New additions to this post added at the end.
A note of warning – If you are thinking about copying or plagiarizing any of the text, ideas or descriptions in this post or using it in 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 my objection will be well publicized. If you believe that you published any of these ideas before I did, please let me know the details in a comment on this article. If you want to make reference to this blog 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.
The idea that Benson’s syndrome or posterior cortical atrophy or PCA, a variety of dementia, is caused or develops in a way that can be seen as the opposite of the synaesthesia linked with exceptional visual memory and literacy skills that runs in my family (this idea has been explored previously in this blog).
The idea that the above cited states develop or are caused in a way that makes them seem like opposites because they both affect the same or similar areas of the brain, but in opposite ways.
The idea that the above described process happens because Benson’s syndrome and our variety of synaesthesia are both mediated by the same or similar natural chemical or cells or biological agent in the brain, one caused by high levels of the mystery substance and the other caused by low levels (a hypothesis that I briefly suggested in January 2011).
The idea that one of the many known or unknown elements of the immune system that impact brain development is the mystery substance referred to above (a hypothesis that I briefly outlined in 2012).
The (implied in above ideas) idea of the immune hypothesis of synaesthesia. (This idea was first published by me in 2012 in a blog post archived here, was I believe plagiarized in 2013 here, and was the subject of my plagiarism claim here.)
The idea that one or more of the complement immune chemicals is the mystery substance referred to above.
The idea that the C3 complement immune chemical is the mystery substance referred to above.
The idea that synaesthesia is linked with one or maybe more immune diseases or conditions caused by low levels of complement.
The idea that genes for synaesthesia stay quite common in the gene pool because of some associated cognitive advantage (probably superior memory) that balances out any disadvantages caused by deficiencies in the immune system.
The idea that some or many people unintentionally experience a memory process that operates in a similar way to the method of loci memory technique in their everyday lives, unintentionally forming long-term associations between individual learned concepts and individual visual memories of scenes (I have named this phenomenon Involuntary Method of Loci Memorization or IMLM).
The idea that IMLM operates in such a similar way to synaesthesia that one could argue that it is a type of synaesthesia.
The idea that synaesthetes are more likely to experience IMLM than non-synaesthetes.
The (implied) idea that the method of loci memory technique is similar to or a type of synaesthesia.
The idea that synaesthetes might have a natural advantage in using the method of loci because the method of loci is similar to or is a type of synaesthesia. This idea that seems likely in light of the case of “S” the Russian memory performer with many types of synaesthesia described by Luria.
The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span.
The idea that IMLM is a phenomenon that is caused by enhanced synaptic plasticity throughout the life span and can thus be used as an indicator of which synaesthetes are synaesthetes due to enhanced synaptic plasticity throughout the life span rather than other possible causes of synaesthesia. Support for this idea comes from the fact that IMLM appears to be a non-developmental variety of synaesthesia that can form new long-term associations in adolescence and adulthood.
The idea that IMLM is a phenomenon that is caused by the unusual possession of levels of synaptic plasticity typical of a young child, during adolescence or adulthood.
The idea that IMLM is caused or enhanced by some characteristic of the immune system that affects the functioning of the brain. Many different elements of the incredibly complex immune system are thought to affect the functioning or development of the brain, and could thus be involved in IMLM, including the complement system, microglia and the MHC class I molecules. Researchers such as Beth Stevens and Carla Shatz have investigated this exciting area of neuroscience. In 2012 I hypothesized at this blog that synaesthesia could be caused by low levels of complement, this idea implying that the immune system is directly involved in synaesthesia (or at least some cases of synaesthesia). I believe these ideas were plagiarized in a paper published in 2013.
The idea that IMLM is similar to the “Proust phenomenon” in that it is very similar to synaesthesia or is a type of synaesthesia and involves episodic or autobiographical memory as a concurrent.
The idea that phonics as a foundational reading skill is similar to or is arguably a type of synaesthesia in that it involves the involuntary association of individual speech sounds with individual printed letters or combinations of letters, as the result of learning in early to mid childhood.
The idea that at least one type of dyslexia is like a deficiency of synaesthesia.
The implied idea that if synaesthesia has as it’s basis hyperconnectivity in the white matter of the brain, dyslexia as an opposite of synaesthesia or a deficiency of synaesthesia is or could be caused by hypoconnectivity in the white matter of the brain (I suspect there might be existing research evidence that supports this idea).
The implied idea that in at least one cluster or grouping of cases synaesthesia is associated with superiority in literacy or reading skill.
The idea that synaesthesia can happen in different regions of the brain, and because of this the experience of various types of synaesthesia can vary in detectable ways because of the influence on the synaesthesia of the varied ways that different areas of the brain operate. This can mean that one synaesthete can experience different types of synaesthesia that operate in very different ways, for example, some types of synaesthesia more rare or spontaneous or intrusive than other types. (I am not completely sure of the originality or the novelty of all of this idea.)
The idea that there is an association between synaesthesia and super-recognition that is not merely coincidental.
The idea that synaesthesia is a type of memory or learning. (Not sure if I’m the first to note this obvious fact).
The idea that synaesthesia concurrents are re-experienced memories, or re-activated “learnings” of concepts, not perceptions. (Not sure if I’m the first to note this obvious fact). In support of this idea I can assert that synaesthesia is like face recognition in that both are visual memory-based phenomena which are subject to the Verbal Overshadowing Effect or something very similar. My assertion that synaesthesia is subject to the verbal overshadowing effect is based on my own observations (outlined elsewhere in this post).
The idea that super-recognizers should or could be trained and employed as expert consultants in the practice of medical genetics.
The idea that medical geneticists and all types of medical specialists need to have a super-recognizer level of face memory or face recognition ability, so that they can intuitively and quickly recognize medical facies.
The idea that there is no clear point of distinction between medical facies or faces associated with genetic syndromes and normal faces.
The idea that super-recognizers could be used to facially identify blood relatives of a person or persons.
The idea that super-recognizers could be used to facially identify the specific ethnicity of a person.
(below ideas added January 28th 2014)
The idea that super-recognition or being a super-recognizer could develop as the result of an unusual level of fascination with the visual appearance of landscapes or scenes, rather than from a fascination with faces, and thus be a side-effect hyper-development of a part of the brain that serves two similar functions.
The idea that super-recognition or being a super-recognizer could, at least in some cases, develop as the result of a general hyper-development of the visual sense to compensate for problems in the auditory sense during childhood such as temporary deafness, recurrent ear infections, glue ear or poor auditory processing.
(below idea added February 1st 2014)
The idea that lexical-gustatory synaesthesia is an exaggerated form of some kind of evolutionary adaptation in the brain that biologically primes the mind to attend to or react to speech on the subject of food (this idea was discussed at this blog in a post dated January 27th 2011, with more consideration in a later post).
(below ideas added February 6th 2014)
The idea that creativity might be immediately enhanced during and only during the duration of physical or visual-spatial activity because the activity activates areas of the brain associated with movement and in turn these areas activate other areas of the brain including those that give rise to conceptual thinking, and the increased activation makes novel associations between diverse thoughts and concepts more likely, and that this process is like synaesthesia or is a type of synaesthesia, and the types of physical activity that are the most effective inducers of this effect might be highly specific, highly specific in effects, highly varied between individuals and highly idiosyncratic, as is typical of synaesthesia inducers and concurrents. Driving a car can act as an inducer of this effect. (I have gone some way to exploring this idea in past posts.)
The idea that mental flexibility might be immediately enhanced by the above effect, which I will name “movement – thought-flexibility synaesthesia”.
The idea that thinking might be immediately enhanced by the above effect.
The idea that memory might be immediately enhanced by the above effect.
The idea that the above effect is similar to embodied cognition or is a type of embodied cognition.
(below ideas added February 14th and February 20th 2014)
The idea that synaesthesia is like the process of face recognition (and vice versa), because they both
– are subject to the verbal overshadowing effect or something similar
– are automatic
– are involuntary
– have a sensory inducer, in face recognition always visual, in synaesthesia I think most frequently visual
– have or can have a concurrent that could be described as a memory, a concept or a personality (I’m comparing face recognition with personification synaesthesias and the synaesthesias that I have described at this blog which have visual memories of scenes as concurrents)
– are or can be visual in both the inducer and concurrent
– typically involve the fusiform gyrus
– involve set pairings of inducers and concurrents (same person’s face seen before then recognized later)
– involve set parings of highly specific inducers and concurrents (I recognize that an employee at my local supermarket has a sister who has just started working there too, as their faces and bodies and hair are near-identical, but for the extra acne and the more receding chin of the new employee. They are very similar in appearance but my discrimination is highly specific, just as I can recognize that the green wall on the lower floor of a public library is close to but not quite the same colour as Tuesday.)
– both can have, but do not always have an actual face as an inducer (we can recognize the faces of celebrities in photos, caricatures and art, even seeing Marilyn Monroe’s face in a pattern of brown coffee cups stuck to the wall at the coffee shop at the art gallery.)
(below idea added February 17th 2014)
“My particular interest in personification is my own theory that personification synaesthesia (as experienced by myself) or something like it gives rise to superiority in face memory (or being a super-recognizer) by naturally making the faces of unknown people more memorable and interesting”
The above is a quote from an article that was published at the blog in October 2013.
(below ideas added February 19th 2014)
The idea that the synaesthesia brain is the result of the developmental influence or shaping from, or the adaptation to, the behavioural phenomenon of “flow” as described by Mihaly Csikszentmihalyi.
The idea that synaesthesia, intellectual giftedness or high IQ and autism or Asperger syndrome seem to coincide more often than chance because gifted and autistic kids are more likely to experience “flow” and this in turn can influence the developing brain in a way that gives rise to synaesthesia.
(below ideas added February 20th 2014)
The idea that the genuine conscious awareness of synaesthesia is a threshold phenomenon that operates in conflict or competition with conscious thinking, meaning that consciously thinking about synaesthesia can inferfere with the perception of concurrents, and synaesthesia must reach a particular level of intensity before it interrupts the experience of consciousness and becomes itself the subject of conscious awareness. I think that the idea that thinking about synaesthesia can interfere with the perception of synaesthesia might be related to the “verbal overshadowing” effect which has been described and debated about by researchers. In fairness I should point out that Mark C. Price speculated in the recently published (2013) Oxford Handbook of Synesthesia that synaesthesia could be subject to the verbal overshadowing effect. My own ideas were arrived upon independently from Price’s writing or work. I base the ideas of synaesthesia being a threshold phenomenon which can also be interfered with by conscious thinking on a number of my own observations. In direct contradiction to what I had expected to find, my scores for accuracy for individual letters and numbers in The Synesthesia Battery (a scientifically-validated online test of synaesthesia) were lower for the numbers and letters that have colours that I find beautiful and which I have thought about to some degree, while my best accuracy was for the numbers and letters that have the dull and ugly colours. It seems the less I think about the concurrents the more accurately I can percieve them when they are evoked. I have also noticed that most of the types of synaesthesia that I experience I was not consciously aware of before I started to think about and examine the idea of synaesthesia. I never realised that I had complete stability in the colours I associate with months and days of the week till I tested myself. While I had a dim awareness of colour colouring my thoughts, I’d not realised that this worked like synaesthesia till I went looking for a pattern using simple testing. My fine motor movement-visual memories of scenes synaesthesia evokes concurrents that are so fleetingly and subtly experienced that they just feel like random thoughts, and indeed I now believe it is possible that the random thoughts of many or even all people are in fact synaesthesia of various types. I have also observed that there are some very unsubtle and intrusive types of syn that I experience, and they are typically rarely experienced and are associated with people, emotions, faces, singing voices or music that I find striking or novel as inducers. Because of the circumstances of these examples of synaesthesia, I think some kind of threshold is being breached when these types of synaesthesia are experienced by me.
The idea that one of the established defining criteria for synaesthesia, that it gives rise to perceptions or concurrents which are “consistent and generic (i.e., simple rather than pictorial)”, is wrong, and specific categories of memories of complex visual images such as faces and scenes, which are processed in the fusiform gyrus, can also be experienced as genuine synaesthesia concurrents. I base this assertion on the fact that I often involuntarily experience synesthesia concurrents of this type, and I have written about such experiences right from the first post in this blog which was published in 2010. I have also named types of synesthesia that have complex visual memories as concurrents: the strange phenomenon, fine motor task – visual place memory synaesthesia, involuntary method of loci memorization, etc. There are also many accounts or scientific observations of synaesthesia with complex visual concurrents in the scientific literature on synaesthesia.
New additions 2020
Is the existence of hyperostosis frontalis interna or Morgagni-Stewart-Morel syndrome as a quite common but typically undiagnosed and untreated condition, and the common characterisation of it as a benign or inconsequential condition, evidence of the medical neglect of older women?
Could hypothalamic hamartoma be an underlying cause of hyperostosis frontalis interna? The hypothalamus, which is affected by HFI, plays a role in regulating calcium metabolism in rats, apparently.
Are many cases of “autism” really undiagnosed cases of hypothalamic hamartoma? How many cases of “autism” could be cured or treated by surgical interventions for HH?
Does autism exist as a diagnosis because health and education professionals have always been unable or unmotivated to diagnose and treat the complexities of epileptic encephalopathy, rare genetic disorders and foetal alcohol syndrome?
Are more males than females diagnosed with autism because many cases of autism are caused by brain damage from a virus and the male immune system appears to be less able to fight at least one viral infection (as evident in the increased rate of male deaths from covid-19 and the greater numbers of females among asymptomatic carriers of covid-19)? Zika, rubella and cytomegalovirus are some viruses that can cause autism or brain damage in people who were exposed in-utero. Should all mothers of children diagnosed with autism be warned and medically-treated as though they were chronically and silently infected with an agent dangerous to a foetus before they plan another pregnancy?
Am I a super-recognizer? 
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
http://www.springerlink.com/content/512306132j162437/
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