Tag Archives: Dementia

So does this mean that folks with an immune deficiency in complement C3 have some kind of protection against Alzheimer’s?

You might have autoimmune diseases and chest infections that take forever to clear, but possibly also less of your brain disappearing with age, if research on mice is relevant to people.

Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice

http://stm.sciencemag.org/content/9/392/eaaf6295

Readers of this blog from back in 2011-2012 could have predicted this, because I pretty-much predicted this with my immune hypothesis of synaesthesia and my immune hypothesis of Benson’s syndrome (a variety of dementia). I wonder how many lives could have been saved and cases of dementia prevented if the world of science had bothered to read my blog and taken my theories seriously back then and set to work finding a therapy that reduces levels of C3? How hard could that be? It happens naturally, so how hard could it be to engineer a similar process? Instead all I got for my ideas and blogging was synaesthesia researchers plagiarizing my ideas shamelessly in a speculative paper about synaesthesia (a mere triviality in the world of neuroscience compared with the tragic and expensive problem of dementia). And all this time funding for dementia research has been counted in the hundreds of millions of dollars and has given the public virutally nothing in the way of effective therapies. How much of that research funding do I get? Not one single frickin’ red cent, because I’m not a scientist. I’m just a housewife with ideas, and a blog.

 

I wish, I wish…

I’d love to be reading and writing about fascinating and largely unexplored topics in neuroscience and psychology such as superagers, super-visualisers and aphantasia, but Christmas and all the associated this and that, and the everyday business of parenting in the summer holidays and housekeeping takes up my time.

Interesting to read that aphantasia was apparently first identified by Sir Francis Galton in 1880, even though it has only recently been given the name aphantasia and come to the attention of contemporary researchers. Galton was also one of the earliest researchers to describe various varieties of synaesthesia, before they were all named as such. Galton was one hell of a scientist, back in the days when a man of means could spend his days exploring vast unknown territories of psychology. Is research so different these days? Science is now a bit more open to women researchers, and there’s still much to explore.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3541673/

https://www.newscientist.com/article/2112820-superagers-with-amazing-memories-have-alzheimers-brain-plaques/

https://www.newscientist.com/article/2104221-superagers-with-amazing-memories-have-shrink-resistant-brains/new

http://www.bbc.com/news/health-34039054

Zeman, A., Dewar, M., & Della Sala, S. Lives without imagery–Congenital aphantasia. Cortex, 3.
https://www.researchgate.net/profile/Adam_Zeman/publication/279234629_Lives_without_imagery_-_Congenital_aphantasia/links/573612f208ae9f741b29cd33.pdf

 

Interesting research on synapses and the neurobiology of forgetting supports model of dementia that appears to compete with mine

The role of GluA2-containing AMPA receptors in sustaining long-term memories and in natural forgetting has been studied by an international team of researchers. They and other researchers have speculated that this process could be involved in the development of dementia. I think they are wrong. I believe that there is a distinction between normal, adaptive forgetting and the forgetfulness of dementia that results from the destruction of the brain. I have previously in this blog outlined my original ideas about the immune system, complement, synaptic pruning and a type of dementia that goes by the names of PCa or Benson’s syndrome. My money is still on high levels of complement as the prime suspect for dementia of the rear parts of the brain. Regarding Alzheimer’s, I still favour the “Prion Hypothesis” but I also understand that obesity and diabetes 2 can damage the brain. Nevertheless, I still find this recently-published piece of research interesting because it seems to shows that forgetting isn’t just the failure of some process, it is a process in itself. I also find it interesting that real memory researchers don’t write about or make sweeping statements about memory in general, they study and write about specific types of memory.

Paddock, Catharine Brain study yields clues about ‘natural forgetting of long-term memories’ http://www.medicalnewstoday.com/articles/308549.php

Paola Virginia Migues, Lidong Liu, Georgina E. B. Archbold, Einar Ö. Einarsson, Jacinda Wong, Kyra BonasiaSeung Hyun Ko, Yu Tian Wang, and Oliver Hardt Blocking Synaptic Removal of GluA2-Containing AMPA Receptors Prevents the Natural Forgetting of Long-Term Memories. Journal of Neuroscience.  23 March 2016, 36(12):34813494; doi:10.1523/JNEUROSCI.3333-15.2016

http://www.jneurosci.org/content/36/12/3481.short?sid=e7babe8d-7f41-4f13-91ca-ae7f9a68afa0

 

Don’t confuse poor face memory with aphasia

I know this fascinating article is from 2013, but it makes such an important point about face recognition that I want to bring it to your attention, if you weren’t already aware of it. The ability to remember a person’s face is a different ability than the ability to name the person the face belongs to. These abilities are evidently processed in different areas of the brain. Unfortunately, there is no direct link to the journal paper this article summarizes, so I cannot quickly determine whether the test using the faces of famous people is the same as the “Famous Faces” test that I have previously mentioned at this blog (and done myself). It does sound similar to one of the tests offered here, free of charge: https://www.testmybrain.org/

Famous faces to help spot early dementia.
Anna Salleh ABC. 13 August 2013.

http://www.abc.net.au/science/articles/2013/08/13/3823757.htm

Radio show about Glenda Parkin living with dementia in suburb of Perth, Western Australia

Below are the details of a recent and very interesting radio interview on Perth public radio with Glenda and Bronte Parkin and Alzheimers WA CEO Rhonda Parker, focusing on Glenda’s experiences as a person who has a form of dementia that goes by a number of names including Benson’s syndrome, posterior cortical atrophy and PCA. This is not the first time that Glenda has shared her story with the media; she previously shared her story with Perth’s daily newspaper, the West Australian, in 2011 and she has recently been interviewed for the Community Newspaper Group.

I have unusual reasons to be grateful that Glenda has shared her story with the mass media. I happened upon her story in a copy of the West while I was enjoying coffee and one of those wonderfully greasy Sausage and Egg McMuffins in a McDonald’s restaurant in 2011, after dropping someone off to a selective school that offers students places based on high ability in the area of literacy and languages. I became intrigued by the fact that the particular type of dementia described in the article appeared to be a mirror-image of the pattern of intellectual gifts that appear to run in our family, associated with synaesthesia, a harmless, genetic, developmental and memory-enhancing condition that is caused by increased connectivity in the structure of the white matter of the brain. I wondered whether there could be an undiscovered developmental basis of Benson’s syndrome that works like the opposite of synesthesia, or could it be caused by some mature-age dysregulation of some chemical that regulates growth in the parts of the brain that seem to be hyper-developed in our family, and attacked, over-pruned or somehow damaged in Benson’s. I wrote about my ideas in this blog soon after. In 2012 my thinking on this theme took an important and exciting leap ahead when I happened across a brief article in New Scientist about research by Dr Beth Stevens on microglia, complement, synaptic pruning and elements of the immune system playing a central role in the development of the brain. I figured that one or maybe more of the complement chemicals could be the chemical that regulates growth or pruning in the parts of the brain that I had written about and attempted to identify in my 2011 blog post. I wrote a brief outline of these ideas at this blog in 2012 in an article that was archived by the Internet Archive Wayback Machine in 2012. In lat 2013 I got a big surprise when I saw my idea linking the immune system with synaesthesia as the main idea of a research paper published in a peer-reviewed neuroscience journal, and all without my permission! That’s another story….

I am sure that many people listening to this radio interview would be fascinated with or even skeptical of Glenda’s account of being able to see but not perceive letters on the cover of a book. Her eyesight is not the problem, the problem lies in the visual processing areas of her brain and because of this a lady who in her impressive career has been an author of books can no longer read text or interpret symbols. Seeing is as much done in the brain as it is done in the eye and optic nerves, and a person who has no apparent problem with their eyes can lose visual perception as the result of dementia or injury or stroke.

“Simple things can be very frustrating” – Glenda and Bronte Parkin on dementia. Mornings with Geoff Hutchison. 720 ABC Perth.
09/07/2014.
http://blogs.abc.net.au/wa/2014/07/simple-things-can-be-very-frustrating-glenda-and-bronte-parkin-on-dementia.html

Jarvis, Lucy Still making a contribution: retired educators share experience of living with dementia. Community Newspapers. 2015

Hiatt, Bethany Penrhos principal’s hardest battle.  West Australian. January 3, 2011. http://au.news.yahoo.com/thewest/a/-/mp/8588194/glenda-parkin/

Postscript March 10th 2015

The West Weekend liftout of the West Australian of February 14-15 2015 has a feature story about West Australians livng with dementia on pages 10-13. he story of Glenda and Bronte Parkin is included in that article and the content makes it clear that although Glenda Parkin has a diagnosis of Benson’s syndrome which has had a negative impact on her ability to recognize symbols, writing and objects, she can still somehow navigate her way in her neighbourhood. I find this interesting as some people who have prosopagnosia, which is an impairment in face memory, also have a similar impairment in visual memory of scenes or landscapes, and thus have serious problems with navigating their way through streets and neighbourhoods. I had thought that Benson’s syndrome, a type of dementia, and prosopagnosia, a developmental disability and also sometimes acquired from brain injury, must be in many ways similar in their manifestations, as they both feature disability in face recognition, but it appears that it is not safe to make assumptions and maybe each case of these two conditions should be considered unique. I do not recall reading about Glenda Parkin’s ability to recognize faces, so maybe I should assume it is still normal, along with her ability to recognize street-scapes and scenes.

Yeoman, William Open minds. West Weekend. p. 10-13 West Australian. February 14-15 2015.

 

Would you like to follow these steps?

First go the the Internet Archive (Wayback Machine):  https://archive.org/

Then copy and paste the web address of this blog into the search form that you will find there, removing the beginning bit, and click on “BROWSE HISTORY”:   https://superrecognizer.wordpress.com/

The results screen that comes up will show you how many times this blog has been archived by the Internet Archive over the years.

Click on the year 2012, then click on the date June 21st 2012.

The Internet Archive will display to you their archived record of the home page of this blog as recorded on June 21st 2012. You will see a blog coloured in green and blue with stories featuring photos of some sculptures seen around Perth, but the thing that you might (or might not) find interesting is the blog post that is third down the page which was first published on June 7th 2012. This is the blog post where I briefly but clearly published my ideas suggesting causal relationships between the human immune system and synaesthesia, and low levels of some of the complement immune chemicals and synaesthesia, all related to the regulation of developmental synaptic pruning and synaptic plasticity involving the activity of microglia, and in this post I also restated my previously-published speculation that the variety of dementia known as Benson’s syndrome or posterior cortical atrophy could be regarded as the opposite of developmental synaesthesia associated with special abilities in visual perception such as super-recognition ability and exceptional reading ability, a cluster of traits that appears to run in at least one family. Got that? The point I’m trying to make is that I published this stuff in June 2012, I thought of these ideas independently and as far as I can tell no one else had previously published these ideas anywhere, including in scientific journals.

Now take a look at this paper in a neuroscience journal which was published in 2013 and was received by the journal as a draft or manuscript on July 31st 2013:  http://journal.frontiersin.org/Journal/10.3389/fnhum.2013.00563/full

Do any of the themes in the paper seem familiar? Does my blog or myself receive any credit or acknowledgement in the paper? Hmm.

Regardless of any issues related to originality or acknowledgement, the important point in all of this is that here we have some ideas about a type of dementia which could conceivably have some medical or scientific use or value. My idea of linking synaesthesia with the immune system is nice but just a step in a possibly much more important sequence of ideas. I’d like to give those ideas another airing, while also restating that I thought of them a long time ago independently and claim all due credit. I hope you don’t mind.

Thank you PubPeer

Thank you PubPeer for (after some fussing about) giving me a place on the internet that is recognized by scientists to publish my objection to some researchers publishing a highly original idea that I had thought of independently and had published at this blog over a year before their draft paper was received by their publisher. I’m certain that this is a case of plagiarism, but other people object to my use of that word, so the only place you will see the word plagiarism used in relation to that matter is here at this blog.

I have already published a very full account of my side of the story at this blog, but unfortunately this blog isn’t recognized as a part of the ecosystem of commentators attached to the world of science, the people and organizations in the league of science journalists, science magazine bloggers and internet services that are supposed to review the science literature but actually appear to be automatically-generated content. PubPeer isn’t like that; it appears to be run by people, but who they are is a mystery. I can completely understand why they wish to remain anonymous. Exposing the many ways in which peer review in science publishing is broken is a pastime that I am sure could be harmful to one’s career in science.

I believe that I can make a greater contribution to science as a blogger who has no job that is in any way connected to any university or any research institution, because I don’t have to deal with career-building and politics that goes with having that kind of career, and as a result I have more “mental bandwidth” free to devote to thinking about actual science. I am not expected to teach half-interested university students or organize conferences or write full-sized published papers or book chapters, and I’m not expected to know my proper place in the scheme of things. Very ordinary physical activities that I do in my everyday domesticated life automatically activate regions of my brain that deal with conceptual thinking and memory, and as a result I am often bombarded by novel ideas resulting from a boundless miscellany of concepts flashing onto the centre stage of my mind and colliding in a quite haphazard manner. I guarantee this kind of involuntary mental activity wouldn’t happen if I spent my days comfortably sedentary inside an airless office, staring at a wall or a dusty old painting. I’ve had jobs like that in the past, and years of study at an austere and ugly university which was also pretty much the staring at a wall lifestyle. I find it ironic that study at a university can offer an environment that has an effect on thought that must surely compare with a lobotomy.

Being a nobody to the world of science has many up-sides. I don’t feel a lot of need to consciously or unconsciously self-censor my ideas and publications to fit in with the beliefs and fashions of researcher peers (whether they make sense or not), and I don’t limit my thoughts to my job description, because I have no job description (and I also unfortunately have no salary, pay or financial benefit of any kind). Having no identity in the world of science means I also have no specialization or niche, leaving me free to see and write about a completely obvious connection between synaesthesia, an area of science typically researched by research psychologists and non-clinical neuroscience/psychiatry researchers, and the human immune system, an area of science that has I guess typically been researched by practicing medical doctors in the specialties of immunology or rheumatology. For sure there have been in the last ten years or so a group of pioneering and original researchers who have researched the incredibly complex ways in which the human immune system impacts on brain development, but I don’t think any of them have linked their work with synaesthesia or any particular type of dementia, as I have.  I’m guessing that they haven’t written about synaesthesia because they feel that it is too trivial a matter for them to bother with, which is probably a defensible point of view, as synaesthesia isn’t a disorder and I’ve never heard of a synaesthete who is looking for a cure. I feel free to write about concepts such as dementia, the complement immune chemicals and synaesthesia that are areas that are beyond my expertise, because I have no recognized area of scientific expertise or any recognized career in science. A lot of words have been written about the concept of intellectual freedom in academia, but I have found that being a non-entity outside of all that is a state that offers the most intellectual freedom. It’s a bit like being the invisible man; you can get up to all kinds of stuff but you can’t hope for recognition, because you have no face and no identity.

Being nobody is a state of freedom but it certainly has it’s frustrations, like having no income as reward for any of the work I put into this blog and the ideas published in it, and having no recognition, not even on the internet, but the most frustrating thing is the way that my most important idea has had no apparent impact in science. I’m not referring to my idea linking the immune system with synaesthesia, which was just an amusing step in my journey to the much more important idea that one particular type of dementia, known by the names Benson’s syndrome or posterior cortical atrophy or PCA, could be caused by an excess of one or more of the complement immune chemicals. Surely this is an idea that could be researched. Surely this is an idea that could lead to a number of different ideas for therapies if it turns out to have some value. Surely this is an idea worth at least checking, for if it reflects reality it surely has the potential to save minds and brains and lives. HELLO! Is anybody listening?

P.S. Late last month an Australian biotechnology company plunged on the stock market following the announcement of the failure of their drug aimed at treating Alzheimer’s dementia during a stage of a study. After years of hoopla and hype about drug companies finding a cure for Alzheimer’s or dementia, and anyone’s guess how much money spent on studies, all they can offer is symptomatic treatments. The story has been one failure after another. Benson’s syndrome is considered by some to be a variant of Alzheimer’s disease. Whether it is or not, maybe it is high time for researchers to stop obsessing about plaques in the brain and look at the immune system and the brain. My money is on C3 and C4 as concepts to focus on in a search for an understanding and cure for dementia. Would it kill you dementia researchers to accept some advice from a Perth blogger who is nobody in particular, and put my name on your research paper if my idea works out?

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

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.

The Opposite of Benson’s Syndrome?

 

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 is 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.

 

Today I had a look through someone else’s copy of today’s West during an idle moment. It’s not much of a newspaper, but one never knows what one might discover in a paper.  On page three I saw a sad but interesting story about the retired principal of a top private school in Perth who has had to cut short her career due to a rare type of dementia, early onset Benson’s syndrome. This is like Alzheimer’s except that it affects specific parts of the brain, and it takes away the ability of the brain to process visual information, among other things. Some of the first symptoms of this disease noticed by Dr Glenda Parkin were an inability to play a card game, an inability to spell and an inability to write notes. This terrible disease robs people of basic visual, literacy and numeracy skills such as reading, spelling, handling money and recognizing familiar objects. Why did I find this particularly interesting, aside from the sadness and the personal courage in the story? Because this disease seemed to be the opposite of the special intellectual gifts that run in our family. We have kids who were early and advanced readers, consistently testing as years ahead of their age peers in reading ability. One of our kids spells effortlessly, tackling long foreign words in their junior primary school years, and picking up a bit of Polish just for fun. I am able to write pieces like this without needing to use a spellchecker. I suspect that this ease in literacy skills is linked with our shared and obviously inherited grapheme-colour synaesthesia, the same variety of synaesthesia that ran in the family of the respected novelist Vladimir Nabokov. I suspect that, like some other synaesthetes, I have a memory for colour that is above average. I can recall the exact colours and the names of the colours of a watercolour set that I was given as a young child. I am also often puzzled by the labels that other people give to colours, which don’t seem even vaguely accurate to me. I know that I have unusually good face recognition abilities because I got a perfect score in the short form of the Cambridge Face Memory Test, which is I believe the state-of-the-art in facial recognition tests. The natural reading skill in our family could be seen as the opposite of the loss of ability to read which is an early symptom of Bensons syndrome or PCA.

Although the story in The West Australian about Dr Glenda Parkin’s battle with Benson’s syndrome did not mention anything about recognizing faces or body language, I was willing to bet that prosopagnosia is one of the symptoms of Benson’s that wasn’t mentioned in the newspaper article. I was curious to find out more about Benson’s syndrome for two reasons – to check if face recognition is indeed affected by it as I predicted, and to also find out which specific parts of the brain are affected by Benson’s, because I thought this would be a good clue about which parts of my brain, and the brains of my blood relatives, are naturally enhanced or over-developed or hyper-connected. I would also discover another fact that shows how different elements of different types of synaesthesia that I experience are connected. I find that if you follow the clues far enough, you will often find that things are connected, especially when you are investigating synaesthesia. I already had a few clues about which parts of my brain are different and give rise to my face recognition abilities and The Strange Phenomenon. The fusiform face area, within the fusiform gyrus were two obvious likely choices. Grapheme-colour synaesthesia, which I have, and which runs in my family, is associated with extra activation in the fusiform gyrus (Rouw and Scholte 2007) and greater volume in the grey matter of the right fusiform gyrus (Weiss and Fink 2008), so I figure this part of my brain has got to be doing strange things. I believe the fusiform gyrus is in the temporal lobe, and the temporal lobe is associated with a love of music, and we do appear to have an emotional connection with music that is above the ordinary in our family, so the temporal lobe in general seems like a likely prospect. I had also formed the opinion that the right side of the brain is likely to be hyper-developed or hyper-connected in me or in our family, based on my reading about face recognition face processing and colour-grapheme synaesthesia.

I did the obvious, I looked up the Wikipedia page for Benson’s syndrome, and from there I clicked on a link that looked like to might be something detailed and professional-level. I found a short paper by a Dr Bernard Croisile, outlining the basics of Benson’s. Indeed prosopagnosia is one of the symptoms of Benson’s, as I predicted. I found a fairly general description of the damage to the brain associated with Benson’s “bilateral parieto-occipital aptrophy, more frequently in the right hemisphere”, and “bilateral atrophy in the parieto- and temporo-occipital areas that is more severe in the right hemisphere.” My prediction about the right hemisphere was on the money, and there seemed to be overlap between my prediction and the reported areas affected by Benson’s, but I’m not a neuroscientist, so I’m not sure about the relationship between the areas affected by Benson’s and the areas of my brain that should be expected to be unusual.

I discovered one thing of interest in Dr Crosisile’s paper that hasn’t apparent in the newspaper report – that Benson’s has two major types of symptoms, the visual agnosia described in the newspaper report, and also apraxia. Apraxia is the loss of the ability to execute or carry out learned purposeful movements despite having the desire and the physical ability to perform the movements. By one account it is caused by damage to specific areas of the cerebrum, and another account states that it is caused by damage to specific areas in the parietal lobes. I’m not sure what to make of this. Why is apraxia of interest to me? Because this seems to be a link between the use of hand movements in the performance of chores and one of the types of synaesthesia that I discussed in my first post, my description of “the strange phenomenon”. I don’t have apraxia, but I do get a type of visual synaesthesia triggered by the types of tasks that are impaired in apraxia. When I perform very specific household chores I experience automatic and involuntary very specific visual memories of places that I have visited in the past. For example, when I squeeze a half a lemon on a citrus squeezer with a twisting action of the wrist, I will invariably experience a vision in my mind’s eye of the backyard of the home of my Godparents, just as it was when I visited the place when I attended a birthday party and child-minding there in my preschool years, around four decades ago. No, I’m not making this up – I travel all around Australia while I do household chores, and usually to places that I don’t much desire to revisit. How is this all connected to face recognition? Please follow me as I take you on a tour of the connections.

The Strange Phenomenon (my strange phenomenon) is a type of synaesthesia that I experience which is associated with face recognition – it is triggered by seeing a specific face under very specific conditions and the experience triggered is the quite old visual memory of another specific face that looks very similar. I only experience two types of synaesthesia that evoke visual memories – The Strange Phenomenon with visual memories of faces and my fine motor chore synaesthesia triggering visual memories of places. Faces and places are linked because they are both things that prosopagnosics are reported to have trouble recognizing. It is reasonable to assume that whatever part of the brain is malfunctioning in prosopagnosics (people who are bad at recognizing faces) should be involved with visual processing of both faces and places. It makes sense to expect that super-recognizers, the opposite of prosopagnosics, might also have unusual visual processing of faces and also of places. This is true of me – my visual memories of places and faces can both also be synaesthesia concurrents (the experience triggered in synaesthesia). I also score like a super-recognizer in tests – further evidence linking me with unusual face processing. So the link between the faces and the places seems clear enough, with a face acting as the inducer / trigger of my synesthesia and another face and scenes of places acting as the synesthesia concurrents. This  leaves only one synaesthesia trigger unexplained – how do fine-motor chores as synesthesia triggers fit into this picture? It now appears that whatever is up with my brain could in some way resemble the opposite of Benson’s syndrome, and Benson’s involves degeneration of whatever part of the brain does skilled familiar movements such as using a key, a pencil or a razor. Synaesthesia is caused by hyper-connections in the brain, and it seems reasonable to predict a high degree of overlap between the parts of my brain that are hyper-connected and the parts of the brain that degenerate in Benson’s syndrome. So it appears that the bits of my brain that are responsible for dreary household tasks such as squeezing lemon juice or scrubbing clean the rounded end of a wooden spoon are hyper-connected, so when I do some of these tasks, the thoughts associated with my movements trigger synaesthesia in which the part of my brain that recognizes faces and also places is activated by some “weird wiring”, resulting in me seeing dated vistas in my mind’s eye.

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 – it would at least partly explain The Strange Phenomenon and confirm that it is indeed a type of synaesthesia because it is based on hyperconnection in the fusiform gyrus, and the idea of the opposite of Benson’s would also explain my fine motor task -> visual place memory synaesthesia as one of only two types of synaesthesia that I have that are the result of hyperconnection between the fusiform gyrus and other parts of the brain that fall within the range of areas affected by Benson’s syndrome. 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.

From this complicated story I have arrived at three conclusions – that one should never pass up the opportunity to read a newspaper, however uninspiring the paper might be, that one should count one’s blessings, and that dementia patients and research into dementia should be supported.

Do you think I’m brainy enough to figure out how my own brain works? I dunno, but it’s sure fun.

Hiatt, Bethany Penrhos principal’s hardest battle.  The West Australian January 3, 2011. http://au.news.yahoo.com/thewest/a/-/mp/8588194/glenda-parkin/

Croisile, Bernard Benson’s syndrome or Posterior Cortical Atrophy. Orphanet. September 2004. http://www.orpha.net/data/patho/Pro/en/PosteriorCorticalAtrophy-FRenPro10748.pdf

Rouw, Romke and Scholte, H. Steven Increased structural connectivity in grapheme-color synesthesia. Nature Neuroscience. Volume 10 Number 6 June 2007. http://www.fmrib.ox.ac.uk/systems-plasticity/jc/potential-papers/rouw_2007.pdf

Weiss, Peter H. and Fink, Gereon R. Grapheme-colour synaesthetes show increased grey matter volumes of parietal and fusiform cortex. Brain (2009) 132 (1): 65-70. doi: 10.1093/brain/awn304 First published online: November 21, 2008. http://brain.oxfordjournals.org/content/132/1/65.full

Postscript February 2013

I’ve got two things to point out. Firstly, if you found the above article interesting, you should read this:

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?

https://superrecognizer.wordpress.com/2012/06/07/is-synaesthesia-caused-by-low-levels-of-complement-is-bensons-syndrome-caused-by-too-much-complement-c3/

Secondly, if you look carefully at the above article I think you can see hints that Benson’s syndrome or PCA affects the parietal lobe. This would very much fit in with my theory that synaesthesia is like the opposite of Benson’s, because it is becoming clear that the parietal lobe plays a major role in synaesthesia. See these papers:

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/

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