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- 07/01/16--18:58: _Newly Discovered EE...
- 07/16/16--19:26: _Professor Richard F...
- 07/22/16--02:53: _A New Twist on Some...
- 07/29/16--19:21: _Clinical Trial for ...
- 08/08/16--03:12: _Scientific Study Sh...
- 08/28/16--15:06: _Healing Prayer and ...
- 08/31/16--23:58: _Music from Your Brain
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- 09/17/16--16:46: _The Neural Lace Tour
- 09/18/16--00:13: _Coming Soon: The Ne...
- 09/29/16--22:14: _Self-Appointed Dest...
- 10/21/16--14:42: _Update on Indie Neu...
- 10/30/16--17:36: _Haunting Delusions ...
- 11/21/16--04:25: _How did Gall Identi...
- 11/28/16--01:44: _Airplane Headache I...
- 12/03/16--03:19: _19th Century DIY Br...
- 12/23/16--01:54: _Bad news for DARPA'...
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- 01/22/17--22:57: _Why Do Political Fi...
- 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
- 07/22/16--02:53: A New Twist on Some Old Brain Myths
- 08/08/16--03:12: Scientific Study Shows Mediums Are Wrong 46.2% of the Time
- 08/28/16--15:06: Healing Prayer and the Brain: Not a Match Made in Heaven
- 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
- 08/31/16--23:58: Music from Your Brain
- 09/07/16--10:27: Pain, Synesthesia, Aging, The Dress, and more
- 09/17/16--16:46: The Neural Lace Tour
- 09/18/16--00:13: Coming Soon: The Neural Correlates of Procrastination
- 09/29/16--22:14: Self-Appointed Destructive Critic
- 10/21/16--14:42: Update on Indie Neuroblogs
- http://www.russpoldrack.org/ feeds/posts/default
- 10/30/16--17:36: Haunting Delusions of Identity
- 11/21/16--04:25: How did Gall Identify his 27 Faculties?
- 11/28/16--01:44: Airplane Headache II: The Sequel
- 12/03/16--03:19: 19th Century DIY Brain Stimulation
- 12/26/16--17:07: Penn's Restoring Active Memory dataset freely available
- 01/15/17--00:31: Neuroscience Can't Heal a Divided Nation
- 01/22/17--22:57: Why Do Political Figures Lie So Blatantly?
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:
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.
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.”
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.
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.
Henry Markram dethroned, @HumanBrainProj under new leadership, with obscure goals. Story of hubris & empty promises https://t.co/CIGXtzxIqL— Leonid Schneider (@schneiderleonid) July 15, 2016
https://t.co/4FqQbP53c9 I didn't resign from HBP. I lead a task. How many other errors in this scurrilous piece? @prsjf@HumanBrainProj— Richard Frackowiak (@prsjf) July 15, 2016
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.
What does this have to do with the HBP?? Nothing. It came along as part of the larger anti-Markram package.
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
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.
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).
lol this RCT actually had a negative result. Fascinating to compare UK vs US media coverage. https://t.co/z4hfC3DSB8https://t.co/Jgk8wsleci— ben goldacre (@bengoldacre) July 27, 2016
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 blue. LMTX 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.
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.
Here's our latest study on mediumship: "Prediction of Mortality Based on Facial Characteristics". Available here: https://t.co/jVMHmF07Dj— Dean Radin (@DeanRadin) May 21, 2016
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.
People can sense #Mortality after brief look at facial photo, & show related brain activity https://t.co/bukFvVUQ1fpic.twitter.com/fE2u6Zaf8E— Frontiers (@FrontiersIn) May 25, 2016
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.
1 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.
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
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.
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):
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
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).
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.
Lutters, B., & Koehler, P. (2016). Brainwaves in concert: the 20th century sonification of the electroencephalogram. Brain DOI: 10.1093/brain/aww207
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.
Stevie Nicks and Elon Musk— finally together in this stunning collection...
I keep my visions to myself
Creating a neural lace is the thing that really matters for humanity to achieve symbiosis with machines— Elon Musk (@elonmusk) June 4, 2016
I need you today
Give to me your leather
Take from me
Who wants to wrap around your dreams and...
Have you any dreams you'd like to sell?
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.
Like a strand in the wind
In the web that is my own
When it rains
Pick your path and I'll pray
Take from me
Take from me
Take from me
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.
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.
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.
Missed all the critic-bashing. Trying to settle on Methodological Terrorist, Methodological Fetishist, or Self-Appointed Destructive Critic— The Neurocritic (@neurocritic) September 23, 2016
I'm very proud to have been appointed Destructive Critic by an admired giant in the field - Max Coltheart!
I hereby appoint you to the position of Destructive Critic. https://t.co/ScExgmBmTq— Max Coltheart (@maxcoltheart) September 24, 2016
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?
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.
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)
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
Independent Neuroblogs, a combined aggregate feed for non-network Neuroscience Blogs, was started on FriendFeed in response to the proliferation of blog networks in 2010. The associated Twitter account @neuroghettohas survived the demise of FriendFeed, Yahoo Pipes, and now twitterfeed. The feeds are currently being shared through the service dlvr.it.
What initially started as a group of 38 neuro/psych blogs in September 2010 grew to a list of
Independent Neuroblogs as part of the science blogging ecosystem
An updated list of the neuroscience and psychology blogs included in the @neuroghetto feed is long overdue. Some of them are no longer active, others may have have updated their url or moved to a different site.
Without further ado, here's the list of 197 RRS feeds included in Indie Neuroblogs:
I have a list of 8-10 more blogs to add. Please leave a comment if you'd like to be added (or removed) from the list.
Delusional misidentification syndromes have fascinated filmmakers and psychiatrists alike. Afflicted individuals suffer under the false belief that persons or things around them have changed their identities or appearance. Classification schemes have varied, but a general outline includes:
from Table 1 (Ellis et al., 1994). Classification and description of the four principal delusional misidentification syndromes (DMS).
Bugs Bunny isn't delusional in the image above, because the mild mannered Dr. Jekyll has actually morphed into the monstrous and hideous Mr. Hyde. Or has he?
Cartoon interpretations of Strange Case of Dr. Jekyll and Mr. Hyde portray the mad scientist's transformation as literal, and why not? It's visually arresting. We needn't dwell on the duality of good vs. evil within, or the harmful effects of repressive Victorian [or 1950s American] mores (although Kevin McCorry makes a convincing case that Hyde and Hare is An Overlooked Masterpiece).
The real syndrome of intermetamorphosis was first described by Courbon and Tusques in 1932 (English translation, 1994):
We present here a woman who, not content with seeing doubles, sometimes has the delusion that people around her are transformed physically and psychologically into other people.
Sylvanie G., 49 years of age (nothing to note from her family history) was admitted to Vaucluse on 9 February 1924 for melancholic depression and paranoia with ideas of persecution. She improved and was discharged on March 1924 but was readmitted 8 years later on 9 March 1932, never having lost her delusions, says the record.
. . .
Objects and animals which she owns appeared to her to be altered or simply displaced: ’They have changed my hens, they’ve put two old ones in the place of two young ones, they had large combs instead of small ones.’ People were transforming her clothes, she goes out in a brand new coat, and everyone around her looking at it is saying that she has a dirty and ripped coat (that is what she perceives). The people that she met were also changing: ’They stretch their ears... I have seen women change into men, young women into old men...’
Here's an incident involving transformation of Sylvanie G.'s husband, who reverted to his actual self just in time to repair the electrical supply:
Her husband changed in appearance, in behaviour, facially and took on the characteristic expression of some neighbour or other; it was this neighbour who had become embodied in him. “In a second my husband is taller, smaller or younger. It’s the individual into whom he is transformed who lives, who is in his skin, who moves. It’s as if you put yourself into his skin, it was you and not him. It was not merely a change, but a true transformation: 'I have changed with age, but have not transformed, I am still the same person.' One day, he changed into young M. Panier. He took on his mannerisms and face, spoke like him; but there was an electricity breakdown and M. Panier, who is not an electrician, tried in vain to repair it.”
The next documented case of intermetamorphosis wasn't published until 1978 (Malliaras et al.). Note the co-occurrence of several delusions, a common theme in these case reports.1
Ms. A, an introverted, shy, and stubborn woman of 19 with high moral standards, is the eldest of two children born to an introverted farmer and a cyclothymic housewife. Her childhood was uneventful and free from neurotic symptoms.
Her illness began when she was 18; she had difficulty in concentration, thought blocks, loosening of associations, and deterioration in scholastic achievement, followed by overt anxiety with psychomotor restlessness, insomnia, feelings of depersonalization and derealization, false memories of familiarity, auditory hallucinations, religious ideas of grandeur, and erotic delusions. Her behavior became strange and unpredictable. Later, delusional misidentifications of the intermetamorphosis type appeared and dominated the clinical picture. They consisted of her conviction that various persons (a taxi driver, a salesman, a pedestrian, a priest) were in fact Mr. B, her theology instructor, who she believed was in love with her. She insisted that these persons were physically and psychologically identical with Mr. B, and her delusional misidentifications continued even after Mr. B left the town to work elsewhere.
The patient was treated with “high doses of [unnamed] major tranquilizers” and started to improve after 6 weeks. Then after 3 months of inpatient treatment, “she was symptom-free and had developed insight into her past psychopathology.” Routine laboratory investigations were considered normal, but her neuropsych testing and EEG were not normal. Her verbal IQ was 120 but her performance IQ was only 82. This 38 point discrepancy strongly suggested that her visual perception, reasoning, memory, and other visual abilities went awry. These deficits are presumably related to her propensity for visual misidentification.
Her EEG showed diffuse abnormalities and frequent paroxysmal slow and sharp waves, especially in the temporal lobes. Stimulation with light produced high amplitude spikes, “associated with jerky movements of the upper and lower extremities (photomyoclonic response).” So even if she wasn't having frank seizures, her EEG activity was similar to what is observed in epilepsy. The authors discussed an organic contribution to her delusions, which was an era-appropriate but now quaint way of saying that something “neurological” was wrong with her brain (as opposed to something purely “psychiatric”). Although delusional misidentification syndromes can occur after brain injury and substance abuse (Silva et al., 1991), they are most often observed in the context of schizophrenia.
Silva and colleagues (1991) reported on 15 cases of intermetamorphosis, which were often accompanied by violent behavior — including murder (n=2), attempted murder (n=1), and other physically harmful behaviors (n=9). In one detailed case report, the authors described a 30 year old male who was recently jailed for violent behavior. He had been experiencing psychotic symptoms for several years. He held the delusional belief that...
...physical duplicates of his family who had different minds wanted to kill him and turn him into robot. ... The beings that inhabited the bodies of his parents and 2 sisters often transformed themselves into animals, including werewolves, vampire bats, snakes, dogs and monkeys. Frequently, he believed these animals wanted to kill him.
The poor man stabbed his sister when he believed she was transformed into a half-sister, half-snake hybrid — truly a living American Horror Story.
After the attack, he indicated that his sister was both a demon and spirit as well as a space creature that wanted to devour his head and replace it with an animal's head. He also reported that she had the power of possession.
Fortunately, his sister survived the attack. But unfortunately, the man didn't respond to antipsychotic medications. He had a history of alcohol abuse, including drinking on the day of the incident. His diagnosis was chronic schizophrenia, paranoid type.
Also fascinating are cases of reverse intermetamorphosis, where individuals believe they themselves have undergone transformation. Clinical lycanthropy, the delusion that one has been transformed into a wolf or other animal, is a special instance of reverse intermetamorphosis.
In Silva et al.'s clinical series, three of the 15 patients believed they were changing their own physical and psychological identities. Religious, social and cultural factors almost certainly influence the content of self-shifting, as is the case for other types of delusions.
1See these papers, for example:
The co-occurence of reduplicative paramnesia, intermetamorphosis and capgras syndrome: a case presentation.
The Comorbidity of Reduplicative Paramnesia, Intermetamorphosis, Reverse-Intermetamorphosis, Misidentification of Reflection, and Capgras Syndrome in an Adolescent Patient.
Coexistence of Reverse Capgras Syndrome, Subjective Double and Cotard Syndrome.
2See these blog posts:
Psychopharmacology of Lycanthropy
Werewolves of London, Ontario
Ophidianthropy: The Delusion of Being Transformed into a Snake
Courbon, P., & Tusques, J. (1994 English translation of 1932 French text). Illusions d'intermetamorphose et de charme. History of Psychiatry, 5 (17), 139-146 DOI: 10.1177/0957154X9400501711
Ellis, H., Luauté, J., & Retterstøl, N. (1994). Delusional Misidentification Syndromes Psychopathology, 27 (3-5), 117-120 DOI: 10.1159/000284856
Malliaras DE, Kossovitsa YT, Christodoulou GN. (1978). Organic contributors to the intermetamorphosis syndrome American Journal of Psychiatry, 135 (8), 985-987 DOI: 10.1176/ajp.135.8.985
Silva, A., Leong, G., & Shaner, A. (1991). The Syndrome of Intermetamorphosis. Psychopathology, 24 (3), 158-165 DOI: 10.1159/000284709
Silva, A., & Leong, G. (1994). Delusions of Psychological Change of the Self. Psychopathology, 27 (6), 285-290 DOI: 10.1159/000284885