Tales From The Science Trenches: The problem of journal addiction

Note: Over the next few months I'll be doing a series of posts critiquing modern peer-review process.  As part of this I'd like to collect stories from other scientists on their experiences trying to get papers through peer-review.  Good or bad, if you have a story you'd like to share, please email me (timothyv[at]gmail[dot]com) or put them in the comments section and I'll post them as I see them.  

Today's guest post comes from Joern Diedrichsen who is one of the smartest, most creative scientists that I know.  He studies motor control at University College London and has a provocative take on the pains of the current peer-review process and the addictive mentality that keeps bringing us back for more.

The problem of journal addiction

"Let’s admit it, we are all suckers for glossy journals. Nature, Science, Neuron, Nature Neuroscience... oh, how we puff up our chest when we have a paper accepted in a high place! How we strut around and announce in talks: “our new paper in xxx shows…”. And how deflated, angry, and bitter are we after a rejection.  How we hate the reviewers and the editors. "Ignorant bastards just do not understand anything."

And of course, we are correct. Our papers are misinterpreted, rejected for selfish reasons, or because of plain ignorance. And the editors do not have the spine to stand up and tell reviewers how petty they are.  And the next time WE get asked to review a paper for this journal – which is really not as good as our rejected paper – we’ll show them! The review request lands in our inbox and we metamorphose into the dreaded reviewer 2. Or 3 (depending on how many hours past lunch it is).

Of course we could boycott the whole system. Retreat to a small island. Only send papers (no matter how good) to PLOSone or Frontiers. But a month later, when the wounds have healed, we find ourselves preparing a cover letter for another submission to one of the hated journals. Talk about addiction.

Do we really think that the title of the journal we publish in means this much? Considering the degree to which professional editors are slaves to fashion, and how random the review process is, we really shouldn’t. I think some of my weaker papers have been published in “better” journals - and vice versa. There is a slight positive correlation – but not very high.  Many of the papers that in retrospect are important, get cited, and have impact on the field are in 2^nd-tier journals. But then again, in terms of careers, candidate selection, and funding decisions, we all like to rely on the fast heuristic of the impact factor, not on how important we think the paper is.

So, rather than go by the journal name, if we all would READ the actual papers, see how clear, compelling and novel the results really are, we should be able to break the yoke that editors and reviewers hold over us, right? So, why are we not online every week making sure that good papers in 2^nd tier journals get their well-earned exposure by posting online evaluations on journal websites? Why do the online debates in PLOS Comp Biology often only consist of statements such as “The reference section is missing a crucial reference: My article, 2011”? Why does Faculty of 1000 seem to be struggling in terms of relevance and in getting enough submissions? I guess we are simply too busy writing angry reviews, rewriting our own papers for the next glossy journal, or arguing with journal editors. And trust me, life as an editor is not rosy either. Talk about a thankless job.

Currently, I do not see a good way out. Do we really think that low-threshold mass-journals like Frontiers and PLOSone are the solution? It seems there is just too much stuff out there, and post-hoc online evaluations by people in the field seem not to work very well. So maybe the traditional peer-review and tiered journal system is – like western democracy and capitalism – the lesser of the evils…. But maybe we can start to not reject because we feel the paper is too novel, doesn’t cite us enough, or infringes on our turf? Maybe we should stop pushing papers by friends in high profile journals for political gain? Maybe we should stop evaluating people based on where they publish and turn our attention to the science they produce instead? Perhaps teach our students some integrity and honesty?

No time for that…. I need to fine-tune that cover letter…"

Tales From The Science Trenches: Case of the missing editor

Note: Over the next few months I'll be doing a series of posts critiquing modern peer-review process.  As part of this I'd like to collect stories from other scientists on their experiences trying to get papers through peer-review.  Good or bad, if you have a story you'd like to share, please email me (timothyv[at]gmail[dot]com) or put them in the comments section and I'll post them as I see them.  

Almost immediately after my post yesterday a friend emailed me to share her story.  I think it sets another good case for why proper editorial management is so important.

If you or a colleague have a similar story or even a positive one about the submission process, please email me your tale.

Case of the Missing Editor

"Hi Tim,

I submitted a manuscript to the International Journal of [redacted] on March 7.  This journal doesn’t have an online submission site, so authors are supposed to email (or paper mail) the submission to the editor.  After several attempts to email the editor with the email address listed on the journal website and on his university web page, none of the emails went through. I also didn’t get a response to an email I sent to someone else on the editorial board looking for the editor’s email address.

So I contacted someone in the office I work in to see if they had ideas about where to go from there.  It turned out the email addresses listed for the editor were incorrect, so they gave me the right one.  I sent in the manuscript, it seemed to go through, but I never received acknowledgement of receipt.  I forgot about it for a while, and figured I’d hear from them with a decision in a few months.

At the end of July, I sent an email to the editor asking for acknowledgement of receipt and information on when I might expect to hear a decision.  He never responded.  At the end of August, I emailed an associate editor at the journal who happened to be at the same university, and asked if he could help me out with getting in contact with the editor about my questions.  He responded right away saying he would get in contact with the editor for me, but I never heard anything from him after that.

At the beginning of September, my advisor emailed the editor asking about my manuscript and another of his that he had sent in May.  The editor responded within a day, saying he received the manuscripts and sent them out for review, and he has a new email address that we should use.

We heard nothing back by the end of October, so at that point I sent another email inquiring about both manuscripts that are under review.  Three weeks later, he responded and apologized for the 'long delay' in his response, saying that he has had a 'high workload.'  He said 'I will be able to inform you about a decision very soon now. You will hear from me before December 15.'

And so we wait.

I’ve considered (many times) pulling my manuscript from the journal and submitting it somewhere else, but haven’t because the topic of my paper just wouldn’t fit well at very many journals, and all of my other journal options have lengthy (2-3 year) waits between acceptance and publication.  Needless to say, I don’t plan on ever submitting to this journal again, at least as long as this person remains the editor."

Tales From The Science Trenches: An open-letter to Frontiers in Human Neuroscience

Note: Over the next few months I'll be doing a series of posts critiquing modern peer-review process.  As part of this I'd like to collect stories from other scientists on their experiences trying to get papers through peer-review.  Good or bad, if you have a story you'd like to share, please email me (timothyv[at]gmail[dot]com) or put them in the comments section and I'll post them as I see them.  

In an ideal sense, the peer-review process is designed to provide useful critiques of scientific manuscripts so that the end result has minimal errors and justified conclusions.

Unfortunately, personal biases, poor editorial oversight and general abuse of the review process can sometimes impair communication of scientific results.  What is described below is one example of the flaws in the process that are sometimes experienced by those trying to publish scientific results.

Recently my colleagues and I tried submitting a manuscript to the journal Frontiers in Human Neuroscience.  Frontier is an open access set of journals that prides itself for a rapid turn-around (i.e., fast review cycles) and a simplified peer-review process focused primarily on methodological validity.  

The manuscript we submitted was a study on the brain activation changes that occur with increasing obesity.   The paper had already been bounced around to several other journals before being sent to Frontiers.  As sometimes happens, the same anonymous reviewer followed us from journal to journal providing the same general (and in our opinion incorrect) critiques of the manuscript.

Now for those of you outside the process, it's generally considered bad manners to agree to review a manuscript that you have already critiqued at another journal.  The logic being that you can't provide an unbiased review of the manuscript because you've already judged it previously.

Unfortunately, this particular reviewer keeps agreeing to critique the manuscript while letting his previous judgements color his critique of our manuscript.  What's worse is that he (I'm assuming the gender because I have a good idea who it is) isn't interested in making helpful criticisms that could expand or fix the paper.  You can see for yourself in the linked documents below.

So we submitted our work to Frontiers and this reviewer followed us there.  He gave his usual critique, ignoring many of the changes we that made to address these concerns.  We then spent a couple of months further revising the manuscript and running control analyses.   Once the revisions were submitted to the journal, this hostile referee immediately withdrew his review (again, rather than address our arguments) while the only other referee signed off on our changes as being sufficient for publication.

Then we waited 8 weeks with no word from Frontiers.  Again, for those of you non-scientists this is a pretty long time to wait for an editorial decision after the reviewers had submitted their responses.  Emails to the editor were ignored and the status remained unchanged.

It turns out that the original editor had retired after we resubmitted our manuscript.  Instead of seeing the submission through to completion (or not agreeing to be an editor in the first place), he simply withdrew as well.  It appears that it took Frontiers almost to figure this out.  Once a new editor was assigned, this individual (Dr. HH in the open letter below) made an executive decision to reject the manuscript based only on the withdrawn review.  He completely ignored our replies and made no mention as to why our carefully constructed retort was incorrect.  

In the end the new editor gave us his subjective opinion, based on the interpretations of an admittedly biased reviewer (he admitted he had reviewed our work at other journals) who withdrew from the review process instead of replying to our arguments. 

Not exactly the thorough, intellectual conversation that the peer-review process plays itself to be.

Had this been my first experience like this, I would let it go.  Disappointment comes with being a scientist.  However, it is sad to say that this isn't an unusual circumstance in modern scientific publishing these days.

So what can I do besides submitting to another journal?  Well I've taken the step of delivering an open letter to the editors at Frontiers in Human Neuroscience to outline my frustrations.  You can read it here or see it below.  

"Why make it an open letter?" you may ask.  I'm not doing it to be vindictive.  I'm doing it in the spirit of open access.  With increasing demand to open up access to articles, I believe it's imperative to also open up access to critiques and criticisms of the review process itself.   We don't have a formal repository of abuses of the peer-review process (i.e., a Yelp of scientific publishing to know editorial, reviewer, or journalistic biases before submitting manuscripts).  Often young scientists only find these out through trial-and-error when trying to publish their results.

Shedding light on the flaws of the peer-review process with your colleagues is the only way to start addressing these problems. Until we have a formal system for bringing these experiences to light, I'd like to start serving that role.   If you have an experience you'd like to share about your own experiences that highlight either errors/flaws or cases where it worked precisely how you think it should, please send them along.  I'll post your stories here on my blog as they come along and respect your privacy.

As of the time of this post, the Frontiers editors have not replied to my concerns laid out in the letter.  I'm not holding my breath.

Epilogue: For those of you interested in what a hostile review looks like, you can read the entire critique from the problematic reviewer and our reply to their critique here since Frontiers won't likely be releasing this anytime soon.

Open letter to the editors of Frontiers in Human Neuroscience:

Dr. HH,

Note: In the letter that follows I speak only for myself and not my fellow co-authors. I will be making this letter open to my scientific colleagues so they can understand what they can expect from Frontiers.

I am extremely displeased with the way in which Frontiers has handled the review of this manuscript. Not only has it been mishandled and delayed due to lack of foresight and administration by the editorial staff, but the reasoning behind the final decision rests on a tautological adherence to the reputation of a reviewer who withdrew from the process altogether without addressing the merits of our arguments. At no place in the decision were our responses acknowledged and shown to be incorrect.

My specific complaints include:

1) Our original editor, Dr. NC removed himself as editor in the middle of the review process instead of either seeing the submission through to completion or not accepting it if he knew he was stepping down.  Dr. NC ignored several email requests from our group asking about the status of the manuscript after we replied to the initial concerns.  We received no correspondence from Frontiers for more than two months and no reply from Dr. NC altogether.

2) It took the Frontiers office almost 8 weeks to revisit our manuscript after the original reviewers had either withdrawn (Reviewer 1) or signed off (Reviewer 2) on our changes. 

3) The editorial board chose to ignore the rude and unprofessional tone of Reviewer 1 (who even admitted that he has been a hostile reviewer of this manuscript at previous journals and yet did not decline the invitation to review).  This reviewer did not provide constructive critiques that could improve the quality of the study. Instead they made rude, accusatory and unprofessional statements that were provably false.  At no point did the editorial board intervene in this review. Further, the editorial decision completely ignored the second reviewer’s positive comments about the manuscript (some of which directly conflicted with the first reviewer).

4) Most insulting of all, rather than find an additional reviewer to replace the hostile referee who withdrew from the review, you made an executive decision based solely on the opinions of the withdrawn review! The arguments laid out in our reply were outright ignored, as was the fact that the reviewer had been withdrawn from the review process. If the reviewer had felt merit in their argument they would have further replied to our revisions.  Instead they chose to simply withdraw from the discussion without providing critical feedback.

5) The basis of your executive decision was based solely on several demonstrably false statements that we laid out in our response and we again describe here.  These include:

a) "One expert in the field of this paper had serious concerns about the design and interpretation of this study. The authors' responses did not alleviate the reviewer's concerns." 

Reply: This comment comes from a withdrawn review so it is unclear whether we actually alleviated the concerns of the reviewer.  However, if the reviewer contacted Frontiers after our reply and did not address our carefully laid out arguments, then this puts us in a grossly unfair position since there is no formal critique with which to make a response. 

b) "In particular, the reviewer was concerned that the 3 groups (normal, overweight, and obese) had major age differences, that these age differences may explain some of the results, and thought that the analysis attempting to factor age out is insufficient. The associate editor and I agree that considering the small number of subjects indeed the age differences cannot be overlooked." 

Reply: This argument is specious and wholly unsubstantiated on several levels.  First, as we carefully lay out in our reply, it is the Overweight group that is slightly older than the Normal and Obese groups.  In fact the ages of the Normal and Obese groups are statistically identical.  Yet our neural effects are Normal < Overweight < Obese in the categorical analysis (specifically Normal < Obese) and strictly linear in the parametric regression analysis.  If age was the driving factor our categorical effect pattern would be Normal < Obese < Overweight and have an inverted-U characteristic in the parametric analysis (Figure 7a).  Therefore this argument fails the simple logic test.

Second, the reviewer's belief that using nuisance regressors is an invalid way of controlling for non-specific effects goes against basic statistical theory.  The argument of accounted variance in nested regression models is the fundamental theory of structural equation modeling and mediation analyses.  Yet, the reviewer mis-quotes one article in a psychiatry journal to make their case.  We clearly demonstrated in the reply that BMI and age are not correlated and therefore (even according to the article cited by the withdrawn reviewer) age can be treated as a valid covariate for the neural effects.

Finally, an N=29 is NOT a small sample-size for conventional fMRI study.  There might be a case for it to under-power the categorical analysis, but in the parametric regression analyses (which supports the categorical findings) this is sufficient even for the conservative sample size recommended by Thirion et al. 2007 which the reviewer himself cites.  

At no stage has the withdrawn reviewer or editor pointed out why any of our arguments are incorrect.  They are simply disregarded without reply.

c) "Moreover, the mere fact that such conspicuous age difference were found, suggests some non-random sampling, which suggests that other factors would covary with BMI. In fact, overweight and especially morbid obesity are associated with numerous factors which may be of importance (e.g. socio-economic factors, health problems, not to speak of comfort in lying in the scanner), but the paper unfortunately does not provide clinical or demographic data on the subjects."

Reply: We fail to see the logic in the argument of "non-random sampling." In fact, with random sampling you will get some inconsistencies between groups.  Equal demographics across groups is only achieved through NON-RANDOM sampling.  Nonetheless, as we carefully laid out in our reply, there is no logical way that age can explain our effects.  As for the other covariates, the slippery slope argument to control for an ever increasing number of factors is a needless "torpedo" argument that can be lodged against virtually any between-group study.  This is a proof of concept study of inhibitory control deficits in obesity.  Once an effect is confirmed, further work can be done to elucidate mechanisms and causes.  But you have to know what you're looking for first.  If we followed your logic to its conclusion, no study could be published until all explanatory factors can be fully accounted for.  For example, differences between younger and older adults could be due to lack of comfort in the MRI environment in older adults.  Differences between borderline personality disorder and controls could be due to emotional reactions to the MRI environment.  Differences between schizophrenics and controls could be due to discomfort and irritation lying in a tight enclosed space.  In short, any between-subject study (including many of those published by the editors of this journal) could be said to have the same limitations as our study.  This in no way undermines studies of age, schizophrenia, borderline personality disorder, autism, or any other disease.  Instead, it emphasizes that despite these limitations in between-group comparisons there can be important information gained.  Similarly, our study on obesity is not immune to these issues, but it does not mean that important information on brain health in obesity could not be gleaned from this work.

d) "Another issue is the fact that since the behavioral results did not in fact confirm the prediction of the authors (more inhibitory problems with obesity), the paper relies heavily on reverse inference – that is, on drawing conclusions from assumptions on the cognitive roles of specific activated brain regions."

Reply: In many brain imaging studies, behavioral effects are weaker or not present where evoked brain dynamics are clearly visible.  In fact, the overall slowing of response times across groups is behavioral evidence for our argument that in higher BMI subjects, it requires more processing power to get the same behavioral output.  Thus all responses would be slower.  Again, this suggests that the manuscript was not clearly read since we make this point very clear in the text.

Given this rude and unprofessional experience, I will request that you no longer ask me to be a reviewer on future manuscripts since I do not wish to participate in such a flawed and obviously biased system.  I will also not be sending any new manuscripts to Frontiers in the foreseeable future. 

Sincerely,

Timothy Verstynen Ph.D.

Research Associate

Department of Psychology

Learning Research and Development Center

University of Pittsburgh

Pittsburgh, PA 15260

Thoughts on the science of brutality

Like many Americans, I couldn't help but sit in astonishment last week as I watched the videos showing University of California police officers hitting and pepper-spraying non-violent student protestors.

My initial reaction was disgust and anger.  How could a reasonable person see this as proportional force to disperse the protesting students?  While it's not as bad as what's happening in Egypt or Syria, this is definitely not behavior we expect to see happen in the land of the free and home of the brave. (I'd like to point out that the "it's worse elsewhere" defense is specious at best).

Many of us direct our anger at the police officers themselves.  I'm guilty of this too.  When I saw the video of UC Davis students being pepper-sprayed, I immediately thought that Officer Pike must be sadistically enjoying the act.  I mean obviously only a sadistic nutcase would do such a malicious act like this right?  A "normal" person would act reasonably and find an alternative, more peaceful way right?

Unfortunately, psychology says that this may not the case.

The science of human behavior consistently demonstrates that conformity is the norm, even for aggressive and abusive actions.  Doing the "right" thing in the face of authority demanding excessive force is the exception to the rule.  All freshmen psychology majors know this story by heart due to the tragic success of the research by Stanley Milgrim and Philip Zimbardo.

Conformity To Power

Stanley Milgrim was an American psychologist who wanted to understand how it was that so many Germans could commit the atrocities that occurred under Nazi control.  Are Germans just a sadistic people inclined towards violence or could anyone be pushed to kill an innocent human being?

To test this, Milgrim took a random sample of people around Yale University and put them in charge of "delivering" electric shocks to "participants" who were answering questions in another room.  Every time the "participant" gave an incorrect response, the test subject was told to deliver a shock and increase the intensity of the electrical stimulus on the next incorrect answer.  Milgrim found that most people (over half) caved to the authority of the experimenter and would deliver even a "fatal" electric shock to the unseen "participant."

Of course the "participant" was just an actor and the "shocks" were never actually delivered, but the conclusion was very clear.  For most people the drive to conform to authority was so strong that they'd even hurt or kill a stranger rather than resist the authoritative figure.  This is even without a threat of violence from the authority figure.

Power Corrupts

About a decade later Phillip Zimbardo showed how context can even affect the authority figures themselves.  In one of the most terrifying experiments in modern psychology, Zimbardo showed that John Dalberg-Acton had a particularly acute insight into the pernicious influence of power on human behavior.

Zimbardo took a random sample of Stanford University students and assigned half to playing the role of "prisoners" and the rest fake "guards" in a mock prison setup in the basement of the Department of Psychology.  Zimbardo himself the role of "warden."  Within a matter of days things quickly fell apart. Otherwise normal, college students found themselves abusing their classmates by playing the role of authoritarian prison guards.  The entire expriment had to be shut down as people fell too deeply into their simulated roles (including Zimbardo himself) and started hurting fellow students.  This was in a setup where everyone knew that their roles weren't real.

The important thing to realize is that in both the Milgrim Study and the Stanford Prison Experiment, it wasn't a subset of people who were pre-disposed to violence that committed abusive acts it was an easy majority each time.  When pressured by authority people will do extraordinary things and left unconstrained those in authority can go too far.  It's simply human nature.

Two Eyes For An Eye

Even in the moment, psychology teaches us that each forceful act is perceived differently by those doing the hitting and those being hit.  Neuroscientist and motor researcher Dan Wolpert wanted to understand why it is that the fights between his two children escalated so rapidly (well really he was trying to understand how the brain optimally predicts sensory stimuli when we move, but it was his kids that apparently gave him this idea for the experiment).

Wolpert had subjects press on a lever attached to a robotic arm.  Another arm delivered the exact same force to another participant seated in the same room.  This participant was then instructed to deliver the force he felt back to the other person using a similar robot setup.  With each cycle the amount of force being delivered would nearly double. This is because our brains underestimate the experience of force when we produce and so it feels weaker than the forces we experience from someone else.  It's the same reason why we can't tickle ourselves.  The sensory signals are sort of cancelled out when we produce them.  When we expect it, our brains make things feel a bit less intense.

Bringing this back to the events of the last few weeks, this may mean that the officers may not fully perceive how rough they are actually being.  Their brains literally don't feel that they are hitting as hard as they are.  So in the moment, it may literally seem as if the hits aren't as strong as they are.  (Of course, who knows if this holds for the experience of pepper spraying.)

Putting The Context In Context

Before I end I need to point out that there are thousands of upstanding police officers in this country who put themselves in dangerous situations every day to keep the public safe and treat civilians in a civil manner.  There are many many officers who treat protesters with dignity and without violence.  Sadly, we often react with more anger to misuses of pepper spray than we react with sadness when an officer is gunned down doing the right thing in the line of duty.

In no way do I mean to imply that because of the context that they are put in, all police officers are going to be abusive or lose control.  I'm just trying to point out that we take a good look at ourselves and realize that many of us, if put in the same situation, would very likely do the same thing as Lt. Pike or the Berkeley police officers.

So what do we do?  Maybe instead of just admonishing the excessive force when we see it, we should also focus on rewarding those officers who stand up against the pressure and internal desires to use excessive force because it's the easy route.  After all, reinforcement works better to change behavior than punishment (we can also thank psychology for knowing that).  But until we start accepting that these actions are not abnormal, but in fact predictable within a context, any acts of punishment against officers who go too far won't change the likelihood of future similar acts

With the exception of psychopaths and saints, if you treat a man like a dog you will get a dog. But treat a man like a man and you'll get a human being.


Shergill, S. (2003). Two Eyes for an Eye: The Neuroscience of Force Escalation Science, 301 (5630), 187-187 DOI: 10.1126/science.1085327

On twitter now....

Thanks to Brad Voytek I have caved and Twittered myself.  Follow me @tdverstynen for my microblogging/ranting in 140 characters or less.

Zombie Brain: Conclusions

This post is the final installment of our collaborative venture (between Oscillatory Thoughts and Cognitive Axon) exploring the Zombie Brain.  We hope you’ve enjoyed this little ride. Sincerely, Bradley Voytek Ph.D.  & Tim Verstynen Ph.D.

Bringing it all together: The Zombie Brain

Over the last ten days we’ve laid out our vision of the zombie brain.  To recap, we’ve shown that zombies:

1) Have an over-active aggression circuit.

2) Show cerebellar dysfunction causing them to move slowly.

3) Suffer from long-term memory loss due to damage to the hippocampus.

4) Present with global aphasia (i.e., can’t speak, can understand language).

5) Suffer from a variant of Capgras-Delusion

6) Have impaired pain perception

7) Cannot attend to more than one thing at a time.

8) Exhibit addictive responses to eating flesh.

9) Have an insatiable appetite.

Together these symptoms and their neurological roots reveal a striking picture of the zombie brain.

Based on the behavioral profile of the standard zombie, we conclude that the zombie brain would have massive atrophy of the “association areas” of the neocortex: i.e., those areas that are responsible for the higher-order cognitive functions.  Given the clear cognitive and memory deficits, we would also expect significant portions of the frontal and parietal lobes, and nearly the entire temporal lobe, to exhibit massive degeneration. Also, the hippocampuses of both hemispheres would be massively atrophied (resulting in memory deficits), along with most of the cerebellum (resulting in a loss of coordinated movements).

In contrast, we would expect that large portions of the primary cortices would remain intact. Behavioral observations lead us to conclude that vision, most of somatosensation (i.e., touch), and hearing are likely unimpaired. We also hypothesize that gustation and olfaction would also remain largely unaffected. Relatedly, we must further conclude that large sections of the thalamus and midbrain, brainstem, and spinal cord are all likely functioning normally or are in a hyper-active state.

Putting these elements together, we have reconstructed a plausible model for what the zombie brain would look like. This is shown in yellow below and presented over a normal human brain for comparison.
 

Overlay (yellow is zombie, gray is human)

It is interesting to point out, from a historical standpoint, that many of the regions we hypothesize to be damaged in the zombie brain are part of what is generally referred to as the Papez circuit. James Papez first identified this circuit in 1936. Much like our current "study", Papez was trying to unify a cluster of behavioral phenomena he had observed into a neuroanatomical model of the brain. He wondered why emotion and memory are so strongly linked. His hypothesis was that emotional and memory brain regions must be tightly interconnected.

To test this theory, he injected the rabies virus into the brains of cats to watch how it spread and he made note of which brain regions were destroyed as a result of these injections. He observed that the hippocampus (important for memory formation) connects to the orbitofrontal cortex (social cognition and self-control), the hypothalamus (hunger regulation, among other things), the amygdala (emotional regulation), and so on. These experiments, conducted almost three-quarters of a century ago, may shed some insight into the nature of the zombie disorder today. We’re not suggesting that some super, brain-eating rabies virus is responsible for zombies. We’re just saying that it’s not not possible.

The profile of damage we have outlined corroborates the behavioral observations we have made from zombie films. From a subjective standpoint, this pattern of cerebral atrophy represents a most heinous form of injury unparalleled in the scientific literature. It would lead to a pattern of violence and social apathy; patients thus affected would represent a grievous harm to society, with little chance of rehabilitation. The only recommendation is immediate quarantine and isolation of the subject.

However, as we learned in GI Joe “knowing is half the battle.”  Based on our observations, we leave you with a few strategies to maximize survival in the event of a zombie encounter.

1) Outrun them: Climb to a high point or some other place they will have trouble reaching. Practice parkour.  The slow zombie variant can’t catch up with a healthy adult human.

2) Don’t fight them: They can’t feel pain and aren’t afraid of dying, so they’ve got the edge in close combat.  If you can simply out run them, why risk the bite?

3) Keep quiet and wait: The zombie memory is so terrible that if you can hide long enough, it will mill around only until something else captures its attention.

4)  Distraction, distraction, distraction: Throw something behind the zombie to capture its attention. Set off a flare, use a flashbang, or whatever you need to do to distract it to get away

5) If you can’t beat them, join them: If you can’t out run them (or are around the fast zombie variant) take advantage of their self-other delusion and act like one of them.

There you have it folks... scientifically validated safety tips for surviving the zombie apocalypse.  Use them wisely the next time you come face-to-face with the living dead.

Zombie Brain: Flesh Addiction

This is yet another installment of multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for another post in this series!

Symptom 8: Flesh addiction

“Braainss... BRAAAINS!” Zombies call out for them like a man calls out for water after a week in the desert. Yet no matter how much they eat, they can never be satisfied. It’s as if the craving to consume brains and/or human flesh is the sole thought running through a zombie’s “mind”. Zombies will even risk loss of “life” and limb to satisfy these urges.

These symptoms mirror those seen in dysfunction of the “reward circuits” in the brain. It’s as if the living dead are addicted to flesh and flesh consumption is a compulsion. 

The sense of reward, or the “high”, that you experience originates first from dopamine cells that rest in an area of the brain collectively known as the ventral striatal reward pathway. This includes a larger network of areas in the neocortex, midbrain and brainstem.

Adopted from Wise (2002)

In many ways this circuit starts and ends in the brainstem with the release of dopamine. Note that these are a different set of dopamine neurons than those involved in the aggression circuit we discussed earlier.  Activating these “reward cells” with stimulation (e.g., drugs, food, sex, etc., in humans, or direct electric stimulation in animals) causes them to transmit dopamine to other regions in the cortex and subcortex such as the striatum. This reinforces the drive for future reward seeking behaviors. 

These signals converge to a set of cells in the nucleus accumbens, which is essential for determining the motivational significance of the reward stimulus, causing the person to think, “Mmmmm that was fun; I’ll do that again.” 

In cases of extreme drug abuse, simply showing pictures of drugs to an addict will engage this reward circuit. The same is true for people addicted to eating: showing them pictures of food can reengage the same reward regions as eating.

In zombies, this dopamine reward circuit is likely in overdrive. Paired with a loss of the feeding “off-switch” in the brain, this could lead to the insatiable appetite that zombies have. Of course, in humans fatty diets cause more hunger and the brain is a highly fatty substance, so unfortunately, the more the zombie eats... the more it wants… But we'll discuss that a bit later.

We expect that if you put a zombie in an MRI machine and showed it pictures of human flesh, you would detect activation in many regions of this ventral reward circuit. In fact, these would be the same activation patterns we'd expect to see in the brain of a (living) drug addict when presented with pictures of their drug of choice.

What fMRI would look like in the zombie brain.

But why isn’t a zombie satisfied even after it has consumed an entire human on its own? Well that's a whole other blog post. Let's just say the zombie brain doesn't know or doesn't care when it's full.


So today's lesson shows us that zombies are depraved flesh addicts who will stop at nothing to get their next fix (i.e., you).

Symptom 7: Stimulus-locked attention

Head over to Oscillatory Thoughts for today's Zombie Brain factoid: Stimulus-locked Attention.

Zombie Brain: Pain Perception

This is part six of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 7!

Symptom 6: Pain Perception

Cut off an arm, yet they keep coming. Shoot them in the chest, they keep coming. Light them on fire, they keep coming. How does the zombie continue to chase us despite wounds that would cause debilitating pain in a normal person?

It's quite simple really. They’re not aware of the damage done to them.  More specifically, they may not be feeling the damage being done.

That toaster's going to leave a mark!

Scientifically we call the sensation of painful stimuli nociception.*  The physiological systems that regulate our experience of pain are incredibly complex.  So I'm going to give you the short and simple version. 


Receptors in the skin pick up mechanical, thermal or chemical changes relay this information to neurons in the spine.  This information goes up the spine through a few different different routes and gets relayed to several cortical regions.  The combined recruitment of these neocortical regions then gives rise that "Ouch! F#$% that hurt!" response.  

The pain pathways (from Basbaum et al. 2009)

A majority of these pain signals are processed in a forward part of the parietal cortex, known as the somatosensory cortex.  These area sits right behind the region of the brain that consciously controls movements.  Now the somatosensory cortex actually regulates our experience of all physical sensations (touch, vibrations, etc.) and processes most of the conscious signals that we are aware of feeling.  However, this area is actually made up of  two distinct areas : the primary and secondary somatosensory cortices. Each regulates the processing of different types of sensory information.

There is also a second pain pathway that regulates our rapid unconscious experiences of pain.  Most of this engages the inappropriately named "fight-or-flight" circuit via the amygdala.  Signals are relayed to a few separate areas such as the cingulate (that processes conflict) and the insula (that, well appears to do everything).  It is thought that these areas regulate the emotional salience of pain.  

Now let's think about this... when was the last time you saw a zombie get emotional about anything let alone a little thing like having a limb chopped off?  This suggests that this second pain pathway is disrupted in the zombie brain.

It’s also clear that zombies can still move and they have an idea of basic sensations (they know where their own bodies are, and they do react reflexively to stimuli), but they don’t appear to have conscious awareness of pain and other sensations. This gives us good reason to believe that the nerves that sense pain, pressure, and so on in the body are intact, because zombies do still react to stimuli. We also know that the spinal cord that transmits those sensations up to the brain (and movement signals down from it) must also be intact. Furthermore, before touch senses get to the brain, they stop in the brainstem where they can be mediated and controlled before entering “conscious” perception.

Thus, we believe that there are a couple of vectors for the zombie’s immunity to pain.

First, their secondary somatosensory regions in the parietal cortices are impaired. This would minimize experiencing some types of painful sensations, but not all.  Note that the primary somatosensory cortex (regulating fine touch, sense of limbs, etc.) is still intact.

More importantly, neocortical regions like the insula and cingulate should also be obliterated in the zombie brain.  This would eliminate any emotional reactions to the residual painful stimuli processed in the somatosensory cortex.

Thus zombies may actually feel pain and really just not give a crap about it.  Just like Chuck Norris.

There you have it folks.  A numb, cold-hearted creature incapable of feeling pain (please save the lawyer jokes for another forum).

* Contrary to popular belief, we don't have just 5 senses.  We probably have closer to 20, and most of them involve different types of physical senses.  There's a sense for feeling your limbs in space (proprioception).  There's a sense of fine touch and vibrations called epicritic touch.  There's the feeling of heat, sharp pain, etc.  

Zombie Brain: Language Deficits

This is part four of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 5!

Symptom 4: Language deficits

Let's face it, zombies aren’t known for their oratory skills. Usually you’ll hear nothing but a collective set of moans as they’re pounding at the barricaded doors. Keep in mind that the most fluent phrase we ever hear Tarman say in Return of the Living Dead is "Braaaaaains!"

Tarman goes on a short lived speaking tour

At best you’ll get a disjointed burst of individual words. For example, a somewhat intelligent zombie might utter into the walkie-talkie of a recently consumed police officer, “send... more... cops...” in order to get a new delivery of fresh meat (as observed in Return of the Living Dead). But that would be considered the Shakespeare of zombies.

This type of speaking is called telegraphia, characterized by the fact that the words are present, but the execution is jammed. Neurologically, this relates to a specific disorder known as expressive aphasia or, as it is classically known, Broca’s aphasia.  

Now in the normal living human, this language production ability is mediated by an area of the brain that rests just behind your temple. More often than not, just behind your left temple.

Broca's area is named after Paul Broca, who described the language deficits of Patient "Tan." Tan was reportedly was unable to say anything but the word "tan" after this region of the frontal cortex was damaged. (Historical side note: Tan could actually say many other things however, they were all just vulgar profanities. Apparently French neurological societies frowned upon the idea of naming him Patient "Foutre!").

Okay, back to zombies!  Zombies don't just have a problem producing language, they also don't seem to be able to comprehend it either. They never respond to verbal commands and rarely seem to stop read road signs (hence they are chronically lost). This inability to comprehend language reflects another type of classical deficit called receptive aphasia, known by it's more common name Wernicke’s aphasia. You guessed it... that's because the guy who discovered it was Carl Wernicke.

Wernicke's aphasia comes from damage to a different region of the brain. This sits farther back in your head, at the junction of the temporal and parietal lobes (basically behind and slightly above your ear).

What does this tell us about the zombie brain? Well it would appear that the frontal language production areas and the temporal/parietal language comprehension areas are both atrophied in the zombie cortex. Since these regions communicate with one another via a large bundle of white matter called the arcuate fasiculus, its safe to say that this “arcuate circuit” is obliterated in the zombie brain, as well as the frontal and parietal language regions. 

Damage to the frontal (Broca’s) region leads to expressive (Broca’s) aphasia, and damage to the parietal (Wernicke’s) region leads to receptive (Wernicke’s) aphasia. Thus, all language and communication skills would be severely disrupted in the zombie brain.


Bottom line: Don't try talking to a zombie. It's not worth your time.

Symptom 3: Long Term Memory Loss

Be sure to head over to Oscillatory Thoughts for our third symptom of the Zombie Brain: Long Term Memory Loss

Zombie Brain: Lumbering Walk

This is part three of our multi-day series on The Zombie Brain. Be sure to visit Oscillatory Thoughts tomorrow for symptom 3!

Symptom 2: Lumbering walk

As soon as zombies rise from the dead, they begin walking. Well not walking... more like lumbering. Each step is slow and arduous. Their stance is wide and steady. This presents us with a very important clue about their brains.

Now a lot has been said about the origins of the zombie “walk.” Given the pervasiveness of the disease, some have argued that zombie movements are like those seen in Parkinson’s disease. Parkinson’s is a devastating neurodegenerative disorder caused by the loss of dopamine neurons in the brain that project to a group of regions collectively known as the basal ganglia. It is partly characterized by a slow decrease in the coordination and ability to move (not spastic, jerking movement as is stereotyped... that’s a side effect from the medications).

However, consider this, persons afflicted with this disease will shuffle when they walk, adopting short sliding movements, and a hunched posture. Shaking and tremors are also present while patients are not moving. This does not sound like the zombie movements we see on the silver screen. Zombies can move quickly when striking and show no signs of a hunched posture or tremor. Therefore, we believe that it’s time to do away with the basal ganglia theory of zombie locomotion!

Example of a Parkinsonian Gait (skip to 0:30 mark)

The lumbering zombie walk more resembles the movements characterized by damage to an area of the brain called the cerebellum.* The cerebellum is a little cauliflower shaped region at the back and base of your brain.

It is involved in many functions (e.g., learning, language, memory, sensations), however it is classically described as a motor coordination region. Indeed, this “little brain” has about half of the neurons in your entire brain!

Example of Cerebellar Ataxia Gait

Patients with degeneration of the cerebellum exhibit a syndrome referred to as spinocerebellar ataxia, which is characterized by uncoordinated movements of many kinds, including a wide-stance and lumbering walk.

Although patients with cerebellar ataxia exhibit many coordination problems, the symptoms are alleviated somewhat with the assistance of vision. This may be another important clue about the zombie brain.

Thus, we contend that zombies suffer from a severe spinocerebellar ataxia.  Well, the “slow zombies” do, at least.

What about fast zombies? Given the terrifyingly coordinated movements that “fast zombies” exhibit (think 28 Days Later or the recent remake of Dawn of the Dead) their cerebellums are likely intact. Thus we can also begin to develop neurological classifications of different subtypes of the zombie disorder that may give important clues to the etiology of the zombie epidemic.

* Truth be told, when we had the opportunity to ask George Romero why he made his ghouls walk they way they did in the Living Dead Movies, he responded “They’re suppose to be dead. They’re stiff. That’s how you’d walk.” Not quite the answer that appeals to our neuroscience instincts, but a good alternative hypotheses to test in the next zombie apocalypse.  Check out part of the interview below.

Symptom 1: Impulsive-Reactive Aggression

Be sure to head over to Oscillatory Thoughts for our first symptom of the Zombie Brain.

The Living Dead Brain: What Forensic Neuroscience Can Tell Us about the Zombie Brain

Dr. Timothy Verstynen & Dr. Bradley Voytek, Zombie Research Society

This is a cross-post between Oscillatory Thoughts and Cognitive Axon. Stay tuned to both sites over the following days leading up to Halloween for updates on our model of the zombie brain.




What can neuroscience teach us about surviving the zombie apocalypse?

What makes a zombie a zombie or, more importantly, what makes a zombie not a human? Philosophers contend that a zombie lacks that qualia of experience that belies normal consciousness.

However this is a less than satisfying explanation for why the lumbering, flesh eating creatures are pounding outside the door of your country farmhouse.

Beyond the (currently) immeasurable idea of consciousness or the whole supernatural “living dead” theory, zombies are characterized primarily by their highly abnormal but stereotyped behaviors. This is particularly true in more modern manifestations of the zombie genre wherein zombies are portrayed not as the reanimated dead, but rather as living humans infected by biological pathogens. They are alive, but they are certainly not like us.

Neuroscience has shown that all thoughts and behaviors are associated with neural activity within the brain. Therefore, it should not be surprising that the zombie brain would look and function differently than the gray matter contained in your skull. Yet, how would one know what a zombie brain looks like?

Luckily, the rich repertoire of behavioral symptoms shown in cinema gives the astute neuroscientist or neurologist clues as to the anatomical and physiological underpinnings of zombie behavior. By taking a forensic neuroscience approach, we can piece together a hypothetical picture of the zombie brain.

Over the course of the next week, Oscillatory Thoughts and Cognitive Axon will team up to show our hypothetical model of the zombie brain. Each day we will present a new "symptom" associated with a zombie behavior and show its neural correlates in our simulated zombie brain.

This entire endeavor is partly an academic "what if" exercise for us and partly a tongue-in-cheek critique of the methods of our profession of cognitive neuroscience. We’ll be breaking up the workload and alternating days (hey... we gotta work our real jobs too) so be sure to check both places for the newest updates on zombie neuroscience.

DISCLAIMER: We need to be very clear on one point. While we sometimes compare certain symptoms in zombies to real neurological patient populations, we are in no way implying that patients with these other disorders are in some way “part zombie”. Neurological disorders have provided critical insights into how the brain gives rise to behavior and we bring them up for the sake of illustration only. Their reference in this context is in no way meant to diminish the devastating impact that neurological diseases can have on patients and their caregivers.

When good science is used badly

In a recent New York Times op-ed piece, branding guru and self-described scientist Martin Lindstrom gives a perfect example of why scientific tools should only be used by professional scientists and not self-trained hacks.  In his article titled "You love your iPhone. Literally." Mr. Lindstrom made the case that we are not addicted to our smart phones, but that we have established a relationship with our technology that is on par with the process of "love."

Mr. Lindstrom would have you believe that he's not just giving his professional opinion as a marketing consultant, but that he has scientific data to validate this claim.  However let's take a close look at these spurious claims.

First, Mr. Lindstrom describes an imaging experiment that he undertook to see if marketed brand names engage the same brain circuits as religious symbols.

"A few years back, I conducted an experiment to examine the similarities between some the world’s strongest brands and the world’s greatest religions. Using functional magnetic resonance imaging (fMRI) tests, my team looked at subjects’ brain activity as they viewed consumer images involving brands like Apple and Harley-Davidson and religious images like rosary beads and a photo of the pope. We found that the brain activity was uncannily similar when viewing both types of imagery."

To someone who doesn't live in the world of brain images all day (like I do), this sounds pretty promising right?  You might think, "Huh? My brain is activated the same way when I see the Apple logo as when I see the Madonna of Brugges."  But that is nowhere close to what these results reflect.  Now I haven't seen the details of his study, so I can't lay claim to the soundness of his methodologies.  However, I can point out two major inconsistencies in his interpretations.

First, seeing "uncannily similar" brain areas engaged when seeing objects and religious symbols is not that surprising. It's not surprising that visual symbols are encoded in the same brain networks.  They're visual stimuli with interpretive meaning.  But that doesn't mean that you value them the same way.  A symbol may just be a symbol as far as the brain is concerned.

Second, Mr. Lindstrom is committing one of the most basic of scientific fallacies.  Not detecting a difference between two conditions isn't the same thing as there not being a difference.  It is called "arguing the null hypothesis".  In science we can't say anything definitive about differences that we don't see, only difference that we do.  Just because monkeys and children pick their noses at the same rate does not mean that they're the same creature.  But this is essentially Mr. Lindstrom's conclusion.

Okay, so he's a bad fMRI researcher.  Big deal... there are a lot of them these days.  Let's look at some of Mr. Lindstrom's other data.

"...I gathered a group of 20 babies between the ages of 14 and 20 months. I handed each one a BlackBerry. No sooner had the babies grasped the phones than they swiped their little fingers across the screens as if they were iPhones, seemingly expecting the screens to come to life."

This again is wrong in so many ways.  As anyone who has ever interacted with children can tell you, they aren't the most coordinated of folks.  In fact the brain systems that regulate our movements aren't fully developed until you're almost a teenager.  Did Mr. Lindstrom give phones to children from countries where iPhones aren't as common for a control group?  Presumably not, but that would be one way to see whether this behavior is just random grasping from people without fully formed cerebellums.

Perhaps most importantly, children imitate adults.  They adopt the behaviors of the people around them as a way of learning the world.  That's a key part of development (as evidenced by these two kids who obviously don't know how to speak, but sure know how to act like it). Just because children are imitating their parents doesn't mean that they value them in the same way as Mr. Lindstrom appears to be suggesting.

Finally, and perhaps most egregiously, Mr. Lindstrom reports on yet another brain imaging study.  In this case he presented either a visual movie of a ringing phone or the sound of a ringing phone.  

"In each instance, the results showed activation in both the audio and visual cortices of the subjects’ brains. In other words, when they were exposed to the video, our subjects’ brains didn’t just see the vibrating iPhone, they “heard” it, too; and when they were exposed to the audio, they also “saw” it. This powerful cross-sensory phenomenon is known as synesthesia."

Had Mr. Lindstrom bothered to go to Wikipedia, he would know that this effect is not synesthesia.  Synesthesia is an inherent, hard-wired "cross connection" in the brain.  It's not learned.

What Mr. Lindstrom is in fact reporting is the very simple result of Hebbian learning: "neurons that fire together wire together."  Seeing visual areas light up with certain auditory (or tactile) stimulation is a fairly commonplace finding in the brain imaging literature.  We often both see the phone light up (or vibrate) and hear it ringing at the same time.  Eventually an association is formed within the brain.  Mr. Lindstrom would probably see the same thing if he showed his subjects a picture of a baby crying, a doorbell, etc.

Finally, there's this last bit of "evidence" (quotes are mine).

"But most striking of all was the flurry of activation in the insular cortex of the brain, which is associated with feelings of love and compassion. The subjects’ brains responded to the sound of their phones as they would respond to the presence or proximity of a girlfriend, boyfriend or family member."

There are a host of other areas that are also associated with "love and compassion" in the brain.  There's not one single area that encodes these concepts.  As far as I know, there is no definitive conclusion about where the concept of "love" is encoded in the brain.

So this becomes a guilt by association conclusion: brain area A is active when experiencing X and Y, therefore X is the same as Y (or worse, X causes Y). If Mr. Lindstrom had seen the same area of the brain engaged when he presented an image of a fire-truck and an image of a t tomato, it doesn't mean that your brain thinks of the truck as being made of tomatos (nor that tomatoes are baby fire-trucks).  Sadly, this is a fallacy that many established neuroscientists also make.  But that's a topic of another post.

As a professional neuroscientist, my reaction to the findings Mr. Lindstrom presents in his op-ed is "So what?" Nothing he reports provides a shred of evidence that we "love" our iPhones, at least neuroscientifically speaking. Nor does he show that the experience of using your smart phone is the same as falling in love or having a religious experience.  All Mr. Lindstrom demonstrated was what can happen when the tools of sciences are placed in the wrong hands.

Perhaps all neuroimaging articles should come with the disclaimer: "Performed by trained professionals, do not try this at home."