Tag Archives: Developmental Synaesthesia

Memory is fallible, but then again, there’s super-recognizers

It appears that super-recognizers (people with very good face recognition ability) are mentioned in the new book The Memory Illusion by Dr Julia Shaw, but I cannot find a preview of that bit of text. I’d be interested in reading what Shaw wrote about supers, because I believe that we are very good evidence against the argument that this book, and some other pop psychology books have offered, that human memory is unreliable and open to interference. I’ve noticed that writing by researchers and authors who offer arguments against the reliability of human memory (such as Elizabeth Loftus) and also those who offer arguments against the idea of natural or inborn talent (such as K. Anders Ericssson) tend to ignore or gloss over the many things that science already knows about face recognition, face memory and super-recognizers.

I’m happy to admit that people who perform amazing feats of semantic memory such as remembering huge lists of random facts or meaningless digits using new or ancient memory techniques have trained their own memories with many hours of practice, but super-recognizers are very different to those people. We do not knowingly or deliberately train ourselves and we do not consciously use tricks or techniques. Maybe we self-train and invent strategies in an implicit manner, but it is also true that super-recognition does seem to run in families, so there seems to be an important genetic contribution to the elite ability or talent, just as there is clearly a genetic component to developmental prospagnosia (very poor face recognition ability).

Face memory researchers have been investigating the phenomenon of super-recognition since it was first described in 2009, and there seems to be ample evidence that supers have very long-lasting, adaptable, and reliable memory of the faces of other humans. We can remember faces across many decades and across changes in facial appearance by forces such as ageing. I believe I am very good at spotting facial family resemblance and facial phenotypes across gender and age. Super-recognizers can also display very accurate face recognition after being briefly shown images of only faces (no hair etc) of a large group of faces of same gender and similar age, some of them very degraded images. This accuracy requires being able to avoid false positives and false negatives. There’s no denying that supers are bloody good at faces. There’s also no denying that some other people are very poor at face memory, so authors of these pop psychology books that denigrate human memory are able to state with a vague air of truth that human memory for faces is fallible. But such a statement ignores what we know about supers, and this is why I have issues with the common practice of psychology researchers of roputinely discarding data from outliers in their studies. If any of that discarded data is from outlier study participants that did incredible well in tests of face recognition or memory, then those participants could be supers and their data tells an important story about human memory and human face recognition.

I think supers are interesting examples of a type of human memory that stands out from other types of human memory as reliable, long-lasting, easily or unconsciously enmcoded and accurate, so one should wonder, why is the face memory of supers so great? My bet is that this niche example of human memory has two characteristics that give it special power: it is disributed across a broad network of neurons throughout the brain (and this is why it might be found along-side synaesthesia), and it is also a type of visual memory, which I can only assume is a very ancient and well-evolved type of human memory that predates stuff like writing and language, that happens in areas of the brain that work amazingly and unconsciously because they evloved well before there ever were humans. I cannot imagine how genuine face memory could ever be interfered with by suggestion or manipulation, because the tricks that some memory researchers have used to fool around with the memories of study participants work on a conscious level communicated by verbal means. Genuine face memory is implicit and visual. It is safe from such nonsense.

The Memory Illusion by Dr Julia Shaw:



Two recently-published attention-grabbing open-access neuroscience journal papers

Shriki O, Sadeh Y, Ward J (2016) The Emergence of Synaesthesia in a Neuronal Network Model via Changes in Perceptual Sensitivity and Plasticity. PLoS Computational Biology. 12(7): e1004959. doi:10.1371/journal.pcbi.1004959


“The model unifies different causes of synaesthesia within a single theoretical framework and repositions synaesthesia not as some quirk of aberrant connectivity, but rather as a functional brain state that can emerge as a consequence of optimising sensory information processing.”


Anders Eklund, Thomas E. Nichols, and Hans Knutsson (2016) Cluster failure: Why fMRI inferences for spatial extent have inflated false-positive rates.
PNAS 2016 ; published ahead of print June 28, 2016, doi:10.1073/pnas.1602413113


“In theory, we should find 5% false positives (for a significance threshold of 5%), but instead we found that the most common software packages for fMRI analysis (SPM, FSL, AFNI) can result in false-positive rates of up to 70%. These results question the validity of some 40,000 fMRI studies and may have a large impact on the interpretation of neuroimaging results.”

Interesting commentary:

Oxenham, Simon Thousands of fMRI brain studies in doubt due to software flaws. New Scientist. July 18th 2016.





Wow, this is interesting

Scientists Find Vessels That Connect Immune System And Brain. June 3, 2015 | by Stephen Luntz. IFL Science.


Structural and functional features of central nervous system lymphatic vessels

Antoine Louveau, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, Kevin S. Lee, Tajie H. Harris & Jonathan Kipnis
Nature (2015) doi:10.1038/nature14432
Received 30 October 2014 Accepted 20 March 2015 Published online 01 June 2015


I find this most interesting for a number of reasons. Firstly, the discovery showing that the human brain has functional lymphatic vessels connecting the brain with the immune system adds to a growing collection of evidence that the immune system plays important roles within the brain, which is an apparent partial violation of the long-held concept of the “blood-brain barrier” (as was described in a dated and inadequate chapter by Dr Karl in his 2013 pop science book Game of Knowns). In 2012 I was apparently the first person in the world, at this blog, to publish the ideas that high or low levels of the “component” immune chemicals at various points in development could be the cause of conditions of the brain such as developmental synaesthesia and Benson’s syndrome or PCA. My ideas were inspired by the very exciting research in areas such as microglia, complement, synaptic pruning and MHC1 molecules.

Another reason why this new discovery linking the central nervous system with the lymphatic and immune systems by researchers from the University of Virginia is so exciting is the fact that it is an unexpected discovery, as one might have thought that human anatomy would have already been thoroughly researched and discovered through the history of medical science to date, but then again, surprising new discoveries in human anatomy have not been unknown in recent years, with discoveries of new features in the human eye, knee and clitoris, the rediscovery last year of a major white matter tract (the vertical occipital fasciculus) at the rear of the brain that could play a central role in skills such as reading, and a new shape of neuron discovered in mouse brains. These new discoveries are exciting and also rather unsettling; exciting because it appears that important new discoveries in human neuroscience and anatomy are still possible, and unsettling because genuinely surprising new discoveries in science seem to indicate that science is not a steady accumulation of knowledge and a path of upward progress, as many believe. This may or may not be surprising to you, depending on which theory in the philosophy of science you favour. I think the discoveries of the VOF and the collection of discoveries about the roles and anatomy of the immune system in the human brain could be interpreted as evidence showing how incorrect ideas in science can become widely-accepted and widely-taught and could also have delayed the progress of new discoveries in neuroscience. How much further might we have come by now in our understanding of the human brain and mind if not for the popularity of the idea that the human brain is quarantined from the immune system? Which other influential ideas about the human brain are holding us back from a clearer understanding of the brain’s workings and diseases?

All those years of neuroimaging research on the brains of synaesthetes has found nothing of substance?

Hupé J and Dojat M (2015) A critical review of the neuroimaging literature on synesthesia. Frontiers in Human Neuroscience. 9:103.


“Our critical review therefore casts some doubts on whether any neural correlate of the synesthetic experience has been established yet”

That is a bit of a shock to read. This isn’t the first time that I’ve gotten a big shock after reading a paper in the journal Frontiers in Human Neuroscience. There was that little matter of some of my most amazing neuroscientific ideas published at this blog being ripped-off and used as the guts of an “opinion article” in that journal in 2013. I haven’t forgotten that episode. Who would have thought so much excitement is there to be found inside a science journal? I should make it clear that the researchers who did that thing in 2013 are NOT the authors of the above paper, but at the same time, I’ve got to wonder where Hupé and Dojat got this idea from

“…synesthesia could be reconsidered as a special kind of childhood memory, …”

Sure, they could have thought of that under their own steam, but I still want to point out that the central, seminal idea of this blog, right from the very first post in 2010, has been the idea that synaesthesia is linked in some meaningful way with face memory, in my case with super-recognizer ability in face memory, and there are many articles in this blog that show and hint that the heart of synaesthesia is memories created in childhood and many different types of synaesthesia operate in ways that are so much like memory that the differences are only quantitative. There was even one article published in 2013 at this blog in which I stated that

“…the Proust phenomenon is considered to be a type of memory and many of my observations at this blog have demonstrated that synaesthesia can involve memory, is an element of the “method of loci” memory technique and I would argue operates like memory. Yes, Yes, Yes, the Proust Phenomenon is a close relative of synaesthesia.”

Some ideas that I’d like to (explicitly) lay claim to (right now) in 2014

Action-packed YouTube video clip

Immune cell in the brain swallows synapses to sculpt neurons during development.

Posted by NIHNINDS (National Institute of Neurological Disorders and Stroke) at YouTube on May 22, 2012.


The green thing is a mouse’s microglial cell. The movie is “courtesy Dorothy Schafer, Ph.D. and Beth Stevens, Ph.D. at Boston Children’s Hospital.” At this blog I have speculated that the kind of process shown in this brief video clip possibly happens less often in the brains of some people because they have lower levels of some of the complement chemicals that are a part of the immune system, with the result being the development of, or the retaining of, childhood or developmental synaesthesia. Some of the complement chemicals mark out synapses for destruction, I believe.

Don’t forget the parietal lobe – the connections are interesting

If you have been reading this blog for a long time you’d know I’ve been trying to figure out which parts of my brain are responsible for my synaesthesia and related experiences. I’ve found that the right fusiform gyrus is a part of the brain that comes up over and over again, in relation to synaesthesia and also face recognition I experience many types of synaesthesia and also have achieved scores in face recognition tests consistent with being a super-recognizer, so this combination seems significant, and despite a lack of any evidence from other case studies linking synaesthesia with superior ability in face recognition, I still think it is a possible relationship that should be scientifically investigated, especially in light of a pattern of associations which I believe suggests that synaesthesia might be a neuropsychological condition that could be seen as the opposite of Benson’s syndrome, which is a type of dementia that involves a loss of visual perception, apparently including a loss of face recognition ability. While synesthesia is generally an inborn developmental condition, and Benson’s or PCA a neurodegenerative condition with a typical onset late in life, I’ve still got to wonder whether inborn factors contribute towards Benson’s. While Benson’s is considered to be a variant of Alzheimer’s, I don’t think anyone knows why it causes deterioration in different areas of the brain as are affected by Alzheimer’s, apparently the same parts of the brain (at the rear) that appear to be enhanced or hyperactive in my brain, and I also doubt that anyone knows why Benson’s has an onset earlier than Alzheimer’s disease. I’m sceptical of the idea that Benson’s is just Alzheimer’s of the back-end of the brain. I suspect that immune system elements microglia and complement might be central to an explanation for Benson’s syndrome. Reading Dr B. Croisile’s paper about Benson’s I’m struck by the many very strange effects of Benson’s on perception, and I wonder at the ways in which a study of it might inform science about  the workings of the brain. I think it is at least as interesting as synaesthesia, which attracts a lot of attention from researchers. Apparently people with Benson’s cannot imitate movements. Does this mean that the mirror-neuron system which so many neuroscientists have gotten so excited about is located at the rear of the brain? I note that the inferior parietal cortex is one of the parts of the brain that are thought to house mirror neurons.

When I set out to write this post I had actually planned to write about a fairly recent review journal paper focusing on recent research about the most common and well-known types of synaesthesia: coloured hearing, coloured graphemes and time units in space synaesthesia. I really like the paper cited below by Professor Karsten Specht from the University of Bergen in Norway, and I’d recommend it to anyone who wants to learn about the latest knowledge about synaesthesia from just one paper. I only have a couple of gripes about he paper. I wouldn’t describe synaesthesia as “rare” as Specht does. Ward, Sagiv and Butterworth wrote in 2009 that around 12% of the population have number forms, and that estimate doesn’t surprise me. Synaesthesia in general can’t be rare if it includes one type that isn’t rare. Time-space synaesthesia or number forms is one type of synaesthesia which the synaesthete can have but not suspect that it is synesthesia, or anything out of the ordinary, so I’d guess it could be very much under-reported and under-estimated. My other gripe with Professor Specht’s paper is this bit; “In recent years, several studies have attempted to investigate whether synaesthesia is primarily a perceptual or conceptual phenomenon.” I think Specht is here presenting the reader with a false dichotomy. In some of the types of synaesthesia and related phenomena which I experience sensory perception, memory and conceptual thinking are connected with synaesthesthetic linkages, so I doubt that there is much point in trying to characterise synaesthesia as one or another type of phenomenon. I was very excited when I read the book Beyond Human Nature by philosopher Jesse Prinz. Professor Prinz argued that we think in mental images rather than in language. He wrote that “It used to be thought that the back part of the brain is used for perceiving and the front is used for thinking. But we now know that the back part of the brain, where most of the senses are located, is very active when people think. Moreover, we know that the front part of the brain does not work on its own, but rather coordinates and reactivates sensory patterns in the back. Recent evidence from Linda Chao and Alex Martin has shown that reading activates the same areas as looking at pictures, suggesting that we visualize what we read.” In a post that I wrote a while ago I described involuntarily “seeing” in my mind’s eye visual images of landscapes and building interiors from imagination and memory while listening to an autobiographical audio-book. I thought it was probably related to synaesthesia, but it appears that everyone’s brain illustrates text with images when reading. Perhaps synaesthetes do this to a greater degree or in a way that is more available to conscious awareness.

Anyway, back to Specht’s paper. Having read it I now suspect that the parts of my brain that are bigger or better connected or more active or something are: the right fusiform gyrus (including the FFA), the left parietal lobe including the left intraparietal sulcus, the right inferior parietal lobe, the hippocampus (I’m sure is involved with IMLM) and the parahippocampal gyrus. I’d guess that these are the places where interesting things are happening. It appears that the role of the parietal lobe in synaesthesia has been understated in the past. It is now thought that synaesthesia does not solely involve the cross-activation of two different sensory areas (as if it was ever that simple!), but it also requires a “binding” process to happen in the parietal lobe. There is no underestimating the importance of this binding.

If you are as interested in synaesthesia and bits of the brain as I am, you might also like to read a much longer journal paper by Rouw, Scholte and Colizoli that was published last year. It is available in full text at no cost, but I don’t think it covers non-colour types of synaesthesia. Details can be found below. One part of the parietal lobe mentioned in that paper, which is cited by a few studies as involved with synaesthesia is the inferior parietal lobule (IPL, Brodmann areas 39 and 40). It is also known as Geschwind’s territory because the neurologist Geschwind predicted in the 1960s that the parietal lobe played a role in language, and was proven right when the IPL was found to include a second connection between Broca’s area and Wernicke’s area, which are of central importance in language. The IPL is very interesting as a part of the brain involved in synaesthesia because according to a 2004 article in New Scientist magazine the IPL matures at a late age, between the ages of five and seven years, which just happens to be time in life when children typically learn the ability to read and write, and it is also the age range in which some children develop grapheme-colour synaesthesia. I find this very interesting because in my family we have at least three closely related grapheme-colour synaesthetes who are unusually high achievers in reading and writing in testing and academic achievement. Two of these synaesthetes were early readers and also talented at language learning. What’s the betting that some gene that alters the development of the IPL is behind this? The author of the most interesting little science magazine article that brought me this news, Alison Motluk, is herself a synaesthete. Is it just a coincidence that a journalist with a well-connected brain has pointed out a number of interestingly related facts that are connected around the conceptual hub of the inferior parietal lobule?

Specht, Karsten Synaesthesia: cross activations, high interconnectivity, and a parietal hub. Translational Neuroscience. Volume 3 Number 1 (2012), 15-21, DOI: 10.2478/s13380-012-0007-z

Croisile, Bernard Benson’s syndrome or Posterior Cortical Atrophy. Orphanet. September 2004. http://www.orpha.net/data/patho/GB/uk-Benson.pdf

Ward, Jamie, Sagiv, Noam and Butterworth, Brian The impact of visuo-spatial number forms on simple arithmetic. Cortex. Volume 45 Issue 10Pages 1261-1265 (November 2009). http://www.cortexjournal.net/article/S0010-9452(09)00213-5/abstract

Rouw, Romke, Scholte, H. Steven, Colizoli, Olympia Brain areas involved in synaesthesia: A review. Journal of Neuropsychology. Special Issue: Synaesthesia. September 2011 Volume 5 Issue 2 p.214-242. Article first published online: 16 SEP 2011 DOI: 10.1111/j.1748-6653.2011.02006.x  http://onlinelibrary.wiley.com/doi/10.1111/j.1748-6653.2011.02006.x/full

Motluk, Alison Two links good for kids’ language comphrehension. New Scientist. Issue 2478. December 18th 2004. p.12. http://www.newscientist.com/article/mg18424784.300-second-link-discovered-in-human-language-circuit.html

Is synaesthesia caused by low levels of complement? Is Benson’s syndrome (PCA) caused by too much complement C3? Could synesthesia and posterior cortical atrophy be considered in some way opposites?

A note of warning – If you are thinking about copying or plagiarizing any of the text, ideas or descriptions in this post and using it as your own work without giving me (C. Wright, author of the blog “Am I a Super-recognizer?”) the proper acknowledgement and citations, then think again. If you do that you will be found out and you will regret it. If you want to make reference to this post or any of the ideas in it make sure that you state in your work exactly where you first read about these ideas. If you wish to quote any text from this post be sure to cite this post at this blog properly. There are many established citation methods. If you quote or make reference to material in this blog in your work, it would be a common courtesy to let me know about your work (I’m interested!) in a comment on any of the posts in this blog. Thank you.

Top of C3 theory post

A quote from New Scientist magazine about a study of microglia responding to changes in synaptic function in mice by Assistant Professor Beth Stevens and colleagues:

“Synapses were marked out for destruction through labelling with an immune chemical called C3”

Immune cells gobble up healthy but idle brain cells. 1 June 2012 by Andy Coghlan New Scientst. Magazine issue 2867. http://www.newscientist.com/article/mg21428675.500-immune-cells-gobble-up-healthy-but-idle-brain-cells.html

A quote about her research at Prof Stevens’ professional web page:

“C1q and downstream complement proteins target synapses and are required for synapse elimination in the developing visual system.”

Beth Stevens, PhD, Boston Children’s Hospital http://www.childrenshospital.org/cfapps/research/data_admin/Site2674/mainpageS2674P0.html

A quote from Wikipedia about synaesthesia:

“This cross-activation may arise due to a failure of the normal developmental process of pruning, which is one of the key mechanisms of synaptic plasticity, in which connections between brain regions are partially eliminated with development.”

Wikipedia contributors Neural basis of synesthesia.  Wikipedia, The Free Encyclopedia, 25 May 2012, 01:45 UTC, http://en.wikipedia.org/w/index.php?title=Neural_basis_of_synesthesia&oldid=494244732

A quote from Wikipedia about Benson’s syndrome or Posterior Cortical Atrophy:

“The disease causes atrophy of the back (posterior) part of the cerebral cortex, resulting in the progressive disruption of complex visual processing.

Wikipedia contributors Posterior cortical atrophy Wikipedia, The Free Encyclopedia, 4 February 2012, 22:34 UTC, http://en.wikipedia.org/w/index.php?title=Posterior_cortical_atrophy&oldid=475033670

Two quotes by me from this blog:

“The idea that I have something like the opposite of Benson’s syndrome would neatly draw together all the elements of some odd phenomena that I have observed over a number of years…”

“I guess the million-dollar question is  – why does Benson’s syndrome affect only some specific parts of the brain? What is it about a certain group of areas of the brain that appear to make these areas prone to hyperconnectivity in some families, and vulnerable to dysfunction in Benson’s syndrome? Is there some magic chemical or process that regulates growth in these areas of the brain? I doubt that the answer could be so simple.”

The Opposite of Benson’s Syndrome? by C. Wright Am I a Super-recognizer? January 4, 2011. https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

My doubt has suddenly evaporated! Could complement be the “magic chemical”? Where’s my Nobel Prize in Physiology or Medicine?

The DOI link in the New Scientist article discussed above doesn’t work, but I’m quite sure this is the journal paper that the article is about:

Dorothy P. Schafer, Emily K. Lehrman, Amanda G. Kautzman, Ryuta Koyama, Alan R. Mardinly, Ryo Yamasaki, Richard M. Ransohoff, Michael E. Greenberg, Ben A. Barres, Beth Stevens Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner. Neuron. Volume 74 Issue 4 691-705, 24 May 2012. 10.1016/j.neuron.2012.03.026 http://www.cell.com/neuron/retrieve/pii/S0896627312003340

A number of other interesting journal papers can be found through Prof. Steven’s web page, some available to read in full text (if you can find the button to click on in the top right corner of the PubMed page). I also found a recently published item by Stevens and colleagues that looks like it is about the same subject as the New Scientist article, published in a conference abstract supplement of the journal Schizophrenia Research, which is a bit of a mystery as I didn’t think the title suggested schizophrenia. You need to pay to read the full text, which I didn’t. http://www.sciencedirect.com/science/article/pii/S0920996412700397

Here’s something else to read, if you’re keen. You can read the whole thing for free:

Marie-Ève Tremblay, Beth Stevens, Amanda Sierra, Hiroaki Wake, Alain Bessis and Axel Nimmerjahn The Role of Microglia in the Healthy Brain. Journal of Neuroscience. 9 November 2011, (45): 16064-16069; doi:10.1523/JNEUROSCI.4158-11.2011  http://www.jneurosci.org/content/31/45/16064.long


C3, C4, C5....

C3, C4, C5….