take a closer look.

Human entorhinal cortex (Schröder et al., 2015)

The entorhinal cortex (EC), located deep within the temporal lobes, projects to the hippocampus, a key region for the formation of episodic memories.3 EC plays an important role in spatial navigation and is famous for containing a spatial map. The EC and its neighbors in the parahippocampal region also receive projections from neocortical association areas, thus serving as a convergence site for cortical input and a distribution center for cortical afferents to the hippocampus.4

from Fig. 1 (Eichenbaum, 2000). The anatomy of the hippocampal memory system.

Suthana et al. (2012) began by reviewing all the potential benefits of entorhinal stimulation:
In rodents, electrical stimulation of the perforant pathway, which originates in the entorhinal cortex and projects into the hippocampus, results in long-term potentiation, release of acetylcholine, and resetting of the theta phase, all of which are associated with improved memory. It has also been shown that electrical stimulation can enhance neurogenesis in the hippocampus. Whether direct stimulation of this entorhinal output to the hippocampus enhances learning is not known.

In the study, seven individuals with epilepsy performed a spatial task where they learned destinations within virtual environments. There were four blocks, each containing six different destinations (that repeated across blocks). In half the trials of blocks 1-3, electrical stimulation (at 50 Hz) was delivered to the EC or hippocampus. No stimulation was given in block 4.

Spatial learning was quantified by determining the actual path traveled by the participant, relative to the shortest possible path. This variable was called excess path length, with shorter “excess” path length indicating better performance. Latency to reach a destination was measured as well.

The graph below shows the results averaged across six patients with entorhinal stimulation. During the three “learning” blocks, stimulation made no difference for (A) latency or (C) excess path length. During the identically structured “retention” block (when no stimulation was actually given), there seemed to be a small difference, with shorter latency and smaller excess path length for the destinations that had been learned with stimulation. No differences in performance were found when the hippocampus was stimulated, which is a little odd. Previous studies have shown that direct stimulation of the hippocampus impairs memory.

Basically, it looks as if the participants were not learning at all without EC stimulation. But the benefits of stimulation were quite modest (p=.03 for both measures), and the error bars were large for non-stimulation trials. Will these findings replicate in a larger sample of patients?

New Findings

Jacobs et al. (2016) tested 49 patients across seven different hospitals and found that 50 Hz electrical stimulation of the entorhinal region during encoding impaired memory in both spatial and verbal tasks. The effects were modest (and not always significant), yet surprising in light of the results from Suthana et al. (2012):
Across all patients and both tasks, entorhinal stimulation impaired memory accuracy (as measured by MS) by an average of 9% (permutation p < 0.02; t[15] = 2.3, p < 0.02). Entorhinal stimulation impaired memory in both the spatial task (permutation p = 0.03; t[5] = 1.7, p = 0.08) and the verbal task (permutation p = 0.09; t[9] = 1.49, p < 0.09).

You can get an idea of the individual variability in the spatial task below, where p < 0.1 and p < 0.05 (one-sided rank-sum test).

The impairments appeared to be more robust with hippocampal stimulation, in contrast to the lack of effect in Suthana et al.:
Stimulation in the hippocampus significantly impaired performance by 8% overall across both tasks (permutation p = 0.002; t[42] = 2.97, p < 0.003). This impairment was present separately in both the spatial task (permutation p < 0.05; t[22] = 1.94, p < 0.05) and the verbal task (permutation p < 0.001; t[19] = 2.3, p < 0.02).

You might notice from the df above that not all patients had electrodes located in the regions of interest: 28 subjects for hippocampus (43 sites) and only 12 subjects for entorhinal (16 sites).

Nothing is Ever Simple

Why the discrepancy between studies?? Jacobs et al. (2016) discussed some potential differences: number of participants, number of independent observations (i.e., greater statistical power in their study), a better test of MTL-based spatial memory, and duration of stimulation (fixed at 10 seconds per trial vs. longer and variable). They also ran a simulation of Suthana et al.'s statistical methods using similar data and reported that “an effect at least as big as the 64% EPL reduction they observed is found in 19% of randomly shuffled data” (meaning that the result is not statistically significant).

What does this mean for the RAM of the future? In an extensive review of the brain stimulation literature, Kim et al. (2016)...
...tentatively suggest that stimulating multiple memory nodes in concert could enhance cognitive processes supporting memory.

Thus, the stimulation studies published so far make the point that for effective modulation of memory performance to be achieved, a network perspective rather than a purely focal stimulation approach should be considered. Declarative memory relies on a distributed network of multiple neocortical and medial temporal regions that serve cohesive roles in memory processes...

ADDENDUM (Dec 24 2016): DARPA has responded, and they're still bullish on closed-loop stimulation for memory restoration. 

One promise of this technology is that when you forget where you went for lunch on Thursday, and what you ate, and where you sat, and what you wore, your implant will kick in and retrieve the memories for you. 

And in response to a reader question, an extended quote from the Kim et al. (2016) network approach is in the comments below.


1 For an extreme example, see Patient H.M.

2 see these posts by The Neurocritic: A Tale of Two BRAINS: #BRAINI and DARPA's SUBNETS and DARPA allocates $70 million for improving deep brain stimulation technology.

3 Synaptic connections in the hippocampus and entorhinal cortex.

from Fig. 1 of Dobrunz (1998). Lateral perforant path (dotted green) and medial perforant path (solid green) provide inputs from the entorhinal cortex to the dentate gyrus of the hippocampus. Perforant path axons form synapses onto dentate granule cells (lateral in yellow, medial in red). Axons from the CA3 region of hippocampus form synapses onto cells in CA1 (purple).

4 Functional overview of the extended hippocampal-diencephalic memory system.


Jacobs, J., Miller, J., Lee, S., Coffey, T., Watrous, A., Sperling, M., Sharan, A., Worrell, G., Berry, B., Lega, B., Jobst, B., Davis, K., Gross, R., Sheth, S., Ezzyat, Y., Das, S., Stein, J., Gorniak, R., Kahana, M., & Rizzuto, D. (2016). Direct Electrical Stimulation of the Human Entorhinal Region and Hippocampus Impairs Memory. Neuron, 92 (5), 983-990. DOI: 10.1016/j.neuron.2016.10.062

Kim, K., Ekstrom, A., & Tandon, N. (2016). A network approach for modulating memory processes via direct and indirect brain stimulation: Toward a causal approach for the neural basis of memory. Neurobiology of Learning and Memory, 134, 162-177. DOI: 10.1016/j.nlm.2016.04.001

Suthana, N., Haneef, Z., Stern, J., Mukamel, R., Behnke, E., Knowlton, B., & Fried, I. (2012). Memory Enhancement and Deep-Brain Stimulation of the Entorhinal Area. New England Journal of Medicine, 366 (6), 502-510. DOI: 10.1056/NEJMoa1107212

Further Reading

Restoring Active Memory Program Poised to Launch (July 9, 2014)
DARPA has selected two universities to initially lead the agency’s Restoring Active Memory (RAM) program, which aims to develop and test wireless, implantable “neuroprosthetics” that can help servicemembers, veterans, and others overcome memory deficits incurred as a result of traumatic brain injury (TBI) or disease.

UCLA and Penn will each head a multidisciplinary team to develop and test electronic interfaces that can sense memory deficits caused by injury and attempt to restore normal function. Under the terms of separate cooperative agreements with DARPA, UCLA will receive up to $15 million and Penn will receive up to $22.5 million over four years...
. . .

Unique to the UCLA team’s approach is a focus on the portion of the brain known as the entorhinal area. UCLA researchers previously demonstrated that human memory could be facilitated by stimulating that region, which is known to be involved in learning and memory. Considered the entrance to the hippocampus—which helps form and store memories—the entorhinal area plays a crucial role in transforming daily experience into lasting memories. Data collected during the first year of the project from patients already implanted with brain electrodes as part of their treatment for epilepsy will be used to develop a computational model of the hippocampal-entorhinal system that can then be used to test memory restoration in patients.
. . .

The Penn team’s approach is based on an understanding that memory is the result of complex interactions among widespread brain regions. Researchers will study neurosurgical patients who have electrodes implanted in multiple areas of their brains for the treatment of various neurological conditions. By recording neural activity from these electrodes as patients play computer-based memory games, the researchers will measure “biomarkers” of successful memory function—patterns of activity that accompany the successful formation of new memories and the successful retrieval of old ones. Researchers could then use those models and a novel neural stimulation and monitoring system ... to restore brain memory function.

DARPA Project Starts Building Human Memory Prosthetics (August 27, 2014)
“They’re trying to do 20 years of research in 4 years,” says Michael Kahana in a tone that’s a mixture of excitement and disbelief. Kahana, director of the Computational Memory Lab at the University of Pennsylvania, is mulling over the tall order from the U.S. Defense Advanced Research Projects Agency (DARPA). In the next four years, he and other researchers are charged with understanding the neuroscience of memory and then building a prosthetic memory device that’s ready for implantation in a human brain.

Work Begins on Brain Stimulator to Correct Memory (April 3, 2015)
If the Penn team is able to identify markers of memory formation, it will try to influence them by stimulating the brain with low doses of electricity. The goal is to test whether it’s possible to coax the brain’s circuitry into whatever state represents a specific patient’s best possible memory function.

Kahana, who is director of the university’s Computational Memory Lab, says it’s too soon to say whether the idea will work. “We want the brain to exhibit a certain pattern of electrical activity,” he says. “It’s a big leap [to say] we can somehow nudge it into that state by giving it a little push.”

Targeted Electrical Stimulation of the Brain Shows Promise as a Memory Aid (September 11, 2015)
. . .

Just over one year into the effort, the novel approach to facilitating memory formation and recall has already been tested in a few dozen human volunteers, said program manager Justin Sanchez. ...

The study aims to give researchers the ability to “read” the neural processes involved in memory formation and retrieval, and even predict when a volunteer is about to make an error in recall. The implanted electrodes also provide a means of sending signals to specific groups of neurons, with the goal of influencing the accuracy of recall.

Initial results indicate that it is indeed possible to capture and interpret key signals or “neural codes” coming from the human brain during memory encoding and retrieval, and improve recall by providing targeted electrical stimulation of the brain.

Top image (from Penn): Illustration showing placement of deep brain electrodes in an epilepsy patient.

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Saturday, December 03, 2016

19th Century DIY Brain Stimulation

Fig. 4 (Wexler, 2016). Lindstrom's Electro-Medical Apparatus (ca. 1895), courtesy of the Bakken.

Think the do-it-yourself transcranial direct current stimulation movement (DIY tDCS) is a technologically savvy and hip creation of 21st century neural engineering? MIT graduate student Anna Wexler has an excellent and fun review of late 19th and early 20th century electrical stimulation devices, namely the “medical battery” designed for home use.

Fig. 2 (Wexler, 2016). An advertisement for one of the few consumer medical batteries that used only direct current (1881, Frank Leslie's Newspaper). Courtesy of the Bakken.

Some highlights (Wexler, 2016):
  • The use of a portable electrotherapy device known as the “medical battery” bears a number of striking similarities to the modern-day use of tDCS.
  • Many features related to the home use tDCS—a do-it-yourself movement, anti-medical establishment themes, conflicts between lay and professional usage—are a repetition of themes that occurred a century ago with regard to the medical battery.
  • Viewed in historical context, the contemporary use of electrical stimulation at home is not unusual, but rather the latest wave in a series of ongoing attempts by lay individuals to utilize electricity for therapeutic purposes.

One notable difference, however, is that contemporary devices make the distinction between cranial and non-cranial stimulation, whereas the medical battery could be applied to anything that ails you: headache, backache, kidney pain, “female weakness”, “premature decline” in men, indigestion, you name it.

Old timey devices designed specifically for the head were unusual, but here are some figures from the patent for a jaunty derby hat that houses a collection of medical batteries. Alas, it never went to market.

Fig. 7. (Wexler, 2016). A medical battery mounted into a hat as depicted in a 1904 patent by George. F. Webb.

Webb (1904): “My invention relates to batteries, my more particular object being to produce a light and compact battery suitable for medical use and capable of ready adjustment without regard to the amount of current to be supplied.”

Clearly, the precursors to Silicon Valley venture capitalists missed out on a great investment. OpenBCI Derby Kickstarter, anyone?

link via @DIYtDCS


Wexler, A. (2016). Recurrent themes in the history of the home use of electrical stimulation: Transcranial direct current stimulation (tDCS) and the medical battery (1870–1920) Brain Stimulation DOI: 10.1016/j.brs.2016.11.081

Sleek and stylish design, then and now.

Fig. 8. (Wexler, 2016). Left: advertisement for the Konzentrator, circa 1927–1928, courtesy of the American Medical Association. Right: Thync electrical stimulation device, 2015, courtesy of Thync, Inc.

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Monday, November 28, 2016

Airplane Headache II: The Sequel

Airline travel during the holidays is one big headache. But for some people, “airplane headache” is a truly painful experience. The headache occurs during take-off and landing, is unique to plane travel, and is not associated with other conditions. The pain is severe, with a jabbing or stabbing quality, and located on one side of the head (usually around the eye sockets or forehead).

Airplane headache was initially described as a rare event in the medical literature. In fact, a 2004 report called it An unusual case of an airplane headache (Atkinson & Lee, 2004):
A 28-year-old man developed severe headache associated with changes in altitude during ascent and descent while flying in an airplane. Jabbing pain over the forehead and between the eyes began within minutes of ascent. It resolved once a cruising altitude was reached, but then returned at the start of descent.

Six years later, another case report noted how rare it is (Domitrz, 2010):
Headache with normal examinations and imaging, occurring during an airplane flight has been rarely reported. We present a young patient with a new type of headache that appeared during flights: take-off and landing of a plane and was not associated with other conditions. This airplane headache is rather rare in population and the pathophysiology of this type is not clear.

This claim is contradicted by 240 miserable passengers who commented on The Neurocritic's 2010 post, which appeared soon after that paper was published. Granted, the comments have accumulated over six years, but they clearly show that it's not an unusual occurrence.

Now, a new Danish survey reveals that up to 8.3% of the respondents suffer from airplane headaches (Bui et al., 2016). The online survey was publicized through the Facebook pages of Scandinavian airlines and related organizations.1 The survey consisted of 14 questions. The first six asked about demographic information, including nationality, age, gender, migraine and history of high altitude headache (HAH). The other questions asked about symptoms, co-occurring medical conditions, and type of flight.

The survey participants were 254 Scandinavian air travelers. Among those, 89 (35%) said they suffer from headaches attributed to airplane travel. However, only 21 (8.3%) met the International Headache Society's diagnostic criteria for airplane headache (e.g., headache lasts less than 30 min, is not due to sinus congestion, etc.).2

The authors defined two groups: the AH group (n = 21; 12 female, 9 male) and the non-AH group (n = 233). The mean age of the AH group was 39 ± 14 years (range 19–67 yrs).
The majority of AH participants (91%) described their headache as unilateral, fronto-orbital or fronto-parietal. The headache was described mainly as “pressing” (43%), but also pulsating (29%) and stabbing (29%). The intensity of headache was described as severe (57%) or moderate (43%).

When asked to provide a possible cause for their headache, changes in cabin pressure during take-off and landing was reported as the most possible cause of their AH (95%).

The AH group was further divided into two subgroups: A medicated-group (n = 5) and a non-medicated-group (n = 16). One person took paracetamol (acetaminophen) and four used triptan drugs (used to treat migraines and cluster headaches). An earlier paper found that triptans may be effective in preventing airplane headaches (Ipekdal et al., 2011).

One caveat of the present study is that the respondents were self-selected: they visited the Facebook pages of airlines and were (probably) more inclined to complete the survey if they suffer from airplane headaches.

What causes airplane headaches? One idea is that reversible cerebral vasoconstriction syndrome (RCVS) could be involved in some cases of AH (Hiraga et al., 2016). The most prominent hypothesis suggests that barotrauma is involved, with pressure changes affecting the trigeminovascular system (Berilgen & Müngen, 2006). The most comprehensive explanation of sinus barotrauma comes from Mainardi et al. (2012), who discuss “the physical changes in the paranasal sinuses due to the modification of external ambient pressure according to Boyle’s Law.” 

But why is it that relatively few people experience this excruciating pain during ascent and/or descent? Mainardi et al. (2012) again:
...the most likely AH physiopathology seems to be related to a variety of multimodal contributing factors: anatomic factors, such as acquired or congenital abnormalities of sinus outlet, environmental factors (cabin pressure, aircraft speed, angle of ascent/descent, maximum altitude), concurrent factors that act by reducing the sinus ventilation, such as a temporary mucosal oedema, possibly worsened, in predisposed individuals...

Airplane Headache: The Discussion

If you suffer from airplane headaches I encourage you to visit my earlier post, and to read the comments, and to share your own experiences.


1 Participants reached the questionnaire through a link that took them to Google Docs. The survey was open from October 15, 2014 to December 1, 2014.

2 I've pasted in the list of diagnostic criteria in its entirety at the bottom of the post.


Atkinson V, Lee L. (2004). An unusual case of an airplane headache. Headache 44:438–439

Berilgen MS, Müngen B. (2006). Headache associated with airplane travel: report of six cases. Cephalalgia 26:707-11.

Bui, S., Petersen, T., Poulsen, J., & Gazerani, P. (2016). Headaches attributed to airplane travel: a Danish survey The Journal of Headache and Pain, 17 (1). DOI: 10.1186/s10194-016-0628-7.

Domitrz I. (2010). Airplane headache: a further case report of a young man. J Headache Pain 11:531-2.

Hiraga A, Aotsuka Y, Koide K, Kuwabara S. (2016). Reversible cerebral vasoconstriction syndrome precipitated by airplane descent: Case report. Cephalalgia Aug 12. [Epub ahead of print].

Ipekdal HI, Karadaş Ö, Öz O, Ulaş ÜH. (2011). Can triptans safely be used for airplane headache? Neurol Sci. 32:1165-9.

Mainardi F, Lisotto C, Maggioni F, Zanchin G. (2012). Headache attributed to airplane travel ('airplane headache'): clinical profile based on a large case series. Cephalalgia 32(8):592-9.

10.1.2 Headache attributed to aeroplane travel

Headache Classification Committee of the International Headache Society (IHS). (2013). The International Classification of Headache Disorders, 3rd edition (beta version) Cephalalgia, 33 (9), 629-808. DOI: 10.1177/0333102413485658


Headache, often severe, usually unilateral and periocular and without autonomic symptoms, occurring during and caused by aeroplane travel. It remits after landing.

Diagnostic criteria:

    A. At least two episodes of headache fulfilling criterion C

    B. The patient is travelling by aeroplane

    C. Evidence of causation demonstrated by at least two of the following:

        1. headache has developed exclusively during aeroplane travel

        2. either or both of the following:

            a. headache has worsened in temporal relation to ascent after take-off and/or descent prior to landing of the aeroplane

            b. headache has spontaneously improved within 30 minutes after the ascent or descent of the aeroplane is completed

        3. headache is severe, with at least two of the following three characteristics:

            a. unilateral location

            b. orbitofrontal location (parietal spread may occur)

            c. jabbing or stabbing quality (pulsation may also occur)

    D. Not better accounted for by another ICHD-3 diagnosis.


10.1.2 Headache attributed to aeroplane travel occurs during landing in more than 85% of patients. Side-shift between different flights occurs in around 10% of cases. Nasal congestion, a stuffy feeling of the face or tearing may occur ipsilaterally, but these have been described in fewer than 5% of cases.

The presence of a sinus disorder should be excluded.

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