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Deconstructing the most sensationalistic recent findings in Human Brain Imaging, Cognitive Neuroscience, and Psychopharmacology

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    New in the journal journal Cortex: four shocking cases of practicing medicine while exhausted  (Dharia & Zeman, 2016). The authors called this newly discovered syndrome “fatigue amnesia.” Why this is is any different from countless other examples of not remembering things you did while exhausted I do not know. Except amnesia for performing a complex medical procedure is a lot more disturbing than forgetting you did the dishes the night before.

    Here are the cases in brief:
    Case 1:  A consultant geriatrician, while working as house officer, treated a patient with chest pain and severe pulmonary oedema in the middle of night. She made an entry in the notes, demonstrating successful initial memory acquisition. She does not remember going to bed that night. On the ward round on the following morning the patient was pointed out to her but she had no recollection of seeing the patient or writing the note.

    Case 2: A senior house officer, now a consultant neurologist, went to bed in the early hours after a busy shift. She was woken soon afterwards to manage a patient with cardiac arrest. The resuscitation was complex and included an intracardiac adrenaline injection. She documented events in the medical notes immediately, demonstrating successful initial memory acquisition. She returned to bed. She was told on the morning ward round that the patient was well and had his breakfast following the cardiac arrest. She was startled by this information, as she had no recollection of the previous night's events.

    Case 3: A consultant microbiologist who was working on a night shift as a house officer clerked in a patient at 11:00 pm and continued to work thereafter throughout the night. On the morning ward round when the patient was pointed out to her she had no recollection of seeing or managing him.

    Case 4: A paediatrician reported memory loss for a complex decision made and instructions given over the phone. While working as a registrar he went to bed in the early hours of morning when on call. He was woken by a call about a complex patient. He went to the ward soon afterwards to find out that the trolley was laid out for Swan Ganz catheterisation. Although he was assured that he had done so, he did not remember giving instructions to prepare the trolley.

    The incidents were not due to alcohol or drugs. Long hours and sleep deprivation were to blame. And fortunately, the amnesic episodes were isolated and did not recur in any of the doctors. Dharia & Zeman (2016) suggested that:
    While the resulting memory gaps can reasonably be described as resulting from a ‘transient amnesic state', the evidence from the medical notes suggest that this phenomenon reflects a novel form of accelerated long-term forgetting (Elliott, Isaac, & Muhlert, 2014), whereby a memory for events is acquired normally but then decays more rapidly than usual.

    Sleep Blogging

    By tomorrow, I will have forgotten that I wrote this...


    Reference

    Dharia, S., & Zeman, A. (2016). Fatigue amnesia Cortex DOI: 10.1016/j.cortex.2016.03.001

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    Recent studies of transcranial electrical stimulation in human cadaver heads showed a 90% loss of current when delivered through the skin (Buzsáki, 2016 CNS meeting).



    This is the one song everyone
    would like to learn: the song
    that is irresistible:

    the song that forces men
    to leap overboard in squadrons
    even though they see the beached skulls

    the song nobody knows
    because anyone who has heard it
    is dead, and the others can't remember.



    Better living through electricity. The lure of superior performance, improved memory, and higher IQ without all the hard work. Or at least, in a much shorter amount of time.

    Transcranial direct current stimulation (tDCS), hailed as a “non-invasive”1 way to alter brain activity,2 has been hot for years. In fact, peak tDCS is already behind us, with a glut of DIY brain stimulation articles in places like Fortune, CBC, Life Hacker, New Statesman, Wall Street Journal, Wired, Slate, Medical Daily, Mosaic, The Economist, Nature, IEEE Spectrum, and The Daily Dot.

    Simply apply a weak electrical current to your head via a pair of saline soaked sponges connected to a 9 volt battery. Current flows between the positive anode, or stimulating electrode (in blue below), and the negative cathode (in red below). Low levels of electrical stimulation travel through the scalp and skull to a region of cortex underneath the anode. Modeling studies suggest that the electric field generated by tDCS in humans is about 1 mV/mm (Neuling et al., 2012). The method doesn't directly induce spiking (the firing of action potentials), but it's thought to alter neuronal excitability. By facilitating neuroplastic changes during cognitive training, tDCS may improve learning, memory, mental arithmetic, and target detection.



    Modified from Fig. 1b (Dayan et al., 2013). Bipolar tDCS electrode configuration, with one electrode over left dorsolateral prefrontal cortex and a reference electrode over the contralateral supraorbital region. 


    And there you have it. High tech performance enhancement for less than $40. Or a siren song for wannabe brain hackers?

    In Symposium Session 7 of the Cognitive Neuroscience Society meeting last week, Dr. György Buzsáki threw a bit of cold water on non-invasive transcranial electrical stimulation (TES) methods, which include tDCS and transcranial alternating current (tACS).




    My understanding of his remarks: Studies of transcranial electrical stimulation (TES) in human cadaver heads showed there's a 90% loss of current when delivered through the skin (which is obviously the case in living humans) vs. through the skull. This implies that a current of at least 5 mA on the scalp would be necessary to generate a 1 mV/mm electric field in the human brain. Based on his personal experience, Dr. Buzsáki reported that 4 mA was hard to tolerate even with anesthetized skin. For comparison, 2 mA is the maximum current recommended by an international panel of experts.

    Others in the audience had similar interpretations:




    This revelation was in the context of work on focused beam stimulation, which is designed to improve the spatial selectivity of TES (Voroslakos et al., 2015):
    We recorded TES-generated field potentials in human cadavers and anesthetized rats. Stimulation was applied by placing Ag/AgCl EEG electrodes over the external surface of the skull.  ... We also measured the shunting effect of the skin during transcutaneous stimulation. In addition to our earlier results, we found that the skin dramatically reduced the generated intracranial electric fields, and alters its geometry.



    image via Sue Peters, @nomorewires


    In turn, the cadaver studies were an extension of very cool research on Closed-Loop Control of Epilepsy by Transcranial Electrical Stimulation. This paper used a rodent model of generalized epilepsy to test a system that (1) records neural activity and (2) triggers TES to quell abnormal activity once it is detected.

    Having such a system that works in humans would be a huge advance for those who suffer from intractable seizures. Human heads are very different from rat heads, hence the need for human cadavers. And hence the bombshell that 1-2 mA current may have less of an effect on neurons than previously expected.

    “But wait!” you say. “Aren't there literally thousands of peer-reviewed articles on tDCS? Surely it must be doing something.”


    How Does It Work?


    Shall I tell you the secret
    and if I do, will you get me
    out of this bird suit?

    –Atwood, Siren Song


    If the effects of tDCS are not directly via neurons, what's the mechanism of action? It's glia! And calcium! Gliotransmission! Maybe.



    “Using a transgenic mouse expressing G-CaMP7 in astrocytes and a subpopulation of excitatory neurons, we find that tDCS induces large-amplitude astrocytic Ca2+ surges across the entire cortex with no obvious changes in the local field potential. Moreover, sensory evoked cortical responses are enhanced after tDCS. These enhancements are dependent on the alpha-1 adrenergic receptor and are not observed in IP3R2 (inositol trisphosphate receptor type 2) knockout mice, in which astrocytic Ca2+ surges are absent. Together, we propose that tDCS changes the metaplasticity of the cortex through astrocytic Ca2+/IP3 signalling.”  (Monai et al., 2016)

    The pre-astrocyte version of purported mechanism based on direct modulation of the affected neurons' resting membrane potential is described in the schematic below (click on image for a larger view).




    But maybe tDCS doesn't really do much in humans after all, as claimed in two recent review articles (Horvath et al., 2015a,b).3

    And remember, transcranial devices are not playthings! (warn Bikson et al., 2013).



    This gentleman discusses his burn injuries at the tDCS reddit.



    Footnotes

    1 But see “Non-invasive” brain stimulation is not non-invasive (Davis & van Koningsbruggen, 2013):
    These techniques [TMS and tCS] have collectively become known as “non-invasive brain stimulation.” We argue that this term is inappropriate and perhaps oxymoronic, as it obscures both the possibility of side-effects from the stimulation, and the longer-term effects (both adverse and desirable) that may result from brain stimulation. 

    2 But see Evidence that transcranial direct current stimulation generates little-to-no reliable neurophysiologic effect beyond MEP amplitude modulation in healthy human subjects: A systematic review (Horvath et al., 2015a):
    Our systematic review does not support the idea that tDCS has a reliable neurophysiological effect beyond MEP amplitude modulation... This work raises questions concerning the mechanistic foundations and general efficacy of this device – the implications of which extend to the steadily increasing tDCS psychological literature.

    3 Not too surprisingly, these papers have not gone unopposed...

    ADDENDUM (April 15 2016)Antal et al. (2015)published one potent rebuttal to Horvath et al. (2015a):

    ...We are concerned about the validity of the conclusions for various reasons. Since this paper reviews a whole field of research and comes to debatable assumptions, it is especially important that basic quality requirements are fulfilled, which is unfortunately not the case.

    First, this review suffers from numerous conceptual flaws and misunderstandings. Second, the work contains relevant design problems, several errors and many incompletely or incorrectly cited data.
    . . .

    In summary, as shown by the examples given above, this review suffers from important flaws with regard to citing and interpreting available literature, non-transparent, and in many cases erroneous data aggregation, citation of study specifics, and discussion of the results.


    References

    Berényi A, Belluscio M, Mao D, Buzsáki G. (2012). Closed-loop control of epilepsy by transcranial electrical stimulation. Science 337(6095):735-7.

    Fertonani A, & Miniussi C (2016). Transcranial Electrical Stimulation: What We Know and Do Not Know About Mechanisms. The Neuroscientist.  PMID: 26873962

    Monai H, Ohkura M, Tanaka M, Oe Y, Konno A, Hirai H, Mikoshiba K, Itohara S, Nakai J, Iwai Y, & Hirase H (2016). Calcium imaging reveals glial involvement in transcranial direct current stimulation-induced plasticity in mouse brain. Nature communications, 7. PMID: 27000523

    M. VOROSLAKOS, A. OLIVA, K. BRINYICZKI, T. ZOMBORI, B. IVÁNYI, G. BUZSÁKI, A. BERÉNYI. (2015). Targeted transcranial electrical stimulation protocols: Spatially restricted intracerebral effects via improved stimulation and recording techniques. Society for Neuroscience. Poster# 257.17/Y3.


    Further Reading

    Invading the brain to understand and repair cognition– CNS Press Release

    When the Hype Doesn’t Pan Out: On Sharing the Highs-and-Lows of Research with the Public– by Jared Cooney Horvath

    Non-invasive direct current brain stimulation for depression: 
the evidence behind the hype– by Camilla Nord and Jonathan Roiser

    Neurostimulation: Bright sparks– by Katherine Bourzac

    DIY tDCS– Keeping Tabs On Transcranial Direct Current Stimulation

    Why 2.0 mA as the limit for TDCS?– reddit thread

    Brunoni AR, Nitsche MA, Bolognini N, Bikson M, Wagner T, Merabet L, Edwards DJ, Valero-Cabre A, Rotenberg A, Pascual-Leone A, Ferrucci R, Priori A, Boggio PS, Fregni F. (2012). Clinical research with transcranial direct current stimulation (tDCS): challenges and future directions. Brain Stimul. 5(3):175-95.

    Davis NJ. (2016). The regulation of consumer tDCS: engaging a community of creative self-experimenters. Journal of Law and the Biosciences. Apr 5:lsw013.

    Davis NJ, van Koningsbruggen MG. (2013). "Non-invasive" brain stimulation is not non-invasive. Front Syst Neurosci. 7:76.

    Dayan E, Censor N, Buch ER, Sandrini M, Cohen LG. (2013). Noninvasive brain stimulation: from physiology to network dynamics and back. Nat Neurosci. 16(7):838-44.

    Edwards D, Cortes M, Datta A, Minhas P, Wassermann EM, Bikson M. (2013). Physiological and modeling evidence for focal transcranial electrical brain stimulation in humans: a basis for high-definition tDCS. Neuroimage 74:266-75.

    Horvath JC, Forte JD, Carter O. (2015a). Evidence that transcranial direct current stimulation (tDCS) generates little-to-no reliable neurophysiologic effect beyond MEP amplitude modulation in healthy human subjects: A systematic review. Neuropsychologia 66:213-36.

    Horvath JC, Forte JD, Carter O. (2015b). Quantitative Review Finds No Evidence of Cognitive Effects in Healthy Populations From Single-session Transcranial Direct Current Stimulation (tDCS). Brain Stimul. 8(3):535-50.

    Kuo MF, Nitsche MA. (2012). Effects of transcranial electrical stimulation on cognition. Clin EEG Neurosci. 43(3):192-9.

    Parkin BL, Ekhtiari H, Walsh VF. (2015). Non-invasive human brain stimulation in cognitive neuroscience: a primer. Neuron 87(5):932-45.

    Santarnecchi E, Brem AK, Levenbaum E, Thompson T, Kadosh RC, Pascual-Leone A. (2015). Enhancing cognition using transcranial electrical stimulation. Current Opinion Behav Sci. 4:171-8.

    Woods AJ, Antal A, Bikson M, Boggio PS, Brunoni AR, Celnik P, Cohen LG, Fregni F, Herrmann CS, Kappenman ES, Knotkova H, Liebetanz D, Miniussi C, Miranda PC, Paulus W, Priori A, Reato D, Stagg C, Wenderoth N, Nitsche MA. (2016). A technical guide to tDCS, and related non-invasive brain stimulation tools. Clin Neurophysiol. 127(2):1031-48.

    MORE! (added April 15 2016): Two recent meta-analyses on tDCS and working memory reported “a mix of significant and nonsignificant small effects” and “some evidence of a beneficial effect ... [but] the small effect sizes obtained, coupled with non-significant effects on several analyses require cautious interpretation” (respectively):

    Mancuso LE, Ilieva IP, Hamilton RH, Farah MJ. Does Transcranial Direct Current Stimulation Improve Healthy Working Memory?: A Meta-analytic Review.J Cogn Neurosci. 2016 Apr 7:1-27. [Epub ahead of print]

    Hill AT, Fitzgerald PB, Hoy KE. Effects of Anodal Transcranial Direct Current Stimulation on Working Memory: A Systematic Review and Meta-Analysis of Findings From Healthy and Neuropsychiatric Populations. Brain Stimul. 2016; 9(2):197-208.




    I don't enjoy it here
    squatting on this island
    looking picturesque and mythical

    with these two feathery maniacs,
    I don't enjoy singing
    this trio, fatal and valuable.

    I will tell the secret to you,
    to you, only to you.
    Come closer. This song

    is a cry for help: Help me!
    Only you, only you can,
    you are unique

    at last. Alas
    it is a boring song
    but it works every time.


    –Atwood, Siren Song

    from Selected Poems 1965-1975. Copyright © 1974, 1976 by Margaret Atwood. Reprinted with the permission of the author and Houghton Mifflin Company in Poetry (February 1974).


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    image:Mihály Vöröslakos / University of Szeged


    Don't Lose Your Head Over tDCS,” I warned last time. Now the infamous cadaver study has reared its ugly hot-wired head in Science News (Underwood, 2016).

    The mechanism of action of transcranial direct current stimulation (tDCS) had been called into question by Dr. György Buzsáki during his presentation at the Cognitive Neuroscience Society meeting.

    ...Or had it?

    To recap, my understanding was that an unpublished study of transcranial electrical stimulation (TES) in human cadaver heads showed a 90% loss of current when delivered through the skin vs. through the skull. This implies that a current of at least 5 mA on the scalp would be necessary to generate a 1 mV/mm electric field in the human brain. Based on his personal experience, Dr. Buzsáki reported that 4 mA was hard to tolerate even with anesthetized skin. For comparison, 2 mA is the maximum current recommended by an international panel of experts.

    But Dr. Tiziana Metitieri left a comment on my post saying this is nothing new. She translated the remarks of Dr. Carlo Miniussi, who said:
    ...but what is reported appear to me not so “new” (http://www.ncbi.nlm.nih.gov/pubmed/?term=Miranda+PC+2006). Of course, if the findings obtained by Buzsáki are confirmed, you may think that tDCS has an effect nearly homeopathic on the brain. Certainly, these type of research is the most needed: systematic studies of animal and human models, comparable in terms of the amount of current that stimulates the brain. Luckily, they are coming out, or, well, we know they exist and we are waiting to read them, as for Buzsáki.  [read more]

    Why is this important to cognitive neuroscientists? Because the behavioral effects of tDCS have been vastly overstated, according to some investigators (e.g., Horvath et al., 2015), and the “homeopathic” level of brain stimulation is one likely explanation.

    But a common refrain of experts in the field [I am not an expert] is that Buzsáki's results are not surprising the low amount of current is old hat. For instance, Dr. Marom Bikson explained in Science News that...
    ...many in the field already accepted that the 1 or 2 milliamps the methods use don't directly trigger firing. It can make neurons more likely to fire or form new connections, he and others believe. Unlike techniques that rely on magnetic fields or higher current to actively trigger neurons ... tDCS and tACS likely subtly alter ongoing brain activity, Bikson says. Using cadavers to test these methods is a “complicated choice” because dead tissue conducts electricity differently from living tissue, he adds.

    Also quoted is Dr. Vince Clark, who...
    ...has found that applying 2 milliamps of current to a person’s scalp for just 30 minutes can double the speed at which they learn a game in which players must detect a concealed “threat”... Several labs have replicated those results, he says, adding that the idea that 10% or less of the current gets through to the brain is not new, and doesn’t necessarily mean the methods are ineffective. “If it works, you know 10% is enough,” Clark says.

    Although some effects may be replicable, Dr. Vince Walsh dropped a stink bomb by saying that the tDCS field is “a sea of bullshit and bad science—and I say that as someone who has contributed some of the papers that have put gas in the tDCS tank.  ...  It really needs to be put under scrutiny like this.” In Wired, Walsh basically said the reason for the “sea of bullshit and bad science” is that the barrier to enter tDCS research is so darn low.


    When Can TES Influence Spiking?

    Returning to Buzsáki's talk, he mentioned a study in rats (Ozen et al., 2010) where a TES-induced voltage gradient of 1 mV/mm at the recording sites could phase-locked spiking (action potentials). However, the current was delivered via electrodes placed directly on the skull or even the dura covering the brain. The stimulation protocol was low frequency sinusoid patterns that mimic slow cortical oscillations, to entrain neuronal spiking activity. That was the goal in humans, but similar TES applied to the scalp produced no discernible change in oscillatory activity. Hence, the cadaver tests.

    These studies used transcranial alternating current stimulation (tACS), which is designed to influence ongoing cortical oscillations by “entraining” or phase-locking to specific EEG frequency bands (as in Kanai et al., 2008). Buzsáki himself actually commented on the Science piece (which I will quote at length):
    "The real question: Is the current which does reach the brain sufficient to perform this ‘extremely weak coupling’ in neural systems?" This is exactly what we investigated. Since we failed to entrain neuronal activity (local fields) repeatedly in the living human brain with the commonly used current intensities, whereas we were very successful in rodents using stimulation electrodes directly on the bone, we looked for answers. The cadaver is the next best possible thing to a living human brain if one wants to know how the currents are distributed inside the brain. We found that most current is lost by the shunting effect of the extracranial tissue. As a result, the voltage gradients that we measured in the brain were way below the values we found in rodents needed to affect population neuronal oscillations. The weak electric fields were just too weak. Of course, there is the principle of stochastic resonance and thus some super weak effect can have some effects occasionally - we cannot and do not want to deny it, but cannot prove it either, therefore cannot rely on it as an explanation for the reported behavioral effects of TES.

    In his talk he mentioned possible effects on astrocytes, and my previous post cited the study of Monai et al. (2016). In his Science comment Buzsáki said, “Glia may be more sensitive to polarized currents than neurons and muscles.” He also mentioned possible effects on peripheral nerves in the scalp (like the vagus nerve), which is something that Dr. Jamie Tyler (formerly of Thync) has said for years:
    Thync tried to replicate some basic tDCS findings on cognition but could not do so. Dr Tyler now believes that tDCS may not directly stimulate the brain at all but instead modulates cranial nerves in the skull...

    During the discussion period at the CNS meeting, Buzsáki was asked about the phenomenon of DIY tDCS. He compared it to alternative medicine.

    On that note, I'll conclude with a nod to the tDCS reddit community, some of whom didn't trash my last critical post as much as I expected. Yay! Others? Not so much. Boo: “There are so many inaccuracies in this article, I don't know where to begin.” And then they don't bother to begin...

    So any- and all-comers can begin by pointing out my inaccuracies in the comments section of this post.


    References

    Horvath JC, Forte JD, Carter O. (2015). Quantitative Review Finds No Evidence of Cognitive Effects in Healthy Populations From Single-session Transcranial Direct Current Stimulation (tDCS). Brain Stimul. 8(3):535-50.

    Kanai R, Chaieb L, Antal A, Walsh V, Paulus W. (2008). Frequency-dependent electrical stimulation of the visual cortex. Curr Biol. 18(23):1839-43.

    Ozen, S., Sirota, A., Belluscio, M., Anastassiou, C., Stark, E., Koch, C., & Buzsaki, G. (2010). Transcranial Electric Stimulation Entrains Cortical Neuronal Populations in Rats Journal of Neuroscience, 30 (34), 11476-11485. DOI: 10.1523/JNEUROSCI.5252-09.2010

    Underwood, E. (2016). Cadaver study challenges brain stimulation methods. Science, 352 (6284), 397-397 DOI: 10.1126/science.352.6284.397


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    NINETY-TWO percent of retired National Football League players have decreased cognitive function, according to a new study:
    “In the NFL group, baseline neuropsychological assessments showed 92% of players had decreased general cognitive proficiency, 86% had decreased information processing speed, 83% had memory loss, 83% had attentional deficits, and 85% had executive function impairment.”

    The Truth?

    The study reported on a self-selected sample of 161 current and retired NFL players recruited via a blog (“The NFL concealed the danger of brain injuries!!”), the Los Angeles Chapter of the Retired NFL Players Association, The Summit (??), and possibly other sources. Perhaps these players were motivated to participate because they had cognitive complaints, or because they wanted an evaluation in advance of the $1 billion concussion settlement. The League's Baseline Assessment Program is a required part of the settlement.1

    The quote above is the full extent of the report on the players' neuropsychological assessments. These were done using computerized test batteries (MicroCog or WebNeuro), which are largely unknown to most clinical neuropsychologists. Was there an adequately matched control population? What norms were used? They don't say.

    THE TRUTH IS, we don't know the extent of cognitive impairment in these football players, or the percentage of all players who are affected, or the severity of impairment in those who are. This new paper (by Daniel Amen, Bennet Omalu, and others) doesn't give us enough information, but it succeeds in sounding the alarm about the dangers of football and the inevitability of memory loss and attention deficits.

    Are blows to the head bad for your brain? Can repeated concussions cause cognitive impairment and chronic traumatic encephalopathy (CTE)? 2  Yes, almost certainly, but we can't rely on biased samples, appeal to celebrity, and Frontline documentaries (“researchers have identified CTE in 96 percent of NFL players that they’ve examined”) as conclusive scientific evidence. What's needed are better sampling methods (in the short term) and longitudinal studies that follow a diverse cohort over time (in the long term).

    The Scans

    Caption for top figure: SPECT brain scans showing abnormal low blood flow in an NFL player compared to a normal healthy control subject.

    The new paper by Amen et al. (2016) was actually focused on SPECT scans, not surprisingly, since these are the backbone of his business at the Amen Clinics. The article claims “90% sensitivity, 86% specificity, and 94% accuracy” in discriminating NFL players from controls. I won't elaborate here, but check out This Neuroimaging Method Has 100% Diagnostic Accuracy (or your money back) and The Dark Side of Diagnosis by Brain Scan for detailed critiques of the methods used here. I will flag one tiny issue, however:
    “All NFL players were male, while 56% of the control group were women.”

    Why?? The authors have a database of 100,000 SPECT scans...


    Footnote

    1  11. What is the Baseline Assessment Program (“BAP”)?
    . . .
    Retired players who are diagnosed with Level 1 Neurocognitive Impairment (i.e., moderate cognitive impairment) are eligible to receive further medical testing and/or treatment (including counseling and pharmaceuticals) for that condition during the ten-year term of the BAP or within five years from diagnosis, whichever is later.

    14. What diagnoses qualify for monetary awards?
    Monetary awards are available for the diagnosis of ALS, Parkinson’s Disease, Alzheimer’s Disease, Level 2 Neurocognitive Impairment (i.e., moderate Dementia), Level 1.5 Neurocognitive Impairment (i.e., early Dementia) or Death with CTE (the “Qualifying Diagnoses”). A Qualifying Diagnosis may occur at any time until the end of the 65-year term of the Monetary Award Fund.

    2ADDENDUM (May 1 2016): I should say, “...cause CTE and/or other neurodegenerative disorders and dementias.”

    Also see: Here’s What We Don’t Know About Head Injuries And Sport
    ...and A Clinical Approach to the Diagnosis of Traumatic Encephalopathy Syndrome



    Reference

    Daniel G. Amen, Kristen Willeumier, Bennet Omalu, Andrew Newberg, Cauligi Raghavendra, & Cyrus A. Raji (2016). Perfusion Neuroimaging Abnormalities Alone Distinguish National Football League Players from a Healthy Population Journal of Alzheimer's Disease : 10.3233/JAD-160207




    Caption (from press materials): SPECT brain scans showing improvement of abnormal low blood flow in an NFL player compared after 3.5 months on a customized brain rehabilitation program.

    ADDENDUM #2 (May 1 2016): The authors'Conflict of Interest statements.

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    When you hear the word “apple”, do you picture a Red Delicious apple or a green Granny Smith? Or neither, because you can't conjure up a visual image of an apple (or of anything else, for that matter)?
    Aphantasia is the inability to generate visual images, which can be a congenital condition or acquired after brain injury (Farah, 1984). The most striking aspect of this variation in mental life is that those of us with imagery assume that everyone else has it, while those without are flabbergasted when they learn that other people can “see” pictures in their head.

    Programming prodigy Blake Ross created a sensation recently with his eloquent essay on what's it's like to discover that all your friends aren't speaking metaphorically when they say, “I see a beach with waves and sand.”

    Aphantasia: How It Feels To Be Blind In Your Mind

    I just learned something about you and it is blowing my goddamned mind.
    . . .

    Here it is: You can visualize things in your mind.

    If I tell you to imagine a beach, you can picture the golden sand and turquoise waves. If I ask for a red triangle, your mind gets to drawing. And mom’s face? Of course.
    . . .

    I don’t. I have never visualized anything in my entire life. I can’t “see” my father’s face or a bouncing blue ball, my childhood bedroom or the run I went on ten minutes ago. I thought “counting sheep” was a metaphor. I’m 30 years old and I never knew a human could do any of this. And it is blowing my goddamned mind.

    It's worth reading Ross's account in its entirety to gain insight into the vast individual variation in our internal mental lives.

    Although the term aphantasia is new (coined by Zeman et al., 2015), the condition isn't; Francis Galton published a paper on the Statistics of Mental Imagery in 1880. Similar to Ross, many of Galton's s friends (male scientists) were shocked to learn that others had imagery:1 
    To my astonishment, I found that the great majority of the men of science to whom I first applied, protested that mental imagery was unknown to them, and they looked on me as fanciful and fantastic in supposing that the words 'mental imagery' really expressed what I believed everybody supposed them to mean. They had no more notion of its true nature than a colour-blind man who has not discerned his defect has of the nature of colour. They had a mental deficiency of which they were unaware, and naturally enough supposed that those who were normally endowed, were romancing.

    The nature of mental images has been a topic of philosophical debate in cognitive science since the 1970s. Are mental images quasi-perceptual representations that activate visual areas of the brain (Kosslyn and colleagues), or non-pictorial, abstract, symbolic descriptions (Zenon Pylyshyn)? The Stanford Encyclopedia of Philosophy's entry on Mental Imagery provides an indispensable background on the philosophical, theoretical, and empirical debates in the field. As well, extensive research on individual differences in mental imagery (e.g., Kosslyn et al., 1984) can inform new studies on aphantasics.


    Aphantasia and Paivio's Dual Coding Theory

    To investigate the role of imagery in verbal memory, I propose a return to classic cognitive psychology experiments of the 1970s. Alan Paivio's Dual Coding Theory specifies two types of mental representations, or codes, for words and mental images (Paivio, 1971). The verbal code and imagery code are both activated by pictures, which can account for the picture superiority effect: pictures are better remembered than their verbal referents (i.e., words). The picture superiority effect should be abolished in those who cannot generate visual images.2

    Even more interestingly, words that are highly imageable (concrete nouns like elephant) are better remembered than words that are rated low in imageability (abstract nouns like criterion). The original ratings from 1968 and the expanded 2004 version (concreteness, imageability, meaningfulness, familiarity) are available online: Clark and Paivio (2004) Norms. Lists of high and low imageable nouns that are carefully matched on other lexical factors (e.g., number of letters, word frequency, complexity) can be presented in a memory test. The recognition memory (or free recall) advantage for concrete, highly imageable words should be diminished or abolished in relation to self-reported imagery abilities.

    I believe this experiment would address the objection of psychogenic aphantasia (“refusing to imagine”), because the concreteness advantage (using imagery during encoding) could not be mobilized as an explicit (or perhaps implicit) strategy. Given the hundreds (if not thousands) of Aphantasics who have made blog comments, joined Facebookgroups and other communities, taken surveys, and of course contacted Dr. Zeman, the sample size might be quite respectable.





    Footnote

    1Aphantasia seems bizarrely overrepresented in Galton's cronies. Here's his explanation:
    My own conclusion is, that an over-readiness to perceive clear mental pictures is antagonistic to the acquirement of habits of highly generalised and abstract thought, and that if the faculty of producing them was ever possessed by men who think hard, it is very apt to be lost by disuse. The highest minds are probably those in which it is not lost, but subordinated, and is ready for use on suitable occasions. 
    2Of note here, some with aphantasia report severe deficits in autobiographical memory.


    References

    Farah MJ. (1984). The neurological basis of mental imagery: A componential analysis. Cognition 18:245-72.

    GALTON, F. (1880). I.--STATISTICS OF MENTAL IMAGERY Mind, os-V (19), 301-318 DOI: 10.1093/mind/os-V.19.301

    Kosslyn SM, Brunn J, Cave KR, Wallach RW. (1984). Individual differences in mental imagery ability: a computational analysis. Cognition 18:195-243.

    Paivio A. (1969). Mental imagery in associative learning and memory. Psychological Review 76: 241-263.

    Paivio A. (1971, 2013). Imagery and verbal processes. Holt, Rinehart & Winston / Psychology Press.

    Zeman, A., Dewar, M., & Della Sala, S. (2015). Lives without imagery – Congenital aphantasia Cortex, 73, 378-380 DOI: 10.1016/j.cortex.2015.05.019


    ADDENDUM (May 7 2016): via @vaughanbell, a new review article by the University of Exeter group (part of their project, The Eye's Mind):

    MacKisack M, Aldworth S, Macpherson F, Onians J, Winlove C, Zeman A. (2016). On Picturing a Candle: The Prehistory of Imagery Science. Front Psychol. 7:515.

    Not only Galton, Paivio, Kosslyn, and Pylyshyn but also Aristotle, Plato, Thomas Aquinas, and more.


    - click on image for a larger view -


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    Left: Belgian physician Dr. Wim Distelmans, a cancer specialist, professor in palliative care and the president of the Belgian federal euthanasia commission.Right: Generic acetaminophen.


    What (or who) is an “Empathy Killer“? An Angel of Death Kevorkian-type who helps terminally ill patients with ALS or cancer put an end their excruciating pain? This is a very selfless act that shows extreme empathy for the suffering of others.

    Or is an “Empathy Killer” a medication that dulls your numerical ratings of empathic concern for fictional characters ever so slightly? If you guessed the latter, you are correct. Here's the actual title of a new paper in SCAN: “From Painkiller to Empathy Killer: Acetaminophen (Paracetamol) Reduces Empathy for Pain.”

    Oh the headlines. Truly painful.

    Paracetamol doesn't just kill pain - it makes us less CARING

    America's Most Common Drug Ingredient Could Be Making You Less Empathetic


    Why Would a Headache Medication Make You Less Empathetic?

    A popular line of research in Social Cognitive and Affective Neuroscience examines the commonalities between physical and social/psychological pain. IFthere is indeed an overlap,1 one might ask some provocative questions about the underlying neural mechanisms. Do drugs that ease physical pain also soothe the pain of social rejection and existential angst?2 Several recent papers have reported that acetaminophen does exactly that (Dewall et al., 2010; Randles et al., 2013; Durso et al., 2015) although some pundits may beg to differ.3

    The latest psychological study on this popular over-the-counter painkiller looks at empathy for another person's pain (Mischkowski et al., 2016). This work is based on the premise that the same neural machinery responsible for feeling our own physical and psychological pain (ACC, AI, mirror neurons don't ask but see Zaki et al., 2016) is invoked when observing the pain of others.


    The Mystery of the Sliding Scales

    [NOTE: Perceived Pain scores standardized in Tables 1, 3, 4 but not Table 2]

    Can Tylenol (aka Parecemetol) lessen the pain you feel for others? I'll go out on a limb here and say probably not. Or not much, especially in a real-world sense. Here's why.

    First, you have to understand that the experimental ratings of empathy were based on two different scales that varied from 1 (No pain at all) to 5 (Worst possible pain) OR from -4 (Worst possible pain) to +4 (Most possible pleasure). For the latter scale, the authors “reverse-coded participants’ ratings, so higher ratings indicated higher empathy for pain.”

    Participants in Experiment 1 were given a placebo drink (n=40) or 1000 mg liquid acetaminophen (n=40). An hour later, they read short scenarios depicting other people in physical pain (e.g., cutting a finger) or social pain (e.g., getting rejected from college). Two major scores were obtained for perceived pain and personal distress. My reading is that these should yield a mean score between 1 and 5 for each measure.

    ADDENDUM (May 18 2016): As pointed out by two Anonymouscommenters, the Perceived Pain scores were standardized in Table 1. The same measure was not standardized in Table 2.

    PERCEIVED PAIN For each scenario, we measured perceived pain with two measures. First, participants rated the pain of each protagonist using a scale from 1 (No pain at all) to 5 (Worst possible pain). Second, participants rated on three items how much each protagonist felt hurt, wounded, and pained on scales ranging from 1 (Not at all) to 5 (Extremely). We averaged items to create perceived hurt feeling measures across physical and social pain scenarios... Within each scenario type, both perceived pain ratings correlated highly... Therefore, we standardized and averaged these measures into indices of perceived physical and social pain.

    PERSONAL DISTRESS Participants also rated their personal distress when reading each scenario. On a scale from 1 (Not at all) to 5 (Extremely), participants rated the extent to which they felt uncomfortable, pained, bothered, unpleasant, distress, as well as wanted to cringe while imagining the feelings of each scenario protagonist. We averaged items to create separate personal distress measures for physical and social pain scenarios...

    My guess is that the authors made a mistake in their Tables, or else I misunderstood the scoring scheme. Let's take a look (click on image for a larger view).




    For the first Dependent Variable, participants rated their own positive and negative feelings on the PANAS. General Affect ratings didn't differ between drug and placebo.

    Next, look at Perceived Pain for Physical Pain Scenarios and Social Pain Scenarios. I won't belabor the p values here. Instead, focus on the red rectangles.[My mistake, Perceived Pain scores were standardized in Table 1. However, this does not affect my next comment.]These values are both close to zero (perhaps not significantly different from zero). But they don't seem to be on the 1 to 5 scale described above. The Personal Distress values ranged from “kind of a little bit” distressed for drug (2.15 and 2.00) to “kind of a little bit more” distressed for placebo (2.75 and 2.45). The participants who received acetaminophen are hardly in the land of the cruel and heartless psychopath. How much would these slight variations in personal distress ratings translate to real world empathy? We simply don't know.

    Next, let's figure out the sliding scale issue. In Experiment 2:
    Participants read the same eight physical and social pain empathy scenarios as in Experiment 1. After reading each scenario, participants rated perceived pain of the protagonist, using a scale from -4 (Worst possible pain) to +4 (Most possible pleasure). We reverse-coded participants’ ratings, so higher ratings indicated higher empathy for pain.

    So here we have a scale that does include negative numbers, perhaps that scale was used for Perceived Pain in Exp. 1. Except ratings in Exp. 2 seems to use the 1 to 5 scale? It's hard to tell at this point. [Perceived Pain scores were not standardized in Table 2.] At any rate, the differences are small, and not significant for some of the comparisons.



    There were other conditions involving noise blasts and watching a person being excluded from a round of cyberball (an old-school ball-tossing video game). Some of the values here were confusing as well. Or maybe I'm just confused... [Yes, I was confused. Perceived Pain scores were standardized in Tables 3 and 4.]


    Noise blasts rated on a scale from 1 (Not unpleasant at all) to 10 (Extremely unpleasant).


    Once again, in Table 4 we see mean values for Perceived Pain that are very close to zero. What does it mean? I will be happy to correct any erroneous interpretations of these Tables.

    Now that I have corrected my mistakes, I still think it's hyperbole to say these differences mean that acetaminophen is an empathy killer in real life.

    Neuroskeptic points out
    Something odd about some of the datapoints... In Table 1, the mean for "perceived pain" for placebo is equal to the mean for acetaminophen * -1 (e.g. 0.22 vs -0.22, 0.19 vs. -0.19). The same is true in Table 4, two different values (e.g. 0.06 vs. -0.06, 0.04 vs -0.04).




    Furthermore, does an Empathic Concern for Ostracized Player score of 1.68 (compared to 2.05) mean you're a less caring person? That acetaminophen has dulled your empathy? An empathy score of 2.05 (out of 5) while on placebo isn't exactly a heart-rending level of concern...




    I could be wrong, but I don't think the Tylenol-fueled collapse of civilization is neigh. Next up? Ibuprofen! 4


    Footnotes

    1 Many have argued that the physical-emotional pain isomorphism is vastly overstated (e.g., Hayes and Northoff, 2012; The Neurocritic, 2012; Iannetti et al., 2013; Woo et al., 2014; Wager et al., 2016).

    2Well sure, you say, people have been self-medicating with opiates and alcohol for centuries. BUT here I mean mild nonprescription medications not known for having psychoactive properties.

    3 Yeah, I've written about this a lot.

    Tylenol Doesn't Really Blunt Your Emotions

    Suffering from the pain of social rejection? Feel better with TYLENOL®

    Existential Dread of Absurd Social Psychology Studies

    Does Tylenol Exert its Analgesic Effects via the Spinal Cord?

    Vicodin for Social Exclusion

    4 I've wanted to see that study foryears.


    References

    Dewall CN, Macdonald G, Webster GD, Masten CL, Baumeister RF, Powell C, Combs D, Schurtz DR, Stillman TF, Tice DM, Eisenberger NI. (2010). Acetaminophen reduces social pain: behavioral and neural evidence. Psychological Science 21:931-937.

    Durso G, Luttrell A, Way B. (2015). Over-the-Counter Relief From Pains and Pleasures Alike: Acetaminophen Blunts Evaluation Sensitivity to Both Negative and Positive Stimuli.Psychological Science 26:750-758.

    Mischkowski, D., Crocker, J., & Way, B. (2016). From Painkiller to Empathy Killer: Acetaminophen (Paracetamol) Reduces Empathy for Pain. Social Cognitive and Affective Neuroscience DOI: 10.1093/scan/nsw057

    Randles D, Heine SJ, Santos N. (2013). The common pain of surrealism and death: acetaminophen reduces compensatory affirmation following meaning threats. Psychological Science 24:966-73.

    Zaki J, Wager TD, Singer T, Keysers C, Gazzola V. (2016). The Anatomy of Suffering: Understanding the Relationship between Nociceptive and Empathic Pain. Trends Cogn Sci. 20(4):249-59.


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    You may have seen headlines such as: Florida Man Woke Up In A Motel Room Speaking Only Swedish. Or: Englishman wakes up speaking Welsh after stroke (“Rare brain disorder left English-speaking Alun Morgan only able to communicate in Welsh”). The first case was likely due to a fugue state, a type of dissociative disorder involving loss of personal identity and aimless wandering (Stengel, 1941). The second seems like an unusual example of bilingual aphasia involving loss of the ability to speak one's native language (rather than the more commonly affected second language).

    Perhaps you've even seen paranormal claims like:

    Under Hypnosis or Past Life Regression, A Physician's Wife Starts Speaking Swedish

    . . .  In sessions conducted from 1955 to 1956, when Tania was under hypnosis, a personality emerged who spoke Swedish, a language that neither Tania nor Ken knew. As such, this represents a case of xenoglossy, where an individual can speak a language that has not been learned through normal means.

    Tania was born in Philadelphia and as such, English was her native language. Her parents, who were Jewish, were born in Odessa, Russia. No one in the family had ever been to Scandinavia and they knew no one who could speak Swedish.

    Xenoglossy is “the putative paranormal phenomenon in which a person is able to speak or write a language he or she could not have acquired by natural means.” Of course, there's always a logical explanation for such cases, but magical thinking leads people to believe that such phenomena are proof of past lives and reincarnation.


    A New Case of False Xenoglossy

    An amusingly written clinical report describes a 50 year old Italian man who stopped speaking his native Italian and insisted on speaking broken and somewhat fake French after a neurological event (Beschin et al., 2016). An abnormality in his basilar artery blocked the necessary flow of cerebrospinal fluid (CSF), with hydrocephalus and brainstem vascular encephalopathy as a result. A typical example of the condition (known as megadolicho basilar artery) in another patient is shown below.



    Fig. 1 (Thiex & Mull, 2006). (A) CSF flow obstruction (arrow). (B) megadolicho basilar artery.


    The man had no previous psychiatric history and retained the ability to speak perfect Italian. The clinical report includes the only instance of the word “fling” that I recall seeing in a scientific journal, so I'll quote at length:
    He had superficially learned French at school, used it in his 20's due to a fling with a French girl but he has not spoken it for about 30 years. In his professional life he used English as his second language. Before brain damage he never manifested a particular attachment to French culture or French cuisine. His accent is not due to dysarthria and he speaks polished and correct Italian, his mother tongue. However, he now states that French is his preferred language refusing to speak in Italian spontaneously.
    . . .

    JC's French is maladroit and full of inaccuracies, yet he speaks it in a fast pace with exaggerated intonation using a movie-like prosody and posing as a typical caricature of a French man. His French vocabulary is reduced and he commits several grammatical errors but he does not speak grammelot or gibberish and never inserts Italian terms in his French sentences. He uses French to communicate with everybody who is prepared to listen; he speaks French with his bewildered Italian relatives, with his hospital inmates, with the consultants; he spoke French even in front of the befuddled Committee deciding on his pension scheme. He claims that he cannot but speak in French, he believes that he is thinking in French and he longs to watch French movies (which he never watched before), buys French food, reads French magazines and seldom French books, but he writes only in Italian. He shows no irritation if people do not understand him when he speaks in French.

    He performed well on picture naming and verbal fluency tests in Italian, although he first tried to name the item in French (substituting category names like ‘vegetable’ for the low frequency word ‘asparagus’). His episodic memory was poor and he could not recall autobiographical incidents from the previous few years (but could recall earlier memories). He performed well on most other cognitive tests. But he did show some psychiatric symptoms that were secondary to the brain injury.
    However, he presents with some delusions of grandeur, sleep disturbances and has some compulsive behaviours: he buys unnecessarily large quantities of objects (e.g., needing two hangers he bought 70) and he makes tons of bread to his wife's chagrin. He also shows unjustified euphoria (which he labels joie de vivre): for example in the morning he opens the windows and shouts bonjour stating that it is a wonderful day. He manifests signs of social disinhibition, for example proposing to organise a singing tour for his daughter's teenage friend or offering French lessons to his neighbours. These symptoms are indicative of secondary mania (Santos, Caeiro, Ferro, & Figueira, 2011) and were drug-resistant.

    This is certainly a highly usual consequence of megadolicho basilar artery, but note that the subtitle of Beschin et al.'s article is “A clinical observation not a mystery.” There is no true xenoglossy here (or anywhere else, for that matter).


    Further Reading

    Man Wakes Up From Coma Speaking New Language: The media’s love of xenoglossy

    Foreign Language Syndrome“There actually isn’t a legitimate foreign language syndrome...”


    References

    Beschin, N., de Bruin, A., & Della Sala, S. (2016). Compulsive foreign language syndrome: A clinical observation not a mystery. Cortex DOI: 10.1016/j.cortex.2016.04.020

    Stengel, E. (1941). On the Aetiology of the Fugue States. British Journal of Psychiatry 87 (369): 572-599.

    Thiex R, Mull M. (2006). Basilar megadolicho trunk causing obstructive hydrocephalus at the foramina of Monro. Surg Neurol. 65(2):199-201.




    Jen speaks fake Italian on the IT Crowd.


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    A recent neuroessay in the New York Times asked, Can Tylenol Help Heal a Broken Heart?
    What’s crazy about the pain of a broken heart is that your body perceives it as physical pain.
    No it does not. Do you feel heartbroken every time you stub your toe?


    Well... I guess the social pain = physical pain isomorphism is a one way street. Anyway, the author continued:
    In research published in 2010, scientists found that acetaminophen can reduce physical and neural responses associated with the pain of social rejection, whether in romantic relationships, friendships or otherwise.
    The pain reliever Tylenol (acetaminophen) lessens the pain of social rejection, according to the 2010 study in Psychological Science[except when it doesn't].1 Acetaminophen also purportedly soothes the existential angst of watching a David Lynch film, blunts your emotions, and kills your empathy.2


    So if you’re hurting from heartache, try popping some Tylenol.
    Do not pop Tylenol after a breakup. It can cause serious liver damage if you take too much.


    But What About Advil?

    A 2014 study in the journal Personal Relationships was the first to break the stranglehold of acetaminophen (Vangelisti et al., 2014). The paper made few headlines (an exception was the Daily Mail), and it was not cited by the Tylenol researchers after its publication. Yet I saw no difference in quality, and even found more to like about it compared to the Tylenol papers (all of which appeared in higher impact journals). One of the Advil authors was Dr. James Pennebaker, chair of Psychology at the University of Texas. Dr. Pennebaker is well-known for his research on text analysis and what word choice can reveal about sex, age, social class, personality, mood, and affective state.

    The focus of the study by Dr. Anita Vangelisti and colleagues was on potential sex differences in the effects of a physical pain reliever on social pain. They cited evidence suggesting that women are more sensitive to physical pain, and men might be more responsive to pain relievers like ibuprofen (Walker & Carmody, 1998).

    Proposed explanations for sex differences in pain and analgesia include the bullet list below (Mogil & Bailey, 2010). These could potentially influence the effects of ibuprofen (and acetaminophen) on social pain.3
    • Socioculturalmanly and stoic machismo
    • Psychological greater negative affect and catastrophizing in women
    • Experiential women may have more experience with clinical pain, which affects current pain perception
    • Opioid receptors and especially their interactions with gonadal hormones
    • Other potential biological factors a long list

    Advil Worsened Social Pain in Men

    Ibuprofen did indeed increase ratings of social pain in male participants, but decreased ratings in female participants Vangelisti et al. (2014). For more details, read on.


    The participants were 138 undergraduates enrolled in communication courses (62 male and 76 female). Half took 400 mg ibuprofen (the dosage in 2 tablets), and half took placebo. In one task, they rated their feelings after being excluded from a ball-tossing video game (Cyberball), similar to the 2010 study of Dewall and colleagues. In the second task, they wrote detailed descriptions about an experience of betrayal by a close relational partner and an experience of physical pain. Participants completed the Positive and Negative Affective Schedule (PANAS) before treatment and after each of the tasks. On the PANAS, respondents rated their experience of 20 different feelings or emotions on a 7-point scale (1 = very slightly or not at all, 7 = extremely).4

    Two additional items assessed social pain or hurt. One required participants to rate the extent to which they felt hurt; the other required them to indicate the degree to which they felt emotionally injured. An average of these two questions comprised the dependent measure of Social Pain (presumably also on a 1 to 7 scale). Another dependent measure used the Linguistic Inquiry and Word Count (LIWC) program to calculate a weighted percentage of Emotion Words and First-Person Pronouns in the written narratives, both of which are indicators of increased social pain. Neither linguistic measure reached statistical significance, so I'll focus on Social Pain ratings.

    Within-subjects comparisons showed that in all cases, Social Pain ratings were higher after the tasks than before.


    Placebo Group
    Before        M = 1.52, SD = 0.86
    Cyberball     M = 2.07, SD = 1.31
    Betrayal      M = 3.12, SD = 1.62


    Treatment Group
    Before        M = 1.54, SD = 1.01
    Cyberball     M = 1.93, SD = 1.11
    Betrayal      M = 3.04, SD = 1.71



    Pre-treatment ratings didn't differ between men and women, but post-treatment Cyberball and Betrayal ratings showed crossover interactions, meaning the effects were opposite in men and women. On placebo, women had higher social pain ratings than men. On Advil, women's ratings dropped but men's increased. Since women are generally lighter than men, these analyses controlled for weight effects on dosage, since everyone got 400 mg.

    - click on image for a larger view - 


    So the women responded in the predicted way, based on past research. But the men did not. Did the subjects' expectations influence the results? The study description specifically stated it “was being conducted to examine the link between physical and emotional pain.” In contrast, the Tylenol studies were a little more vague: “advertised as a general assessment of the cognitive and emotional impacts of acetaminophen” for the study of existential angst, and “Tylenol and social cognition” for the blunted emotion experiment.

    The authors proposed a social cognitive model:
    Because men are comparatively likely to curb their emotional pain, it is possible that men who take a physical pain reliever will display a disinhibition effect. That is, when men take a physical pain reliever, their cognitive response may act to blunt or inhibit their tendency to suppress their emotional pain. The cognitive processes underlying such a disinhibition effect are akin to [a] reverse placebo effect.

    This didn't make sense to me, but then I found a paper that manipulated expectancy for physical pain relief in a within-subject design (Butcher & Carmody, 2012). The sample size was small (10 men, 10 women), but the participants came in once a week for 4 weeks to experience all of these conditions:
    1. Subjects told they were receiving ibuprofen and received ibuprofen (positive expectancy).
    2. Subjects told they were receiving ibuprofen but received placebo (positive expectancy).
    3. Subjects told they were receiving placebo but received ibuprofen (negative expectancy).
    4. Subjects told they were receiving placebo and received placebo (negative expectancy).
    The subjects were exposed to experimentally-induced pain (electrical stimulation of the earlobe) and assessed for analgesia response (change in pain tolerance). Ibuprofen dose was 800 mg (4 tablets).

    Pain tolerance in women did not differ for any of the four conditions. But pain tolerance in men conformed to their positive expectations: pain tolerance increased in both the ibuprofen and the placebo conditions when told they would receive ibuprofen. There was also negative placebo effect (a true negative placebo effect), but this was not statistically significant.

    What does this mean for social pain? Although the Butcher and Carmody (2012) findings need replication, Vangelisti et al.'s disinhibition model seems to be based on expectation, not on a direct relationship between physical and social pain.

    Other quibbles include the between-subjects design and small or marginal effects for some of the statistical comparisons — both of which are true for the Psych Sci Tylenol studies with their overblown interpretations. For instance, one headline from APS had this fun cure: Experiencing Existential Dread? Tylenol May Do the Trick.

    To their credit, Vangelisti et al. didn't oversell their results.5 An article in The Alcade, the University of Texas alumni magazine, asked the same question as the NY Times neuroessay Can Ibuprofen Mend a Broken Heart? but arrived at a more prudent answer.
    So does that mean we should all start popping ibuprofen whenever our feelings are hurt? Absolutely not, says Vangelisti.“In time, we may see psychiatrists prescribing painkillers for social pain—judiciously, I hope—but right now there are too many unanswered questions that our study has raised for this to be considered a viable treatment.”

    I'll leave you with this quote from Woo et al. (2014), who found that representations of physical and social pain are clearly separable in the brain.
    [Our] findings demonstrate that separate representations underlie pain and rejection despite common fMRI activity at the gross anatomical level. Rather than co-opting pain circuitry, rejection involves distinct affective representations in humans.



    Thanks to @thebyrdlab for linking to the Advil paper.


    Footnotes

    1 In the Cyberball fMRI study of Experiment 2 (Dewall et al., 2010), the participants on placebo vs. those on drug did not differ in their social distress ratings after being excluded from the game.

    2 Not surprisingly, I disagree with all of these overblown interpretations. See Acetaminophen Probably Isn't an "Empathy Killer".

    3 By and large, social psychology researchers don't seem particularly concerned about the mechanisms of action of these drugs. I haven't written about ibuprofen, but see Does Tylenol Exert its Analgesic Effects via the Spinal Cord?

    4 I thought the PANAS was on a 5-point scale, but the paper said 7-point.

    5 On the other hand, we have this unfortunate statement:
    "It's possible that taking physical pain relievers provides men with more cognitive resources to express the pain they feel," said Vangelisti. "There's some evidence that, for men, the part of the brain that enables them to regulate their emotions is linked to the part of the brain that processes physical and social pain. If that's the case, taking a physical pain reliever may affect men's ability to hide or suppress their social pain." 

    References

    Butcher, B., & Carmody, J. (2012). Sex differences in analgesic response to ibuprofen are influenced by expectancy: A randomized, crossover, balanced placebo-designed study. European Journal of Pain, 16 (7), 1005-1013. DOI: 10.1002/j.1532-2149.2011.00104.x

    Dewall CN, Macdonald G, Webster GD, Masten CL, Baumeister RF, Powell C, Combs D, Schurtz DR, Stillman TF, Tice DM, Eisenberger NI. (2010). Acetaminophen reduces social pain: behavioral and neural evidence. Psychol Sci. 21:931-7.

    Mogil JS, & Bailey AL (2010). Sex and gender differences in pain and analgesia. Progress in brain research, 186, 141-57 PMID: 21094890

    VANGELISTI, A., PENNEBAKER, J., BRODY, N., & GUINN, T. (2014). Reducing social pain: Sex differences in the impact of physical pain relievers. Personal Relationships, 21 (2), 349-363 DOI: 10.1111/pere.12036

    Walker JS, Carmody JJ. (1998). Experimental pain in healthy human subjects: gender differences in nociception and in response to ibuprofen. Anesth Analg. 86(6):1257-62.

    Woo CW, Koban L, Kross E, Lindquist MA, Banich MT, Ruzic L, Andrews-Hanna JR, & Wager TD (2014). Separate neural representations for physical pain and social rejection. Nature Communications 5: 538.






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  • 06/23/16--04:41: In Oxytocin We Trust


  • Oh oxytocin, you cuddly hug drug, you fine upstanding moral molecule, why are you so maligned by critics? That's because you're overrated, and misunderstood by those who look to you as a beacon of empathy, trust, love, peace, and prosperity. Sure, you're all about pair bonding in monogamous prairie voles — we have no beef with rigorous animal studies — but in humans, you're downright complicated. Yes, you can be magnanimous and romantic some of the time. But you're not always a moral molecule. You can promote antisocial behaviors such as envy and schadenfreude and aggressive tendencies. And even in voles, too much of a good thing can backfire.

    Four new papers on oxytocin in humans have been published this week.1 Collectively, there's something for nearly everyone to complain about:

    Oxytocin and Epigenetics

    Of the four, the one that has garnered the most media attention is on epigenetics and sociability (Haas et al., 2016, published in PNAS). DNA methylation in the promoter region of the oxytocin gene (OXT) was quantified as an indicator of OXT expression. Lower methylation is presumably associated with higher OXT expression, and all sorts of sociable characteristics such as “more secure attachment styles, improved ability to recognize emotional facial expressions, greater superior temporal sulcus activity during two social-cognitive functional MRI tasks, and larger fusiform gyrus gray matter volume.”

    Are these findings plausible from a mechanistic standpoint? Assuming that OXT expression was higher in the sociable sorts, which in turn assumes that methylation in saliva is a good proxy for expression in brain, how did “more“ oxytocin have all these effects? And on what time scale?

    The Daily Mail was predictably credulous and hyperbolic,2 using terms like “breakthrough”, “a ‘chatty’ gene which makes people sociable”, and [the kicker] “new treatments for autism”. The autism reference comes from the paper itself (and from the university press release):
    "Participants with greater methylation of the OXT gene were less accurate in describing the emotional states of the people they saw in pictures," [first author Brian W. Haas] said. "That's a typical characteristic associated with autism, for example."

    But it's not that simple. Let's look at the relationship between emotion recognition and OXT methylation. The task was to view 10 sec video clips of human faces morphing from neutral expressions to happy, sad, fearful and angry, and to identify the emotion as soon as it was detected. This led to 10 different dependent measures: reaction time and accuracy for each of the individual expressions, and for the mean of all expressions. The (conservative) Bonferroni corrected significance level is α = .05/10 = .005 [but the authors said it should be .025]. Overall accuracy is shown below.




    Not all that impressive, eh? Another scatterplot was based on self-report questionnaires. The association between an anxious and insecure attachment style and OXT methylation fared better (p=.005), but the association between OXT methylation and avoidant attachment style was not significant. Why?


    Oxytocin and Spirituality

    The next paper, on oxytocin and spirituality (Van Cappellen et al., 2016), has gained traction on Twitter. Dan Quintana has already written an inspired blog post about it (Spray and pray: Does intranasal oxytocin increase spirituality?), so you should go and check it out. Dan has published at least 7 papers on oxytocin, so his critique is more informed than mine. I'll highlight his main points and then add a few of my own.

    Good news:
    First, the authors should be congratulated for posting the data for the paper on Open Science Framework (OSF). It’s great to see this dataset online considering the hype surrounding oxytocin...

    Here’s a few other things I liked about this paper (or a list of things that oxytocin papers often don’t do): i) Effect sizes and confidence intervals are reported, ii) the alpha for the main outcome was adjusted for multiple tests, and iii) the placebo spray was a “true” placebo that contained all the same ingredients as the oxytocin spray, except the actual oxytocin (i.e, not just saline spray). It’s much easier to taste the difference between oxytocin and saline so this is an important point.

    Bad news, genetics:
    The authors included an “exploratory analysis” (their words in the intro and a section of the results) of three oxytocin pathway polymorphisms (rs53576, rs6449182, and rs3796863). There are about 10–15 candidate oxytocin pathway SNPs the could be analysed so it’s not clear why these three were chosen rather than others. Sure, rs53576 has been studied a lot, but so have many other oxytocin pathway SNPs (especially rs2254298).

    Bad news, religious affiliation:
    ...it appears that there was a main effect of condition on both spirituality scales. However, a close read of table 1 reveals that this was after correcting for religious affiliation. Now this is reasonable when you consider that someone who’s an atheist is likely to report that spiritually is “not at all” important in my life. In fact, the data bears this out as the average spiritual rating (which can range from 0 to 7) for the atheist/agnostic group was 1.97 during the experimental visit and 1.88 a week later, whereas the average rating for the religiously affiliated group was 4.8 during the first visit and 4.9 during the second visit (I was able to calculate this from their posted dataset — isn’t open data great!).

    It’s plausible for someone who identifies as agnostic or atheist to report “not at all” on both occasions — and many did. In fact, when you look at the agnostics/atheist group alone, there’s a statistically significant increase in spirituality after oxytocin compared to placebo both during the lab visit and 1 week later... However, there was no significant difference when assessing the religiously affiliated group.

    (or not)

     Dr. Quintana concluded his post by advocating pre-registration and replication.


    Oxytocin, Meditation, Positive Emotions, Negative Emotions, Oxytocin Receptor Gene (OXTR rs53576), CD38 (rs6449182 and rs3796863), Religious Affiliation, and Spirituality After Intranasal Oxytocin Administration in 83 Predominantly White Middle Aged Men

    My unwieldy subheading includes only a small subset of the 161 variables in the study of Van Cappellen et al. (2016). Granted, some of these variables (e.g, the answers to individual items on questionnaires) were never examined in isolation — they were part of a composite score. Nonetheless, I think we can tick the “Ridiculously large numbers of variables” bullet point. We also have “Intranasal oxytocin administration” and “Small n candidate gene studies” (with n's below 20 in some cells). Bonus bullet point of “Between subjects design” is a personal pet peeve. I'd really like to see some within-subjects studies.

    And there's a mysterious element to some of the data not included in this paper:
    The data presented here are part of a larger study testing additional hypotheses not related to the present ones. For the larger study and to test a larger model, based on power calculation, a sample of 240 participants was targeted with a breakdown female-male of 125-115... Data collection ... stopped at 239 but despite recruitment effort, the sample is skewed toward females. This report focuses only on the 83 males who took part in the study... Growing evidence suggests that the effects of oxytocin are different for males and females (Feng et al., 2015) and most of the current evidence on intranasal oxytocin’s psychological effects, which support the current hypotheses, come from studies with exclusively male samples. A separate analysis of female participants, controlling for a series of additional variables related to natural variations in oxytocin is ongoing.

    The larger study also included a task using Chinese pictographs, since the ability to read Chinese pictographs was an exclusionary criterion “applied to another task unrelated to the current investigation.” I'm generally not a study pre-registration evangelist, but one can really see the point here.




    In Oxytocin We Doubt

    I'll conclude on a pessimistic note (what else is new?). Some highly critical reviews of the oxytocin literature have appeared recently.

    Evans SL, Dal Monte O, Noble P, Averbeck BB. Intranasal oxytocin effects on social cognition: a critique. Brain Res. 2014 Sep 11;1580:69-77.

    Leng G, Ludwig M. Intranasal Oxytocin: Myths and Delusions. Biol Psychiatry. 2016 Feb 1;79(3):243-50.
    Despite widespread reports that intranasal application of oxytocin has a variety of behavioral effects, very little of the huge amounts applied intranasally appears to reach the cerebrospinal fluid. However, peripheral concentrations are increased to supraphysiologic levels, with likely effects on diverse targets including the gastrointestinal tract, heart, and reproductive tract. The wish to believe in the effectiveness of intranasal oxytocin appears to be widespread and needs to be guarded against with scepticism and rigor. Preregistering trials, declaring primary and secondary outcomes in advance, specifying the statistical methods to be applied, and making all data openly available should minimize problems of publication bias and questionable post hoc analyses. Effects of intranasal oxytocin also need proper dose-response studies, and such studies need to include control subjects for peripheral effects, by administering oxytocin peripherally and by blocking peripheral actions with antagonists. Reports in the literature of oxytocin measurements include many that have been made with discredited methodology. Claims that peripheral measurements of oxytocin reflect central release are questionable at best.
    --- there is a retort to Leng and Ludwig by Quintana and Woolley:  Intranasal Oxytocin Mechanisms Can Be Better Understood, but Its Effects on Social Cognition and Behavior Are Not to Be Sniffed At.

    Walum H, Waldman ID, Young LJ. Statistical and Methodological Considerations for the Interpretation of Intranasal Oxytocin Studies. Biol Psychiatry. 2016 Feb 1;79(3):251-7.
    ...Our conclusion is that intranasal OT studies are generally underpowered and that there is a high probability that most of the published intranasal OT findings do not represent true effects. Thus, the remarkable reports that intranasal OT influences a large number of human social behaviors should be viewed with healthy skepticism...

    McCullough ME, Churchland PS, Mendez AJ. Problems with measuring peripheral oxytocin: can the data on oxytocin and human behavior be trusted?Neurosci Biobehav Rev. 2013 Sep;37(8):1485-92.


    It might be time to order Liquid Trust...



    Footnotes

    1 Actually, the number of articles is closer to ten, but I'll just list these four for now.
    1. Van Cappellen P, Way BM, Isgett SF, Fredrickson BL. Effects of Oxytocin Administration on Spirituality and Emotional Responses to Meditation. Soc Cogn Affect Neurosci. 2016 Jun 17. PMID: 27317929.
    2.  
    3. Haas BW, Filkowski MM, Cochran RN, Denison L, Ishak A, Nishitani S, Smith AK. Epigenetic modification of OXT and human sociability. Proc Natl Acad Sci. 2016 Jun 20. PMID: 27325757.
    4.  
    5. Simons RL, Lei MK, Beach SR, Cutrona CE, Philibert RA. Methylation of the oxytocin receptor gene mediates the effect of adversity on negative schemas and depression. Dev Psychopathol. 2016 Jun 20:1-12. PMID: 27323309.
    6.  
    7. Gao S, Becker B, Luo L, Geng Y, Zhao W, Yin Y, Hu J, Gao Z, Gong Q, Hurlemann R, Yao D, Kendrick KM. Oxytocin, the peptide that bonds the sexes also divides them. Proc Natl Acad Sci. 2016 Jun 20. PMID: 27325780.
    2 Hyperbolic and inaccurate. They called methyl groups "proteins".


    References

    Haas BW, Filkowski MM, Cochran RN, Denison L, Ishak A, Nishitani S, Smith AK. Epigenetic modification of OXT and human sociability. Proc Natl Acad Sci. 2016 Jun 20. PMID: 27325757.

    Van Cappellen P, Way BM, Isgett SF, Fredrickson BL. Effects of Oxytocin Administration on Spirituality and Emotional Responses to Meditation. Soc Cogn Affect Neurosci. 2016 Jun 17. PMID: 27317929.


    Further Reading

    The Ed Yong Collection:

    Oxytocin: the hype hormone

    One Molecule for Love, Morality, and Prosperity?

    Oxytocin: Still Not a Moral Molecule

    The Weak Science Behind the Wrongly Named Moral Molecule

    The Neurocritic Back Catalogue:

    Oxytocin and Mind Reading...

    LEARN TO TRUST YOUR OWN EYES

    ABC News Says: 'Trust Drug' Oxytocin Unbelievable For Now

    Paul Zak, Oxytocin Skeptic?

    Your Brain on Coupons?

    Neuroskeptic Posts:

    More Doubts Over The Oxytocin And Trust Theory
    (about: Failed Replication of Oxytocin Effects on Trust)

    Psychologists Throw Open The “File Drawer”
    (about: Is there a publication bias in behavioral intranasal oxytocin research on humans?)

    Sofia Deleniv:The Dark Side of Oxytocin

    Nature News:Neuroscience: The hard science of oxytocin


    Old ad for Liquid Trust


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    Texting Zombie (by Ian Aberle)


    Contemporary consumers of science infotainment “need” to understand that the brain responds to modern technology in an unprecedented and potentially sinister way. Or at least, that's what you'd think, based on the number of books and essays on how The Internet and Digital Technologies are destroying our brains. The latest entrée into this lucrative genre of mild techno-paranoid is from Elsevier, with their press release about a poorly controlled observational study in a relatively obscure journal:

    Sending text messages on a smartphone can change the rhythm of brain waves, according to a new study published in Epilepsy & Behavior.
    . . .

    Dr. Tatum, professor of neurology and director of the epilepsy monitoring unit and epilepsy center at Mayo Clinic in Jacksonville, Florida found a unique 'texting rhythm' in approximately 1 in 5 patients who were using their smartphone to text message while having their brain waves monitored.

    The publishing giant spawned a flood of news stories which claim that texting triggers a Unique, Never-Before-Seen Brain Rhythm that Actually Changes the Way Your Brain Thinks.

    But here's what we don't know about the 'texting rhythm'. We don't know:
    • That the signal represents brain activity, rather than a biological artifact (e.g., eye movements) or an electromagnetically-induced artifact produced by the smartphone
    • That the 'texting rhythm' has never been seen before, given the lack of systematic studies
    • That it occurs in people without epilepsy
    • That it has any direct relation to how we think

    In a series of two [largely overlapping]studies, Tatum and colleagues (2016a, 2016b) recorded noninvasive EEG (brainwave) activity from inpatients undergoing continuous video monitoring for potential seizure activity. In the more recent paper (2016b), records from 129 texting patients were reviewed for the presence of a reproducible texting rhythm (TR), defined as “a distinct, paroxysmal, time-synched, rhythmic, generalized, frontocentral, 5–6 Hz, monomorphic, theta rhythm repeatedly induced by text messaging” (based on their 2016a study with 100 patients).



    Fig. 1 (adapted from Tatum et al., 2016b). (B) unilateral texting with the right hand (picture insert) during video-EEG monitoring. Note the presence of the TR as a 5–6-Hz frontocentral monomorphic rhythm (blue boxes) at the start and termination of texting (solid blue arrows).


    It's hard to see what's going on here, so I've zoomed in on the lower box, which shows activity from two bipolar derivations. The Fp1-F3 trace shows eye movements and the F3-C3 trace shows the TR. It appears to be more rhythmic in these left hemisphere electrodes contralateral to the texting hand, but the TR can also be seen in the F4-C4 derivation in Fig 1B.


    Although I'm just making qualitative guesses here, I don't think the EEG was quantified with spectral power or time-frequency analyses. In other words, epochs of EEG during texting vs. other activities (audio telephone use, thumb/finger movements, cognitive testing/calculation, scanning eye movements, and speech/language tasks) were eyeballed for the presence or absence of TR. We learn that the TR lasted from 2 sec to continuous runs of  >10 sec. We don't know the number or duration of epochs during the various control activities, but the authors declared a startling significance level:
    The TR was highly specific to this text messaging (p < 0.0001). A similar waveform during baseline activation with motor, speech/language, and cognitive tasks performed independently was absent in all patients and was not observed during auditory–verbal smartphone communication (p < 0.0001).

    The TR didn't habituate with repeated texting, wasn't specific to iPhone vs. Android, and “was observed in a patient using an iPad, though we did not observe it during the use of a laptop.”

    But most texting patients undergoing video EEG monitoring did not show a TR. The percentage of patients with a TR was 24.5% (24 out of 98) and 22.6% (7 out of 31) in a separate Chicago cohort (Tatum et al, 2016a), and only 20.9% (27 of 129) in the 2016b paper. Having a TR wasn't related to age, sex, type of seizure (focal, generalized, epileptic, non-epileptic), or presence/absence of brain lesion on MRI. And we have absolutely no explanation for why that might be, which inspired this hilarious, overly honest headline:

    Neuroscientists just found that texting alters your brainwaves, but they can’t explain why

    Does using a smartphone fundamentally alter the way that your brain works? ...a group of researchers at the Mayo Clinic recently discovered that text messaging elicits a change in the regular rhythm of brain waves, completely different than the waveforms created by any other activity.

    “The big deal with discovering this ‘texting rhythm’ is that the number of new brain waves that are identified on EEG are extremely rare at this point in time,” Dr. William Tatum, the lead author of the study, tells Digital Trends.

    Dr. Tatum says that the new brain waves were discovered by accident when analyzing the day-to-day cortical rhythms of people suffering from epilepsy. This discovery triggered an investigation into the neurological effects of smartphone use, which ultimately grew to include nearly 130 participants over a period of 16 months. Only around one in five participants demonstrated the “texting rhythm,” although it didn’t appear to conform to any single gender, ethnicity or age group. Nor is it known exactly what aspect of texting prompts the effect: since text messaging includes a variety of different skills, such as finger dexterity, formulating succinct communications and more.

    What we do know is that cell phones and other devices can produce artifacts in EEG recordings (Sethi et al., 2007; Rasquinha et al., 2012; Myers et al., 2016), and this was not discussed in the paper.


    Dr. Ranjith Polusani, Artifacts in EEG


    EEG Artifact Recognition: Electrical and Environmental Artifacts[cellphone]


    But I don't mean to be so pedantic. William O. Tatum, D.O. is a neurologist and member of the American Board of Clinical Neurophysiology who has published Handbook of EEG Interpretation, Second Edition, How not to read an EEG (Neurology, 2013), Artifact-related epilepsy (Neurology, 2013), and more (see References). In fact, here's another image of a telephone artifact from Tatum et al. (2011). Dr. Tatum presumably knows a non-physiological artifact when he sees one.



    So does that mean I believe the TR is real? I'll withhold judgment until the results from carefully controlled, quantitatively analyzed, statistically rigorous experiments in participants with and without epilepsy are in. Meanwhile, speculating on the origin, meaning, or relevance of the 'texting rhythm' is premature...

    “The question we’re trying to answer right now is whether this is a destructive process or an active process,” Dr. Tatum says. “We think it’s probably an active process through an entrainment of normal cortical rhythms. What’s strange is that it appears to be a destructive frequency that’s more typically identified in people that have a slowing of their brain waves.”


    References

    Myers KA (2016). Cell Phone Saccades: EEG Artifact for the 21st Century. Pediatric Neurology. Available online 25 June 2016.

    Rasquinha RJ, Moszczynski AJ, Murray BJ. (2012). A modern artifact in the sleep laboratory. J Clin Sleep Med. 8(2):225-6.

    Sethi NK, Sethi PK, Torgovnick J, Arsura E. (2007). Telephone artifact in EEG recordings. The Internet Journal of Neuromonitoring. 5(1).

    Tatum WO, Dworetzky BA, Schomer DL. (2011). Artifact and recording concepts in EEG. J Clin Neurophysiol. 28(3):252-63.

    Tatum WO. (2013). How not to read an EEG: introductory statements. Neurology 80(1 Suppl 1):S1-3.

    Tatum WO. (2013). Artifact-related epilepsy. Neurology 80(1 Suppl 1):S12-25.

    Tatum WO, DiCiaccio B, Kipta JA, Yelvington KH, Stein MA. (2016a). The Texting Rhythm: A Novel EEG Waveform Using Smartphones. J Clin Neurophysiol. Jan 7. [Epub ahead of print]

    Tatum WO, DiCiaccio B, Yelvington KH. (2016b). Cortical processing during smartphone text messaging. Epilepsy Behav. 59:117-21.


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    A neuroimaging pioneer, distinguished Professor Richard Frackowiak, has come out in favor of retirement:
    I retired aged 65 – I am known for being very pro-retirement. Older scientists should advise, if asked, by the next generation, which they trained. They should refrain from occupying leadership positions or directing implementation – the time for that is past.

    This is an important public stance to take in a time of dwindling resources and opportunities for junior scientists. On the one hand, with the steady increase in life expectancy since 1935, many aging Boomers plan to work well into their 70s. But on the other hand, this glut of working elders deprives many talented young researchers entrée into tenure track positions. The fact that a senior scientist wants to move aside to allow the next generation to occupy leadership positions is notable, in my view.

    Prof Frackowiak's opinion on retirement was included in his comment on a post about Henry Markam and the Human Brain Project (HBP). In The laborious delivery of Markram’s brainchild, science journalist Leonid Schneider takes Markram to task for his dictatorial HBP leadership, his publishing empire (Frontiers), and most of all his hubris (e.g., 2009 TED talk):
    “I hope that you are at least partly convinced that it is not impossible to build a brain. We can do it within 10 years, and if we do succeed, we will send to TED, in 10 years, a hologram to talk to you”.

    Frackowiak found the post “scurrilous” and specifically objected to Schneider's mischaracterization of his own retirement as “resigning” from the HBP:
    I note one mistake that could easily have been checked. Makes me wonder about the accuracy of this scurrilous blog. I did not resign from the HBP. I remain a task leader in the Medical Informatics Platform.  




    But many have objected to the goals and governance of the HBP from the very beginning. In fact, two years ago, 156 Principal Investigators (eligible for HBP funding) and 660 others signed an Open message to the European Commission concerning the Human Brain Project. I won't rehash those issues (see further reading below).

    Schneider ends with some pointed links to highly embarrassing Frontiers papers, including one endorsing chemtrail conspiracy theories. Frontiers has issued an Expression of Concern about this paper:
    An expression of concern on
    Human and Environmental Dangers Posed by Ongoing Global Tropospheric Aerosolized Particulates for Weather Modification
    by Herndon, J.M. (2016). Front. Public Health 4:139. doi: 10.3389/fpubh.2016.00139

    With this notice, Frontiers states its awareness of several complaints and serious allegations surrounding the article “Human and Environmental Dangers Posed by Ongoing Global Tropospheric Aerosolized Particulates for Weather Modification” published on 30 June 2016. Our Chief Editors, Joav Merrick and Anwar Huq, will direct an investigation in full accordance with our complaints procedures. The situation will be updated as soon as the investigation is complete.

    UPDATE (17 July 2016): The chemtrails article has been retracted by Frontiers (via @Neuro_Skeptic):
    Based on information discovered after publication and reported to Frontiers in July 2016, the article was examined, revealing that the complaints were valid and that the article does not meet the standards of editorial and scientific soundness for Frontiers in Public Health. The retraction of the article was approved by the Field Chief Editor of Frontiers in Public Health and the Specialty Chief Editor of Environmental Health. The author considers the retraction to be unwarranted and therefore does not agree to the statement. 


    What does this have to do with the HBP?? Nothing. It came along as part of the larger anti-Markram package.


    Further Reading

    Guest post: Dirty Rant About The Human Brain Project

    Interview: What’s wrong with the Human Brain Project?

    Markram et al. (2015). Reconstruction and Simulation of Neocortical Microcircuitry. Cell. 2015 Oct 8;163(2):456-92.

    Behold, The Blue Brain

    More Fringe Science from Borderline Publisher Frontiers





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    1. We only use 4 to 5% of our brains.

    The usual ten percent myth is wrong, according to Brain Vizion. We have even more untapped potential waiting to be unlocked!
    Brain is the most complex organ in the human body & serves as the center of the nervous system. Brain is the amazing organ as we go deeper we realize the miracles of the GOD. If all information of all books in the world is loaded into the brain, human brain will never be full. Do you know, we are using at the most 4% to 5% of potential of our brain?. Potential of human brain is beyond our imagination. Full potential is a result of proper education (mental development). Think what will happen if we use whole brain?





    2. Left Brain, Right Brain, Mid Brain

    Everyone knows the left brain/right brain myth. But did you know that you should stimulate your mid brain?
    Mid-brain activation is a method to stimulate and balance the left and right brains. Mid brain Activation allows the middle brain act as a control panel for left and right hemispheres. This activates both parts of the brain and enhances the capacity and ability to learn.

    What is the middle brain?
    Mid brain manages functions of left and right brain. Mid brain is the ‘bridge’ between left and right hemispheres. [No, that would be the corpus callosum.] Once the mid brain gets activated, information will exchange more efficiently in between both hemispheres which leads to more efficient in learning and absorbing information.Mid brain activation allows the brain to function as a whole, rather than only utilizing one part of the brain.




    3. Left Brain is Beta, Right Brain is Alpha.

    Did you know that each hemisphere has a unique pattern of oscillatory brain activity, operating at separate frequency bands?
    One type of brain function belongs to left brain which operates at Beta wave frequency (14Hz to 30Hz cycles/sec). This is the brain we are most familiar with, having developed this brain in traditional academy settings. ... The right brain works at Alpha wave frequency (8 to 13 hertz cycles per second). This is the frequency of the brain associated with a relaxed alert state of mind such as in meditation, just before getting out of bed or while listening to music. It is not the type of brain activity which determines whether something is right or left brain oriented, but rather the brain wave that is operating at the time (Alpha or Beta).




    4. Move over theta, it's time for THEATA wave learning.

    Back to our magical friend, Mid Brain Activation:
    In order to awaken this part of the brain, it is necessary to stimulate a hormonal discharge by sending a special vibration. For this scientific alpha-theta level music are played where apparently only children can receive these waves effectively. In general, theta and alpha waves belong to babies and children. Since these waves belong to the subconscious mind babies and children feel easier to learn something or receive and follow somebody else’s words.  

    Wait, I thought alpha waves belong to the right hemisphere...

    Mystical brain training outlet Brain Vizion has clearly moved from common brain myths into ESP territory here:
    During the mid-brain activation, a child learns how to enter the condition of meditative trans in order to be able to ”see” with eyes closed (Blind-folded).
    . . .

    Blindfold activation ... is a form of extra sensory perception.Our activated mid-brain’s brain-wave may detect objects nearby & appears in our mind as a form of visualization.Science have proven that even animals are able to perform such ability when moving around or looking for food.e.g.Bats.In human beings , in Blind-fold activation intuition play an important role.

    OK then. What can THEATA wave training do for you?
    Children will be given an opportunity to do activities of ALPHA & THEATA level vigorously throughout the workshop.Conventional school emphasize predominantly on BETA waves & neglect the importance of ALPHA & THEATA wave learning environment which are for more conducive.


    The benefits of their Brain Stimulation program also include improvements in attention, mood, motivation, energy, pain, sleep, performance enhancement, and stress reduction.

    It gets even weirder, with the quackery known as the Dermatoglyphics Multiple Intelligence Test (DMIT).




    What is the Relation between Human Brain and Fingerprints? Don't click unless you want to see pictures of anencephalic babies. Instead, if you really want to read more about DMIT, Hand Reading News & Reports has a comprehensive review of its history, pseudoscientific claims, and scams.


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    So which is it? Ineffective or unprecedented?

    TauRx Alzheimer's Drug LMTX Fails in Large Study Although Some Benefit Seen

    Wednesday, 27 Jul 2016 | 11:23 AM ET

    TauRx Pharmaceuticals' experimental Alzheimer's drug LMTX failed to improve cognitive and functional skills in patients with mild to moderate Alzheimer's disease, a large, late-stage study showed.

    But in a perplexing twist, the drug did show a significant benefit in about 15 percent of patients in the trial who were not taking other standard Alzheimer's drugs, according to the findings released on Wednesday at the Alzheimer's Association International Conference in Toronto.


    LMTX was ineffective in a clinical trial of 891 patients with Alzheimer's disease (AD), although a post hoc analysis in a small subgroup of patients showed a benefit for those taking no other medications for AD (when compared to an inappropriate control group).


    Ben Goldacre, Chris Chambers, and others on Twitter took the UK media to task for their misleading articles on the outcome of the trial conducted by TauRx Pharmaceuticals.

    As the name implies, TauRx is developing Alzheimer's treatments based on disrupting tau protein, which accumulates in pathological tangles in the brain. Tau aggregation inhibitors are presumed to disrupt these tangles, thereby slowing neurodegeneration and memory loss. The degradation of tau aggregates in vitro was first demonstrated 20 years ago (Wischik et al., 1996), using the stain methylene blueLMTX is a variant of methylene blue, which turns urine blue. For that reason, the placebo group in the TauRx trial received a tiny amount of the drug for blinding purposes.

    The clinical trial protocol is NCT01689246, Safety and Efficacy Study Evaluating TRx0237 in Subjects With Mild to Moderate Alzheimer's Disease. The original enrollment across 121 sites was estimated at 833, and the original duration was 12 months. The duration was changed to 15 months about a year later, and five other outcome measures were added. And a secondary outcome measure (ADCS-ADL23) and a primary outcome measure (ADCS-CGIC) were swapped.

    The company press release used a vague headline (TauRx Reports First Phase 3 Results for LMTX®) to announce the results, but led off with the subgroup analysis (no surprise):

    TauRx Therapeutics Ltd today announced Phase 3 clinical trial results that show treatment with LMTX®, the company's novel tau aggregation inhibitor, had a marked beneficial effect on key measures of Alzheimer's disease in patients with mild or moderate forms of the disease.

    While the TRx-237-015 study in 891 subjects failed to meet its co-primary endpoints, clinically meaningful and statistically significant reductions in the rate of disease progression were observed across three key measures in patients who were treated with LMTX® as their only Alzheimer's disease medication. These three key measures comprised a cognitive assessment (ADAS-Cog), a functional assessment (ADCS-ADL) and an assessment of the level of brain atrophy (lateral ventricular volume, LVV, as measured by MRI). An abstract of the results will be presented during an open session at the 2016 Alzheimer's Association International Conference (AAIC) in Toronto, Canada this afternoon by Dr. Serge Gauthier, CM, MD.

    The ADCS-ADL was originally a secondary outcome measure, and hippocampal volume (not reported) was included as an “Other” outcome measure along with the lateral ventricle volume measurements. Keep in mind these results are preliminary (not peer-reviewed). However, given the possibility of a true positive treatment effect, I can understand why publication would be of secondary importance. There should be no delay in starting AD patients on an effective new and proven treatment (which this is not).

    It took a while to find the conference abstract by Gaultier et al. (2016), but an excerpt is below. The actual results were not included the abstract aimed to “highlight the potential therapeutic value” of LMTX (also called LMTM and TRx-0237)  but the text did mention the “85% were taking approved AD treatments” aspect of the study.

    Gaultier et al., AAIC 2016

    LMTM (TRx-0237) is a novel stabilized reduced form of the methylthioninium moiety with potential for efficacy in treatment of Alzheimer's disease. ... It acts as a selective tau aggregation inhibitor in vitro and in transgenic mouse models  The present 15-month double-blind, placebo-controlled trial (NCT01689246) was performed in patients with probable AD, MMSE score in the range 14-26, Clinical Dementia Rating 1-2 and age < 90 years. Patients were randomized 3:3:4 to receive oral LMTM at doses of 150 or 250 mg/day or placebo (containing 8 mg/day, to maintain blinding) respectively. Primary efficacy outcomes were change from baseline on cognitive (ADAS-Cog) and functional (ADCS-ADL) scores. Three-monthly assessment included magnetic resonance imaging (MRI) as a disease modifying outcome. Other secondary outcomes included ADCS-CGIC and MMSE. Results: A total of 891 patients were randomized, of whom 62% were female. Approved AD treatments were being taken in 85%. The mean age was 70.6 (SD 9.0) years and baseline MMSE score was 18.7 (SD 3.4). ... The study efficacy and safety outcomes will be reported. The outcomes of this phase 3 trial will highlight the potential therapeutic value of tau aggregation inhibitor therapy in AD. A second phase 3 trial of LMTM for AD will be completed and reported later in 2016.

    [The entire abstract with authors and affiliations is at the end of this post.]

    The 15% who benefited from LMTX® were the patients who were not taking any other medications for dementia (e.g., acetylcholinesterase inhibitors). This monotherapy subgroup was compared to the entire placebo group, not to the subgroup of placebo patients not on any other dementia meds (as pointed out by @bengoldacre). It was nice to read critical coverage of the TauRx spin (and media reporting) at Forbes, BuzzFeed, and Quartz.


    Meanwhile, New Scientist updated their headline (and url) to more accurately reflect reality.




    Is it worthwhile for TauRx to pursue a proper clinical trial of LMTX as a monotherapy?  Maybe. The big mystery is why LMTX didn't work in patients taking the usual medications for dementia. There's no convincing mechanism to explain that odd result (Wischik: “other Alzheimer’s treatments help to clear toxic material out of the brain, and may also clear away LMTX too”). Or it could be a p-hacked false positive, or a function of milder severity or diagnostic issues or study site in the 15%. If TauRx is truly confident that LMTX taken alone can slow the progression of AD by 80%, then run another randomized controlled study where LMTX + no AD meds is compared to placebo + no AD meds.

    Meanwhile, exaggerated reporting on “the first drug to halt Alzheimer’s” is highly unethical.


    AAIC Conference Abstract

    Phase 3 Trial of the Tau Aggregation Inhibitor Leuco-Methylthioninium-Bis(hydromethanesulfonate) (LMTM) in Mild to Moderate Alzheimer's Disease

    Serge Gauthier, MD1; Howard H Feldman, MD2; Lon S Schneider, MD, MS3; Gordon Wilcock, MD4; Giovanni B Frisoni, MD5; Jiri Hardlund, MD6; Karin Kook, PhD7; Damon J Wischik, PhD6; Bjoern O Schelter, PhD8; John M Storey, PhD6,8; Charles R Harrington, PhD6,8 and Claude M Wischik, MD, PhD6,8, (1)McGill University Research Centre for Studies in Aging, Verdun, QC, Canada, (2)University of British Columbia, Vancouver, BC, Canada, (3)Keck School of Medicine of USC, Los Angeles, CA, USA, (4)Oxford University, Oxford, United Kingdom, (5)Universite de Geneve, Geneve, Switzerland, (6)TauRx Therapeutics Ltd, Aberdeen, United Kingdom, (7)Salamandra LLC, Bethesda, MD, USA, (8)University of Aberdeen, Aberdeen, United Kingdom

    Background: Leuco-methylthioninium-bis(hydromethanesulfonate) (LMTM; TRx-0237) is a novel stabilized reduced form of the methylthioninium (MT) moiety (Harrington et al. J Biol Chem 2015;290:10862) with potential for efficacy in treatment of Alzheimer's disease (AD). A previous trial using the oxidized form of MT identified dose dependent absorption limitations (Wischik et al. J Alzheimers Dis 2015;44:705). LMTM is better absorbed and tolerated (Baddeley et al. J Pharmacol Exptl Therapeutics 2015;352:110) permitting higher doses to be tested. It acts as a selective tau aggregation inhibitor in vitro (Harrington et al. J Biol Chem 2015;290:10862) and in transgenic mouse models (Melis et al. Behav Pharmacol 2015;26:353). Methods: The present 15-month double-blind, placebo-controlled trial (NCT01689246) was performed in patients with probable AD, Mini-Mental State Examination (MMSE) score in the range 14-26, Clinical Dementia Rating (CDR) 1-2 and age < 90 years. Patients were randomized 3:3:4 to receive oral LMTM at doses of 150 or 250 mg/day or placebo (containing 8 mg/day, to maintain blinding) respectively. Primary efficacy outcomes were change from baseline on cognitive (Alzheimer's Disease Assessment Scale cognitive subscale; ADAS-Cog) and functional (Alzheimer's Disease Cooperative Study Activities of Daily Living; ADCS-ADL) scores. Three-monthly assessment included magnetic resonance imaging (MRI) as a disease modifying outcome. Other secondary outcomes included ADCS-CGIC and MMSE. Results: A total of 891 patients were randomized, of whom 62% were female. Approved AD treatments were being taken in 85%. The mean age was 70.6 (SD 9.0) years and baseline MMSE score was 18.7 (SD 3.4). Dementia was of moderate severity (MMSE score 14-19) in 61%. The study efficacy and safety outcomes will be reported. Conclusions: The outcomes of this phase 3 trial will highlight the potential therapeutic value of tau aggregation inhibitor therapy in AD. A second phase 3 trial of LMTM for AD will be completed and reported later in 2016.


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    Not a very good showing, eh?


    In the study,
    “Participants were asked to press a button if they thought the person in a photo was living or deceased. Overall mean accuracy on this task was 53.8%, where 50% was expected by chance (p < 0.004, two-tail). Statistically significant accuracy was independently obtained in 5 of the 12 participants.”

    The abstract claims the participants showed better than chance performance, but even if we accept this level of accuracy at face value (so to speak), the mediums were wrong 46.2% of the time. Remember that before your next psychic reading.

    And of course we should not accept the results at face value. Let's take a closer look at the paper (Delorme et al., 2016), which was published in Frontiers in Human Neuroscience



    Actually, let's take a closer look at the authors first. Arnaud Delorme, Alan Pierce, Leena Michel,  and Dean Radin are all affiliated with the Institute of Noetic Sciences (IONS), a parapsychology research institute in California. Dr. Delorme is also affiliated with UC San Diego. Along with Scott Makeig, he developed EEGLAB, a Matlab toolbox that's widely used to analyze EEG data. Delorme and Makeig (2004) has been cited 5738 times (as of this writing).

    Why is Delorme doing parapsychology research?? He's a long-time Zen meditator, according to his IONS biography. Why is Frontiers publishing parapsychology research? Here's one opinion.


    Dead or Alive?


    Figure 1 (Delorme et al., 2016). Process involved in creating a group of photographs of “Alive” and “Deceased” individuals.


    Photographs of known alive and dead people were selected from three internet databases: (D1) school portraits from 1939–1941; (D2) school portraits from 1962–1968; and (D3) politicians (US senators excluded) and businessmen. Why? Why use pictures of US Representatives and state politicians outside of California? Even though the subjects said they didn't recognize them, there could be a vague sense of familiarity with some of these faces.

    Photos of 404 individuals were presented, and the 12 participants pressed keys to indicate “deceased,” “living,” or “do not know”. 1

    The participants all “claimed to be able to experience feelings of vitality from facial photographs alone. ... They were required to have been performing professional ‘readings’ for clients...” THERE WAS NO CONTROL GROUP.  In other words, participants who did not claim any psychic or clairvoyant abilities were not included in this study. Thus, there was no way to know if the marginal ability to discern whether a person was alive or dead was based on mediumship.

    And marginal it was. Basically, they were terrible at determining whether people in old yearbook photos were dead or alive. Terrible. No better than guessing. 2




    Given the number of statistical tests, we should only consider values with *** (p<.001), of which there were two (out of 35 possible comparisons). Therefore, the evidence for mortality prediction (clairvoyance) should not be taken seriously, despite the authors' conclusion:
    We do not rule out the hypothesis that subjects might have had access to information in ways that are not currently understood by modern physics and could potentially go beyond classical information delivered by facial features.

    Paranormal physics do not apply to old photographs, however.

    And the EEG data were equally unconvincing. The face-specific N170 component did not differ based on dead or alive, correct or incorrect. The earlier P1 component showed a small difference between correct and incorrect responses for the deceased only, but there was no good explanation for this (“Future research could assess if low-level visual image characteristics and attentional modulation were important factors in leading to this difference in electrocortical activity”).

    The truth is out there, but this study provides no proof that the ‪#‎Supernatural‬ actually exists.


    Footnote

    The “do not know” responses were not included in the analyses, and we have no idea of how many such responses were recorded.

    2 Oh here's a fun fact. S06 indicated that 90% of the people in the photos were dead.


    Reference

    Delorme, A., Pierce, A., Michel, L., & Radin, D. (2016). Prediction of Mortality Based on Facial Characteristics. Frontiers in Human Neuroscience, 10.  DOI: 10.3389/fnhum.2016.00173





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    Activity of the medial prefrontal cortex after psycho-spiritual healing (Baldwin et al., 2016).


    Everything we do and feel and experience changes the brain. Psychotherapy, juggling, taxi driving, poverty, reading, drugs, art, music, anger, love. If it didn't we'd be dead. Why should prayer be any different? The trick is to accurately determine the structural or physiological changes that are unique to a specific activity. And when assessing the effectiveness of clinical interventions, how the changes compare to an adequately matched control intervention. Plenty of high profile studies have failed to do that, including a recent one on emotionally focused therapy.1 

    I feel bad about criticizing a study on the neural correlates of healing prayers. I'm not one of those smug atheists who lord their intellectual superiority over the unwashed religious masses. Certain atheist organizations claim they're all about promoting scientific literacy and a secular worldview. But I think these New Atheists are detrimental to science literacy, since they alienate the vast majority of the population.

    So why am I blogging about a prayer intervention for depression? It's not to sneer at the authors. And it's especially not to sneer at the participants, who were recruited from Houston-area churches. My interest is the unholy alliance between brain imaging and a psychological intervention with no control condition. As I've said before...
    ...neuroimaging studies of psychotherapy that have absolutely no control conditions are of limited usefulness. We don't know what sort of changes would have happened over an equivalent amount of time with no intervention. More importantly, we don't know whether the specific therapy under consideration is better than another form of psychotherapy, or better than going bowling once a week.

    Healing Prayer, Trauma, and Forgiveness

    This is especially true for a treatment that is based on faith and a strong belief that the intervention will work — a Christian form of prayer focused on forgiveness and psycho-spiritual healing (PSFH). A prayer minister “led the subject through three different phases: (1) a prayer of forgiveness for the perpetrator of the hurtful event; (2) a prayer of blessing on the perpetrator; and (3) a prayer to heal the emotional damage caused by the traumatic event.”



    Study design for the 6 week healing prayer intervention (Baldwin et al., 2016).

    The 18 participants had moderate to severe levels of depression on the Hamilton Depression Scale (HAM-D). Oddly, post-traumatic stress disorder (PTSD) was not assessed before or after the intervention. This was a major weakness, given that the purpose of the intervention was to forgive the perpetrator of childhood abuse and to heal from emotional trauma. In this sense, PSFH is akin to more formalized psychotherapies such as forgiveness therapy.

    It's no surprise that a non-randomized, unblinded prayer intervention in religious persons resulted in dramatically reduced HAM-D scores in the 14 participants who completed the study (11 of whom were available for a one year followup).


    Who am I to criticize a practice that helps suffering people? I won't do that.

    What I will do is point out difficulties in task design that make it nearly impossible to interpret some aspects of their fMRI study. The task used a symptom provocation paradigm using 3 key words to evoke memories of the traumatic event (15 seconds) and feelings of the traumatic event (15 seconds), separated by a 2 second blank screen.2 Is it possible to separate traumatic memories from the feelings they evoke, and to switch between them on such short notice? Certain therapies (such as prolonged exposure) are designed to do just that. The authors stated that anecdotally, this appeared to be the case here as well:
    In this and our previous study, subjects frequently mentioned informally that PSFH results in a separation of the traumatic memory and associated feelings: while the memory remains intact, it no longer associates with traumatic feelings.


    Activity of the precuneus to Bad Feelings was higher before psycho-spiritual healing(Baldwin et al., 2016).


    It is, however, difficult to interpret a 23 voxel decrease in precuneus activity in 14 subjects as a reflection of such a complex therapeutic change, especially since this brain region is involved in both self-referential processing and episodic memory retrieval.

    But to be even more fair, the authors listed ten caveats to their admittedly preliminary study.3 When all is said and done, how can this study reveal ANYTHING about the neural correlates of healing prayer?




    Or in this case, nothing fails like a non-randomized, unblinded, not-placebo-controlled fMRI study of prayer. Or of any other intervention, for that matter.

    Nothing-Fails-Like-Prayer image by Henry Ruddle


    Footnotes

    1Johnson SM, Moser MB, Beckes L, Smith A, Dalgleish T, Halchuk R, Hasselmo K, Greenman PS, Merali Z, & Coan JA (2013). Soothing the threatened brain: leveraging contact comfort with emotionally focused therapy. PloS one, 8 (11).

    Also see two blogposts by Dr. James Coyne.

    2These Bad Memory/Feeling blocks were also compared to Neutral Memory/Feeling blocks that evoked memories and feelings about a neutral topic (e.g., the weather). This is the pre/post contrast shown in the first figure of the post.

    3To shorten and paraphrase the overly honest Limitations section of Baldwin et al. (2016):
    • the number of subjects was small (n=14) 
    • recruitment was largely done at churches, which might affect generalizability
    • individual minister effects could not be ruled out
    • there was no control population receiving an alternative therapy
    • only subjects who completed the study were included, which may have skewed the results
    • life events such as changing employment status, marriage stability, family, health, and economic changes were not assessed
    • possible confounding effects between the role of PSFH and intercessory prayer for the participants by others [NOTE: some of us may discount this as a confounder]
    • cannot rule out an effect of being exposed to the task in the MRI twice
    • demand characteristics participants answered worse at the beginning and better at the end to fulfill researcher’s expectations 
    • outcomes were rated by non-blinded observers

    Reference

    Baldwin, P., Velasquez, K., Koenig, H., Salas, R., & Boelens, P. (2016). Neural correlates of healing prayers, depression and traumatic memories: A preliminary study Complementary Therapies in Medicine, 27, 123-129 DOI: 10.1016/j.ctim.2016.07.002

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  • 08/31/16--23:58: Music from Your Brain


  • The journal Brain has a new review on the history of converting the electroencephalogram (EEG) into sound (Lutters & Koehler, 2016). The translation of data into sound, known as sonification, has been applied to brain waves since the 1930s. In addition to early scientific and medical applications, sonification of the EEG has been used in the field of experimental music.




    In 1965, physicist Edmond Dewan and composer Alvin Lucier collaborated on Music for the Solo Performer:

    Sitting on a chair, eyes closed, Lucier’s brainwaves were recorded from his scalp, amplified and channelled to numerous loudspeakers scattered around the room. As the amplified alpha rhythm was below the human audible range, the loudspeakers were put ‘right up against’ various percussion instruments, which were then activated by means of vibration. While Lucier attempted to refrain from mental activity, percussion sounds slowly started to fill the room, which were suddenly disrupted when he opened his eyes, engaged in mental exercise, or when his attention was drawn towards sounds from the audience (Kahn, 2013).





    The article also reviews more contemporary translations of EEG activity into music:

    By the end of the century, advances in EEG and sound technology ultimately gave rise to brain–computer music interfaces (BCMIs), a multidisciplinary achievement that has enhanced expressive abilities of both patients and artists (Miranda, 2014).


    Image credits:

    Edmond Dewan and his brainwave control system (1964). From Kahn D. Earth sound Earth signal: Energies and Earth magnitude in the arts. Los Angeles: University of California Press; 2013. p. 96. Image courtesy of Brian Dewan.

    Lucier practicing brainwave control in the Brandeis Music Studio (1965). From Kahn D. Earth sound Earth signal: Energies and Earth magnitude in the arts. Los Angeles: University of California Press; 2013. p. 91. Image courtesy of Alvin Lucier.


    Reference

    Lutters, B., & Koehler, P. (2016). Brainwaves in concert: the 20th century sonification of the electroencephalogram. Brain DOI: 10.1093/brain/aww207


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    Vote for your favorites in the 2016
    Brain Awareness Video Contest!




    You can submit up to two votes for The People's Choice Award. You don't need to be a member of the Society for Neuroscience.

    Deadline: September 30, 2016.


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  • 09/17/16--16:46: The Neural Lace Tour

  • Stevie Nicks and Elon Muskfinally together in this stunning collection...

    Elon
    You have the limbic system, 
    the cortex 
    and a digital layer above the cortex 
    that could work well and symbiotically with you



    Stevie:
    Now here I go again, I see the crystal visions
    I keep my visions to myself

    --Dreams, Fleetwood Mac




    Stevie:
    I need you to love me
    I need you today
    Give to me your leather
    Take from me
    My lace

    --Leather and Lace, Stevie Nicks


    Elon:
    If you assume any rate of advancement of AI,
    um.......
    we will be left behind
    by a lot

    --We are already cyborgs | Elon Musk | Code Conference


    Stevie:
    It's only me
    Who wants to wrap around your dreams and...
    Have you any dreams you'd like to sell?

    --Dreams, Fleetwood Mac


    Neural Lace

    The concept was first thought up by Iain M. Banks in his Culture novels. In these novels, a neural lace is a mesh-like device that would be implanted in a person directly through the bloodstream, controlling the release of certain neurons using the power of thought.

    Musk’s version of the neural lace doesn’t work exactly like that. Musk’s lace seems to be a mesh that would allow such AI to work symbiotically with the human brain. Signals will be picked up and transmitted wirelessly, but without any interference of natural neurological processes. Essentially, making it a digital brain upgrade. Imagine writing and sending texts just using your thoughts.


    Stevie:
    And the days go by
    Like a strand in the wind
    In the web that is my own

    --Edge of Seventeen, Stevie Nicks


    Elon:
    You have a digital version of yourself
    a partial version of yourself
    online
    in the form of your e-mails and social media
    and all the things you do...

    --We are already cyborgs | Elon Musk | Code Conference


    Stevie:
    The clouds never expect it
    When it rains

    --Edge of Seventeen, Stevie Nicks


    Elon:
    We're IO bound
    particularly output bound

    --We are already cyborgs | Elon Musk | Code Conference



    Stevie:
    Heartless challenge
    Pick your path and I'll pray

    -- Gold Dust Woman, Fleetwood Mac


    Elon:
    Something
    I think
    is going to be quite important
    — I don't know of a company that's working on it seriously —
    is a neural lace



    Stevie:
    Give to me your leather
    Take from me
    My lace
    Take from me
    My lace
    Take from me
    My lace 

    --Leather and Lace, Stevie Nicks


    Scientists Just Invented the Neural Lace

    A group of chemists and engineers who work with nanotechnology published a paper ... about an ultra-fine mesh that can merge into the brain to create what appears to be a seamless interface between machine and biological circuitry. Called “mesh electronics,” the device is so thin and supple that it can be injected with a needle — they’ve already tested it on mice, who survived the implantation and are thriving. The researchers describe their device as “syringe-injectable electronics,” and say it has a number of uses, including monitoring brain activity, delivering treatment for degenerative disorders like Parkinson’s, and even enhancing brain capabilities.




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    by @bahniks - click on image for a larger view


    By now, those of you familiar with the “methodological terrorism” controversy (PDF) are probably sick of  it. I won't go into any detail, other than to say that disagreements between the communities of (1) traditional psychologists who respect the current peer review process, and (2) reformers who advocate replication, post-publication peer review in social media, and alternate modes of dissemination, have been heated. In a nutshell, are the new media bad for science or good for science?

    Here, I'd like to examine some ideas in isolation from their source(s). This is to avoid the appearance of an ad hominem attack and to maintain a civil tone. Ultimately, we may learn that abusive argumentation and incivility are less common than expected. Or not well-defined, at least.


    Ad Hominem (Abusive) Argument.

    “Attacking the person making the argument, rather than the argument itself, when the attack on the person is completely irrelevant to the argument the person is making.”

    Does this really happen all that often?1 Does questioning someone's motives for maintaining the status quo constitute an ad hominem attack? If a researcher receives widespread media attention for their findings, can we find fault with their public statements, or is this ad hominem too? Off-the-cuff remarks on Twitter are the most likely place for attacks that meet the “abusive argument” definition. We should avoid it, or else it supports the trash-talk allegations.


    Tone.

    What is the appropriate tone for online debate? Who decides? Adults have criticized the language and attitudes of youth since the beginning of time. One person's funny irreverent witticism is another's destructo-criticism.

    I know I've been misunderstood. A lighthearted spoof with a bold red disclaimer (and advance apologies) was interpreted as sneering, ridiculing, and bullying (of a very senior figure). Another post, Spanner or Sex Object?, wasn't meant as methodological fetishism (so to speak). Some might say the images were objectionable, but they were included along with substantive critiques of the findings and their interpretation, not of the authors.

    In the the wider world of the internet, there's no doubt that the level of hostility, trollish behavior, abusive threats, racism, and sexism have risen dramatically (just ask Leslie Jones about her Twitter experience). Let's hope that we can monitor our behavior and filter out mean spirited, personal attacks.


    Peer review is more civil.

    Like many others, I've suffered from the tone of anonymous peer review at journals.  My very first review as a graduate student was one paragraph long. “The current work doesn't add to the literature, it detracts from it” (or something like that). The decision was made on the basis of only one reviewer. One paragraph. Overly harsh.

    That was real encouraging. Enough to drive a fledgling researcher out of the field, eh? “Don't take it personally” is the recommended mantra. Don't take it personally. Don't take it personally.


    Destructo-Critic



    I'm very proud to have been appointed Destructive Critic by an admired giant in the field - Max Coltheart!


    Arguably, I am the first destructo-critic, given that I started The Neurocritic blog back in 2006. This was well before the current replication crisis in social psychology.2 My inaugural entry critiqued an fMRI paper on empathy, followed by posts on lie detection, HARKing,3media sensationalism, ubiquitous anterior cingulate and insular activation, the insufficiency of fMRI for explaining qualia, mind reading, and anonymous peer review. I didn't notice any ad hominem attacks back then. Have I become more snarky over time?

    As Neuroskeptic wondered, when the critics of critics don't name names, how are we to know who are the objectionable ones, and who are the ones aiming to improve the field? Perhaps it's time for some self-examination, and that's true for stakeholders on both sides of the fence. My aim has always been to improve the field I love. Or else, why would I have persisted for so long?


    Self-Destructive Critic

    In real life I am my own harshest critic. It's a pernicious and intractable element of my disease. I never apply the same standards to other people. I always try to frame criticism (whether in person or in anonymous peer reviews) in as positive a light as possible. “It might be better if the authors tried this...” Try to find the positive elements. Most people would say I'm very considerate.

    In real life I am a self-destructive critic of the self. And this is my truth.


    Footnotes

    1 I can think of one notable exception, a very high profile public figure in the UK... and even then, much of the criticism is of her views.

    2 It's mostly called The Replication Crisis in Psychology, but the strong focus has been on social psychology. Neuroimaging research (fMRI) has come under fire as well. Initiatives for data sharing (e.g., OpenfMRI and Neurovault and the fMRI Data Center well before that) and reproducibility are on the rise.

    3 Hypothesizing after the results are known (Kerr, 1998)


    Further Reading

    Promoting open, critical, civil, and inclusive scientific discourse in Psychology

    The Day the Palm hit the Face

    Some thoughts on methodological terrorism this one is particularly indispensable

    Weapons of math destruction

    Terrorist Fiske Jab: On “Destructo-Criticism”

    “Methodological terrorism” and other myths

    We talked to the scientist at the center of a brutal firestorm in the field of psychology

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