Tag Archives: Visual Cortex

Have my ideas been plagiarized in a paper published in a neuroscience journal? I believe they have.

Top of C3 theory post

Middle of C3 theory post

End of C3 theory post

This post replaces a brief temporary posting which was previously published here, with the notice that it would be added to at a later date when I had more time. I’m a busy parent who gets paid nothing to write and I have struggled to find the time to give this important matter proper attention. Do not be surprised if you find this post edited or altered.

I’ll get to the point straight away. I believe that I am the victim of plagiarism. At the very least, I believe that I have scientific priority in regard to a group of related scientific ideas or hypotheses, and my priority in regard to two of those ideas has not been recognized, and as a result some ideas which I published at my blog in 2012 have been presented in a journal paper that was published this year as though those ideas were new. The two ideas which were re-published by others in 2013 as though they were their original ideas are the idea that synaesthesia could be caused by unusually low levels of complement (a group of immune system chemicals) and also the idea implied by that idea that synaesthesia could have as its origin some peculiarity in an element of the immune system which plays a dual role in the development of the brain. The complement chemicals are certainly not the only elements of the immune system which are thought to influence the brain. I am not alleging that plagiarism in the form of word-for-word copying of text has happened in regard to the documents cited below. I am alleging that plagiarism of ideas has happened, and even though this type of plagiarism is not easy to prove, I can prove that I published my blog article introducing my ideas over a year before the journal  paper by the others was even received as a manuscript by the journal which would eventually publish it.

Below are the details of my blog post published in June 2012 which contains the ideas which I believe have been plagiarized:

Wright, C. 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? Am I a super-recognizer? June 7, 2012.

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

and permanently archived by the Internet Archive Wayback Machine on June 21st 2012: http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

Below are the details of the published journal paper which includes what I believe is plagiarism of my ideas, or at the very least the re-publication of my ideas without any acknowledgement of me or my writing:

Carmichael, Duncan A. and Simner, Julia The immune hypothesis of synesthesia. Frontiers in Human Neuroscience. 2013; 7: 563.

Published online 2013 September 11. doi:  10.3389/fnhum.2013.00563

Received July 31, 2013; Accepted August 23, 2013.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/?report=classic

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3769635/    (see the “article notes” at this version to view all the dates relevant to publication of this paper.)

http://www.frontiersin.org/human_neuroscience/10.3389/fnhum.2013.00563/full

https://pubpeer.com/publications/13259457EAEBF97186167E7BDFB6B3

Please note the dates cited relating to the process of getting this paper published. There is nothing in those dates that could serve as evidence that these authors independently thought of the ideas in the paper before I published my blog piece. I published my blog piece in June 2012 and the above paper was received by the above journal in July 2013. The authors could have been wildly plagiarizing during the thirteen months or so after I published my piece and before their paper reached the offices of the journal.

I think it is important to point out that I had no contact or communication with either of the authors of the above journal paper about my ideas about synaesthesia and the immune system during the period before their paper was published. I did not inform them about or discuss my ideas on this subject privately and I did not privately grant them permission to use or publish my ideas, and I am not one of the “anonymous reviewers” who made “helpful comments” on the manuscript of the above paper, who were mentioned in the acknowledgements section of the above paper. Shortly before I published my ideas about synaesthesia and the immune system I did have a short and one-sided email correspondence about some of my ideas with a microglia researcher and I also sent a non-specific email off to a local medical specialist. The authors of the above journal paper did not privately inform me about any ideas or theories linking the immune system with synaesthesia before the publication of my blog post on that subject. It is my sincere belief that my ideas in that post were new and original and had not previously been published. I also did not receive any information or “leaks” about the work of the authors of the journal paper from any third party.

If you take a careful look at the details of my blog post you might notice that one of my scientific hypotheses is presented within the internet address of that posting and also within the title of the posting, and the internet address also contains details of the date of publication. Like all of the internet addresses of the posts at this blog, it was automatically generated by WordPress when I published the post. The date of publication is also automatically added to the blog post during publication, as is the name of the author. Unfortunately, the date of blog posts can be altered post-publication, with this alteration reflected in the web address of the post and the situation of the post in the chronological sequence of the blog. While the blog can be altered, one cannot alter blog readers’ memories of my blog posts and any records that they might have kept of them, and this blog has a diverse and steady readership. In situations demanding proof of the date and also the content of a document published on the internet, one free resource on the internet is invaluable; the Internet Archive Wayback Machine. This internet archiving service archived my June 7th 2012 blog article on two different dates in two different forms. The earlier archived record was recorded on June the 21st 2012 with the blog post included in a record of the whole home page of my blog on that date.

http://web.archive.org/web/20120621071430/https://superrecognizer.wordpress.com/

This date was only a fortnight after the post was first published and over a year and a month before the others’ journal paper was received as a manuscript by the journal that would later publish it. This proves that my blog post was published on the internet at least before June 21st 2012, a long time before the journal paper was published online or in hardcopy, or was even received by the journal publisher. The content of my blog post as was published then is also documented and can be checked. The blog post was also archived in November 2013 within an archive of a month’s blog posts.

In addition to citing the archived old record of my blog post as evidence, there is other evidence that I can cite to show a long history of me expressing ideas such as those in my blog post, ideas that overlap with ideas presented in the journal paper, and many more novel, original and inter-related ideas besides. The origin and development of the ideas in my blog piece can be traced back a long way in time within my own writing at my blog. I theorized not only that synaesthesia could be caused by low levels of the immune chemical complement, I also theorized that a form of dementia, which to my knowledge has never by anyone else been linked to or contrasted with synaesthesia in scientific discussion, could be caused by excessively high levels of complement. I also theorized that this type of dementia, Benson’s syndrome or PCA, could be seen as the opposite of synaesthesia or at least the opposite of the cluster of unusual functional characteristics of my own brain. Implied within this theory is the idea that there is some kind of network within the brain of parts that are especially sensitive to some factor that influences growth or pruning or cell death, because the same mental functions appear to be boosted at least since early childhood in the brains of me and some of my first-degree relatives which decline in Benson’s syndrome. I have no reason to believe that the early specific cognitive enhancements are some unknown facet of Benson’s, because there is no particular history of dementia in my family. I still see the two conditions as opposites, potentially with one common factor (extreme levels of some influential chemical) unlocking the mystery of both. My post published in June 2102 was not the first place where I published my own ideas about Benson’s syndrome being the opposite of synaesthesia. I had first written about this apparently original and new idea in a blog post published in January 2011:

https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

This blog article was archived and recorded by the Internet Archive Wayback Machine in March of 2011:

http://web.archive.org/web/20120308215442/https://superrecognizer.wordpress.com/2011/01/04/the-opposite-of-bensons-syndrome/

It is clear that my ideas in my June 2012 blog post were a development of ideas that I had already published at this blog in January 2011, indeed I quoted from my earlier blog post in my latter blog post. My earlier blog post has been archived by a third party and stands with other related blog posts as a record of the direction and date of the development of my ideas, which are very congruent with the many ideas expressed in my June 2012 blog post. In contrast, it appears to me that that the authors of the journal paper which I believe is a plagiarism of ideas in my blog post cannot demonstrate any published and/or archived set of documents that show the development of their ideas towards any theory linking synaesthesia with any element of the immune system. I believe this because I have done a quick check of the lists of past publications of both authors. I have not been able to trace any development of theories about synaesthesia in their work or academic collaboration that might lead them to look at the immune system, and I was not able to find any hint or explanation in the journal paper itself about why these researchers arrived at a theory about the immune system. In my opinion, their theory linking synaesthesia with the immune system appeared “out of the blue” within the context of their own published research and published papers. If anyone can identify any dateable and/or archived document by either of the authors of the journal paper that shows an early development of the idea of linking synaesthesia with the immune system then I would be very interested to see that document, and I request that a comment detailing such document be left at this blog. The apparent absence of evidence of a theoretical progression or development towards “the immune hypothesis of synaesthesia” in the published work of the two authors of the journal paper is one reason why I cannot believe that they conceived of the immune hypothesis of synaesthesia independently as a team or as individuals.

The immune hypothesis of synaesthesia would not have been proposed had it not been for the work of researchers who investigate the dual roles of elements of the immune system which also play a role in brain development and neuroplasticity. The authors of the journal paper have primarily cited the work of Assistant Professor Lisa Boulanger who studies MHC Class 1 proteins, while in my blog post I concentrated on the work of Assistant Professor Beth Stevens who studies microglia and complement. It appears to me as though the authors of the journal paper have made a deliberate decision to anchor their theoretical ideas onto a different existing body of research in molecular biology than the body of research that inspired my theories. I believe they had the aim of distancing or differentiating the content of their paper from the content of my blog post. I first learned about the work of Beth Stevens from reading a June 2012 article in New Scientist magazine. Although the authors of the journal paper evidently at some point in time developed an interest in the work of Boulanger and consulted her during the writing of the paper, it is not clear why in 2013 they should be publishing a paper at least in part inspired by her work, because the papers of hers cited were published in the years 2004, 2009 and 2010, hardly the latest news in neuroscience. The most recent items in the journal paper’s references list relating to the immune system and the brain are a 2012 paper by Elmer and McAllister and a 2012 paper by Beth Stevens and two other authors. Boulanger does molecular biology at Princeton University in the United States while the authors of the journal paper do psychology and psychiatry at Edinburgh University in the UK, so it seems unlikely that the three by chance swapped ideas over lunch.

I have noticed an absence of mention of or enthusiasm for the immune hypothesis of synaesthesia in 2012 and 2013 media coverage and conference presentations featuring either of the authors of the journal paper, and I find this curious. It appears that they deliberately kept quiet about the hypothesis before it made it into publication. Why?

One of the authors, Duncan Carmichael, was interviewed for the British radio show The Naked Scientists on October 7th 2012, and his research on synaesthesia was the subject of the discussion:

http://www.thenakedscientists.com/HTML/content/interviews/interview/2269/

Even though this interview was conducted roughly nine months before Carmichael’s and Simner’s journal paper about synaesthesia was received by the journal as a manuscript, no evidence of a conception of the idea of an immune hypothesis of synaesthesia can be found within Carmichael’s answers in this interview. He spoke about a genetic study, but said not a thing about the immune system. I find it hard to believe that a researcher who gave such an ordinary account of the contemporary state of knowledge and research on synaesthesia was a member of the team who generated one of the most original ideas in synaesthesia research for a long time. Wouldn’t he have been barely able to contain his excitement about the novel scientific theory? I know that is how I felt about it when I thought of it.

This is a university web page outlining the work of Duncan Carmichael:

http://www.anc.ed.ac.uk/dtc/index.php?option=com_people&func=showall&userid=387

I cannot find evidence of a lot of originality in thinking or the development of ideas about the immune system in the work detailed at this page. It looks like some standard ideas about synaesthesia explored by a PhD student whose background in psychology and psychiatry is pretty standard for synaesthesia researchers.

An abstract of a conference presentation delivered and co-authored by Duncan Carmichael can be found at the below link and a link to what appears to be the slide images used in that talk can also be accessed at the below link:

http://www.synesthesia.info/recent.html

This conference was the Tenth Annual National Conference of the American Synesthesia Association held in Canada May 31 through June 2, 2013, roughly two months before the immune hypothesis of synaesthesia paper was received by the journal as a manuscript. I looked at the abstract and also the slide show and I found a spelling error and some questionable unexplained assumptions in the slide presentation but I found no hint of the development of the immune hypothesis of synaesthesia. I find it remarkable that Carmichael could have co-written and submitted a publishable a paper containing some highly original and paradigm-shifting ideas barely a couple of months after giving talks at a conference about the same general area of research which gave no clue about the intellectual development of the novel ideas. When I look at the highly conventional and ideas about synaesthesia in Carmichael’s written work, media appearance and May-June 2013 conference presentation I find it impossible to believe that he is a part of the team that theoretically wed synaesthesia with the immune system for the first time based on their own ideas. One could argue that Carmichael was deliberately keeping the new theory a secret, but what can account for the contrast between the conventionality of his other work and the originality of the immune theory?

Perhaps the originality of the novel idea was the contribution of the other author? I’ll happily admit that Dr Julia Simner’s work on synaesthesia has consistently been interesting and she has made important and fairly novel contributions, but I could likewise find nothing in her work or in her academic background to indicate a curiosity about or knowledge of the immune system. Dr Simner categorizes herself as a cognitive neuropsychologist, and her academic background is in “psychology, languages and linguistics”.

This is a link to her university web page in which Carmichael is listed as a student supervised by Simner:

http://www.ppls.ed.ac.uk/people/julia-simner

Two 2013 media appearances are listed at the above page. One was at the Guardian Edinburgh International Television Festival. These are pages related to an August 2013 talk by Dr Simner at that festival:

http://www.audionetwork.com/content/whats-new/events/geitf/julia-simner-q-and-a

http://www.audionetwork.com/blog/author/dr-julia-simner/2013/8/27/synaesthesia—a-merging-of-the-senses.aspx

http://www.audionetwork.com/show-article.aspx?id=386

Unfortunately a recording of that talk appears to be no longer available. The talk was presented while the immune theory paper was in the process of being published but I found no hint of the paper’s theme in the page about Dr Simner’s talk.

This is the page about an appearance that Dr Simner made at the Edinburgh International Science Festival on April 1st 2013:

http://www.sciencefestival.co.uk/whats-on/categories/activity/sensory-dining-1404

A PDF of the festival’s 2013 programme can be accessed here:

http://www.sciencefestival.co.uk/uploads/EventImages2013/Edinburgh%20Science%20Festival%202013%20brochure.pdf

There’s nothing related to the immune system to be found in info about that appearance.

A Word document of Dr Simner’s CV can be downloaded from Simner’s university page:

http://www.psy.ed.ac.uk/people/view.php?name=julia-simner

Simner’s CV includes a quite up-to-date list of the publications. I searched her CV and found only one mention of any word that I can think of that is related to the immune system, and it was in the title of the paper under dispute. I couldn’t even find one example of use of the words “synapse”, “synaptic”, “plasticity”, “pruning” or “neuronal” in Simner’s CV, which I take as an indication that Simner’s research on synaesthesia could hardly be described as “biomedical”, except for that one paper which stands out like dog’s balls within the contexts of the other work by Simner and by Carmichael. I invite you to check for yourself and let me know if I have missed something.

Here are some other links to information about Dr Simner:

http://www.biomedexperts.com/Profile.bme/1310901/Julia_Simner

http://www.research.ed.ac.uk/portal/en/persons/julia-simner(616de62b-07c6-430d-b217-d18880744549).html

http://ukcatalogue.oup.com/product/9780199603329.do

http://community.frontiersin.org/people/u/68706

I have argued that the originality of the immune hypothesis of synaesthesia stands in contrast with the conventionality of Carmichael’s other work and also stands in contrast with the lack of medical or molecular biology focus in Simner’s other work. I could also argue that the originality and the molecular biology of the immune hypothesis stands in contrast with synaesthesia research in general. Stale old models of synaesthesia proposing hyper-connectivity in the brain, inhibition of the process of neuronal pruning or disinhibited or hyper-excitable neurons have been doing the rounds forever. Researchers seem to be satisfied with explaining the biological basis of these theorized neurological peculiarities by suggesting that there are genes for these features, as though that is any explanation at all. The traditional models of synaesthesia seem to owe a lot to a layman’s understanding of simplistic models of psychiatric illnesses and neurodevelopmental disorders (endless guff about neurotransmitters and brain “wiring”) or owe a lot to a superficial resemblance between synaesthesia and hallucinogenic drugged states of mind. There have been genetic studies of synaesthesia and there have been brain scan studies as well, but I don’t think you will find a lot of molecular biology in pre-2013 synaesthesia research.

If the authors of a journal paper read my blog post and took my ideas in that post and used them in their journal paper without acknowledging me, could they have any possible excuse? It is perhaps worth noting that at my blog my name as the author of the posts (my blog is not a collaborative one and only has one author) is not shown on posts at the main page of the blog, but the author’s name in blog posts is displayed when individual posts are selected for viewing, along with any comments about the post. There is no information about me (the author) at the main page of my blog, so I guess it is not inconceivable that a reader might assume my blog is an anonymous publication. Nevertheless, if one wanted to properly cite any of the posts at my blog or the blog itself the title of the blog could be cited. It is a standard practice to cite the first few words in the title of a book or other type of document instead of the author’s name if the author is unknown, and if the author is known to be anonymous they should be cited as “Anonymous”. There is no technical or formal reason why any of the pieces of writing at my blog can’t or could not have been cited.

I can see one possible objection to my claim of having scientific priority regarding the idea of linking synaesthesia with complement and the immune system. It could be argued that my idea was never properly published as my idea, because it was published at a blog and was not published as my idea in a paper or some other document in a scientific journal. Such an objection would be based on the assumption that scientific publication can only happen within a select and specialized type of publication that is widely recognized as a scientific publication, and cannot legitimately be self-published or published in a print publication or internet web site which is not specifically devoted to the publication of scientific research and scientific theories. My answer to this objection is that it is snobbery and it is also at odds with the current realities of our online world. Such an idea seems to be based on the belief that science is an enterprise that legitimately operates like a closed society in which membership is only open to those who have particular credentials or those who have jobs in particular types of institutions (universities or research institutes for example) or those who have the resources and social connections to be able to successfully submit a full-length paper for publication in a peer-reviewed science journal. But the history of science is peppered with examples of scientists who done important work outside of universities, of amateur scientists and gentlemen scientists who have made very important contributions, and of scientists who have offered interesting and respected theories outside of the fields in which they are qualified. There are also plenty of examples of crackpots who present themselves as legitimate scientists and of researchers who have made laughable blunders while straying outside of their areas of specialization. There are also too many examples of scientists who have made serious blunders because they apparently did not know about important and relevant facts or knowledge from areas of science beyond their limited field or from beyond the world of academia. I can also think of some great examples of scientists who have only been able to make important discoveries once they have had the courage to question accepted scientific or medical knowledge. My point is that science is not a neat, closed and orderly enterprise. It can and it should be informed by non-scientists who have specialized expertise and amateur scientists. Science can be seriously failed by academics who are blinkered or who over-reach the limits of their knowledge or who engage in scientific misconduct. If science was a perfect and orderly enterprise we would call it The Church of Science and lecture theatres would be places of worship. Science belongs to everyone; everyone benefits from it and anyone who has good ideas and a respect for evidence can play a part, and should be given due credit.

Even if there were no plagiarism in the journal paper by Simner and Carmichael there are still plenty of things in that paper which I find objectionable. As a synaesthete I am personally offended by the frequent use of negative language in reference to synaesthesia in the paper. Here’s a list of words and phrases from the paper: “neurological condition”, “excess cortical connectivity”, “excess connectivity”, “excessive connectivity is indeed a feature of the synesthetic brain”, “failing to supress non-relevant activation”, “excessive activity of excitatory neurons”, “aberrant connectivity”, and ”misregulated feedback mechanisms”. This repeated use of terminology with negative connotations regarding synaesthesia is certainly not typical of scientific or popular literature on the subject. It is rather amusing when one reflects that these authors are being so negative about the type of mind which I believe provided them with the central idea of their journal paper. Talk about biting the hand that feeds! Even more offensive and stupid is the authors’ described quest to find a link between developmental synaesthesia and the degenerative nervous system disease multiple sclerosis (MS). They aren’t even being as bold as researching a link between diagnosed cases of MS and synaesthesia, they are only looking at “people with the radiological profile of multiple sclerosis”, whatever that means. Developmental synaesthesia is a generally stable inherited neuropsychological variation characterized by white matter in the brain that has been described as having greater volume, greater connectivity or being “more coherent”. It is not considered to be an illness or a disorder, and it appears to be associated with superiority in memory. Multiple sclerosis is an inflammatory disease typically with an onset in adulthood which damages the myelin covers of nerves in the brain and in the spinal cord. While there are some genetic risk factors it is not considered to be a hereditary disease. Vitamin D deficiency and infectious agents have been suggested as causes or triggers. MS causes a wide range of mental and physical problems and disability and substantially reduces life expectancy. It is not known whether is caused by an autoimmune process or a failure of the myelin-producing cells. The only apparent commonality between MS and synaesthesia appears to be that they both feature white matter that differs from the average state, but those differences could be characterized as opposite states, not similar. Simner and Carmichael’s idea that synaesthesia might be more common in those who look like MS cases strikes me as at best bizarre, but apparently they have submitted a paper on this subject. I think I know where that paper might belong.

To offend in so many ways certainly takes some doing, and I do acknowledge that there is a large difference between the amount of effort that went into the writing of my blog post and the amount of work that would have gone into writing and obtaining publication of the journal paper, but I believe that it is also true that the guts of that paper was an idea of mine, and I believe there would have been no paper to work on without my idea.

If I accept the proposition that this apparent case of plagiarism was really a case of two different parties reaching the same conclusion independently and within a year or so of each other, with the others being unaware of the existence of my prior publication, and then they innocently published their own paper as the first to introduce these ideas to the world, then I must ask why they were not aware of the existence of my blog post. Did they think they only had to search the traditional scientific literature to check whether their ideas were truly novel and original? I find that hard to believe, in this online, open-access world. Before I published these ideas at my blog I searched the internet and bibliographic databases to check whether my ideas were really as novel as I thought they were. I found nothing comparable. I am completely sure that my blog post would have been retrieved within the first page of a results display from a simple Google search on the terms “immune” and “synaesthesia” or “synaesthesia” performed in the months and year after I published my blog post. My blog has always done very well in Google searches.

I believe that the immune hypothesis of synaesthesia is the product of a synaesthete brain, my synaesthete brain. If anyone can show evidence that counters this, please let me know by leaving a comment. I have demonstrated that I was the first to publish the immune hypothesis of synaesthesia. I believe that I should have been acknowledged as the creator of this idea by the authors of the journal paper. I’m not pleased with what has happened. I do want my ideas which I have published at my blog to be read, considered and developed by other people. I am not a hoarder of ideas and I’m not out to make trouble. I just want to be contacted, asked and acknowledged, and properly acknowledged in print in the conventional manner if my original ideas are used or referred to in someone else’s work.  I don’t think that is too much to ask.

Scenes, scenes, scenes, my idle thoughts are filled with scenes

While trying to get my finger into the groove on the inner side of sticks of celery to wash them properly scenes of Leederville around the area of the Luna Cinema and the Leederville TAFE or tech or whatever they call it these days flashes into my mind automatically. There is no logical or temporal connection between celery and Leederville that I know of. This is just another example of my fine motor task – visual place memory synaesthesia. I named it myself. As far as I know I’m the first person to ever describe this type of synaesthesia in detail. I experience it all the time, and it is such an ordinary part of my life that I barely notice it. I’ve also described other types of synaesthesia that are either triggered by seeing scenes or which have visual memories of scenes as the surprising thing that is triggered by doing things such as household manual chores or thinking about particular concepts or reading or listening to a narrative story or non-fiction account that has scenes in it.

The stuff of thought is scenes and visualizations. In my opinion the front of the brain is over-rated for importance in thought compared to the back end and the under-side of the brain, which does visual processing. I believe we need to take a new LOOK at the way the brain works.

I don’t see what you see, and vice versa

This blog post from Dr Kevin Mitchell, a synesthesia, brain connectivity and developmental neurogenetics researcher from Trinity College in Dublin at his interesting blog Wiring the Brain is well worth a read, and I think is very relevant to finding an explanation for my gifts and peculiarities in visual perception. I was amazed by the normal variation in size of visual processing areas of the brain, which is probably genetic in origin and isolated from other traits. Australian cognitive science researcher Dr Jon Brock at Macquarie University left a comment suggesting a related possible area for research into autism.

“A negative correlation that has been observed between size of V1 and size of prefrontal cortex in humans might be consistent with such an antagonistic model of cortical patterning.” Fascinating! I’ve got to wonder if this has any relevance to understanding Benson’s syndrome or posterior cortical atrophy or PCA.

Dr Mitchell’s blog has been in my blogroll for a long time, and if you are looking for some interesting holiday reading about the psychology of visual processing or neuroscience, a good starting point might be my blogroll.

Do you see what I see? by Dr Kevin Mitchell December 12th 2012 Wiring the Brain. http://www.wiringthebrain.com/2012/12/do-you-see-what-i-see.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….

Grapheme-colour synaesthesia and enhanced cortical excitability – I find this research quite exciting, but maybe that’s just me

“He found that neurons in the primary visual cortex were more active than expected.”

This is a quote about a study of some grapheme-colour synaesthetes. I’m a grapheme-colour synaesthete, and I’m wondering if this enhanced cortical excitability in the primary visual cortex which they wrote about in New Scientist last November is also an explanation for my superior face memory and the many other atypical visual perception experiences that I’ve had, and have described in this blog. It’s exciting research.

Hyperactive neurons build brains in synaesthesia. New Scientist. 23 November 2011 Issue 2840 p. 18.  http://www.newscientist.com/article/mg21228405.400-hyperactive-neurons-build-brains-in-synaesthesia.html

Thomson, Helen Hyperactive neurons build brains in synaesthesia. New Scientist. 17 November 2011  http://www.newscientist.com/article/dn21183-hyperactive-neurons-build-brains-in-synaesthesia.html

Enhanced Cortical Excitability in Grapheme-Color Synesthesia and Its Modulation. Current Biology. Vol 21 Issue 23 2006-2009, 17 November 2011. 10.1016/j.cub.2011.10.032 http://www.cell.com/current-biology/retrieve/pii/S0960982211011936

A very interesting idea from Dr Simner but I’ve got my doubts

This is a quote from Dr Julia Simner’s thought-provoking paper in the British Journal of Psychology about defining synaesthesia:

“To avoid this circular evidence of what synaesthesia is and is not, we might instead define synaesthesia in terms of it neurological basis, and then allow ourselves to consider what types of variants this synaesthesia might then include. If indeed the condition were defined by inherited atypical cross-talk, we might find synaesthesiae in unexpected places. For example, if an inherited predisposition for neurological hyper-association manifested itself, say, in the fronto-temporal language regions that mediate semantics, lexical-forms, and syntax (e.g., see Tyler & Marslen-Wilson, 2008, for review) what would this mean? It might mean we could find ‘synaesthetic’ individuals with unusually strengthened connections in spoken language processing.”

I happened across this picture that is apparently from The Human Connectome Project, or at least from a paper by Liza Gross that was published in PLoS Biology in 2008: http://www.abc.net.au/radionational/programs/allinthemind/the-human-connectome/3706910  I’m guessing that the coloured larger blobs represent the most connected hubs in the brain, and I’m guessing these bits would be made of white matter? I know that there is one type of synaesthesia that is associated with some kind of functional enhancement of white matter, and in general, synaesthesia is thought to be due to hyperconnectivity in the brain, which I guess might mean that it operates the most in regions of the brain that are the most connected? Well, looking at the picture with the red and pink blobs, it seems as though the parts of the brain that are the most connected are towards the rear of the brain, maybe the parietal, occipital and part of the temporal lobes, with most of the frontal lobe and Broca’s area (important in language processing)  left pretty much out of the loop. So I’ve got to wonder how realistic is Dr Simner’s theoretical idea of a type of person who is especially articulate due to a hidden type of synaesthesia based in the “fronto-temporal language regions”. I certainly do think it is probable that there are non-obvious and undiscovered types of synaesthesia linking brain functions that researchers haven’t already known to be hyperconnected, but I suspect that researchers will also find that synaesthesia is more likely in some regions of the brain than others. I’ve long ago noticed that most types of synaesthesia that are known to science (and to me) involve the sense of sight in one way or another (scenes, colours, shapes, faces, visual-spatial landscapes etc), and where is vision processed in the brain? At the rear, where so many of those red blobs are found.

Simner, J. (2012), Defining synaesthesia. British Journal of Psychology, 103: 1–15. doi: 10.1348/000712610X528305  Article first published online: 11 MAR 2011 DOI: 10.1348/000712610X528305 http://onlinelibrary.wiley.com/doi/10.1348/000712610X528305/full

Gross L (2008) From Structure to Function: Mapping the Connection Matrix of the Human Brain. PLoS Biol 6(7): e164. doi:10.1371/journal.pbio.0060164  http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0060164

Human Connectome Project  http://www.humanconnectomeproject.org/

Are the flashbacks that are an element of Post-Traumatic Stress Disorder a troublesome variety of synaesthesia and/or related to the Tetris effect?

I’m going to explain why I think this question is worth considering.

I have recently been reading a most interesting book that has been descibed as a “medical memoir”. I have read that the fiction writer Siri Hustvedt has mirror-touch synaesthesia, and I was rather interested in reading about that, but the main topic of Hustvedt’s book The Shaking Woman is her search for an explanation for her seizure-like shaking episodes that are triggered by public speaking.

One thing that I’ve noted is that both Siri and her late father have experienced PTSD-type flashbacks of traumatic memories (warfare, car accident). Like myself, Siri Hustvedt has also experienced the Tetris effect, which is like PTSD flashbacks in that it is an involuntary experience of a visual memory. I don’t experience the Tetris effect much these days, but when I do it is typically in response to a full day of weeding or some other outdoor repetitive work. I don’t think scientists know how common the Tetris effect is, and if it is a thing that everyone experiences then it wouldn’t mean a thing that the novelist and I both experience it. I have at least one other close blood relative who has also experienced the Tetris effect quite a few times. The Tetris effect operates through an unknown memory system, possibly related to procedural memory, according to the Wikipedia. I would think that the Tetris effect would have some type of visual memory system as its basis. It is interesting that Hustvedt’s mysterious shaking episodes were dampened-down but not completely cured by the drug propranolol, which (according to the book) is also used to treat high blood pressure, migraine, performance anxiety and PTSD. Hustvedt seems to have a lot of whatever mechanism is the basis of PTSD, which I guess might be a very strong or hyperconnected visual memory system in her brain. I would think this system is also probably responsible for the Tetris effect. Another reason to believe that the Tetris effect and PTSD operate in the same brain system is that a study described in the Wikipedia found that playing a Tetris-like video game soon after a traumatic event “….reduces the number of flashbacks that are experienced afterwards”. I guess a specific memory system becomes overloaded with memories if the game is used as preventative treatment, so less of the traumatic memories can be encoded properly for long-term storage.

Hustvedt and I have quite a few things in common. We are both synaesthetes, we have both experienced the Tetris effect, we have also both experienced and migraine headaches, and we have both apparently had brain-based experiences of involuntarily-retrieved visual memories. In her book Hustvedt did not spell out explicitly that her flashbacks included visual content, and she did mention the memory of sound, but I’m happy to assume that anything labelled as a “flashback” included visual content. My involuntarily-retrieved visual memories are two different types of synaesthesia which I’ve experienced which trigger visual memories of scenes or a face. Hustvedt’s shaking episodes are like synaesthesia in that they have a very specific trigger (public speaking) and a very specific manifestation (violent body tremors without apparent anxiety, or under the influence of propranolol, an “electric buzz” quiver throughout the body).

There seem to be a lot of things here that are inter-connected. My experiences of my fine-motor->visual memories of scenes synaesthesia and The Strange Phenomenon, which is I believe a hybrid of face recognition and synaesthesia in which seeing one face under very specific conditions triggers an involuntary experience of a very old memory of the face of another person, show that synaesthesia concurrents or triggered additional sensory experiences can be in some ways similar to PTSD flashbacks, but without any accompanying psychological distress. My fine-motor-triggered visual memories are very subtle and hardly noticeable, while the face memory evoked in The Strange Phenomenon is more of an intrusion into ordinary consciousness. I’d like to put forward the theory that the flashbacks of PTSD (and not any of the other distressing features of PTSD) are synaesthesia concurrents that just happen to be distressing visual or sensory memories. I guess they must have some type of trigger, and I guess could be something purely sensory, very subtle or ordinary. I have never experienced PTSD myself, probably because I have fortunately never been in the type of extremely traumatic situation that causes this psychological syndrome, so I can only guess at what PTSD flashbacks are really like from what I’ve read. Are PTSD flashbacks the result of a type of synaesthesia that can manifest as quite a subtle experience, but are only troublesome or exceptional because of the very unpleasant nature of the memories evoked? Are synaesthetes more likely to develop PTSD if exposed to trauma than non-synaesthetes exposed to equivalent situations? It’s just a theory!

Wikipedia contributors Tetris effect. Wikipedia, The Free Encyclopedia. http://en.wikipedia.org/w/index.php?title=Tetris_effect&oldid=448999724

The Shaking Woman. The Book Show. Radio National. April 22 2010.  http://www.abc.net.au/rn/bookshow/stories/2010/2878610.htm

Wish I had time to read this – journal paper from last year about Williams syndrome, music and synesthesia or synaesthesia-like experiences

What exactly do people who have Williams syndrome experience when they listen to music?

 

Auditory Attraction: Activation of visual cortex by music and sound in Williams syndrome.

Tricia A. Thornton-Wells, Chris J. Cannistraci, Adam Anderson, Chai-Youn Kim, Mariam Eapen, John C. Gore, Randolph Blake, and Elisabeth M. Dykens
Am J Intellect Dev Disabil. Author manuscript; available in PMC 2011 March 1.
PMCID: PMC2862007

Published in final edited form as: Am J Intellect Dev Disabil. 2010 March; 115(2): 172–189. doi: 10.1352/1944-7588-115.172.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862007/