• Author: Emily L. Williams
• Comments: 26

• Autism
• Neurobiology

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<a href="http://leftbrainrightbrain.co.uk/?p=3470">The ‘Connectivity’ Link between Autism and Dyslexia</a>

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26 Responses to “The ‘Connectivity’ Link between Autism and Dyslexia”

1. 
   Laurentius Rex
   November 4th, 2009
   20:27:45

   Oh he of Charles Bonnet Syndrome ( I told him jokingly some time ago that I though he had it as he was the only one who could see his microcolumns.

   FWIW some people have been positing a link between so called dyslexic difference and autism for some time within a broader neurodivers phenotype if you want to get all scientific and regular about it.

   Why are these scanner wallahs so slow?

2. 
   Raymond Andrews
   November 4th, 2009
   23:00:07

   What about Dyslexics that have Dyspraxia and/or ADHD. I have a history of Dyslexia,Dyspraxia,and ADHD

   It’s very common for neurodivergents to have more than one neurodivergent condition.

3. 
   Sullivan
   November 5th, 2009
   00:59:46

   Emily,

   welcome!

   Sometime I need to communicate with Dr. Cassanova. He has done some interesting work. However some of his early descriptions of TMS (in the press, not papers) were questionable, talking about reversing magnetic regions in the brain with TMS. The more recent interviews I’ve read have not mentioned those theories.

   I am very hesitant about anyone publishing in Medical Hypotheses. That journal has been used for too much questionable purpose by others in the autism communities.

   I haven’t read the JADD article yet, but I’m interested to see how the short and long range connectivity is defined and measured.

4. 
   Laurentius Rex
   November 5th, 2009
   01:14:42

   To be honest it is too early to be sure that Dr Casanova has discovered anything as he is one of these scientists who is currently out on a limb without the replication of observations that would tend to confirm his hypotheses.

   For all that the new techniques in scanning have revealed about general neurological funtion it is still all too easy to get led astray when it comes to seperating out particular disorders, nothing is clear cut in the way you can see a tumour or major lesion or whatever, it is all in the statistics and number crunching and there in lies the problem.

   I wish I could find the papers on this, there is more than one, but one of the problems I believe is the way in which the voxels are counted more than once in statistical analysis magnifying (at least I think that is what it does) the significance of any variance that is observed, it is a bit a bit like turning up the image enhancement on a scan of the martian surface and seeing pyramids and faces. The referene to Charles Bonnet syndrome is not altogether flippant, and I am sure Dr Casanova understands that well enough which is why I considered it a nice “in joke” to share with him when he was presenting his material at IMFAR last year. Essentially our brain fills in the gaps when data is missing, and so do the statistics if they are given significance that is not supported by the mathematics, something all researchers need to be aware of when analysing data, not to rely on the machines without understanding what they do.

5. 
   Laurentius Rex
   November 5th, 2009
   01:27:46

   Oh yeah another caveat, does not “in press” signify that the article has been tentatively accepted but has not yet been finally cleared for publication and that revisions are likely before publication.

   It is another of those tricks used by research departments to circumvent the wait for the proper appearance (or not) of an article. This smacks altogether of a press release statement. You won’t find it in JADD just yet.

   I have seen it before when the articles have not materialised, and it is damned annoying, I have been caught out that way myself citing something I ought not to have done before it found its final resting place, one of the reasons an article of mine has yet to see publication as it was sent back for revision (which I have yet to get round to) so in press may be innocent on the one hand, but on the other it can cover a multitude of sins if it is used as an academic sleight of hand.

6. 
   Laurentius Rex
   November 5th, 2009
   01:58:10

   That is the problem isn’t it Mike, that whilst the internet has undoubtedly democratised access to a lot of material and allowed the lay person to trawl databases for citations, it has also allowed for a lot of sloppy practice and outright cheating.

   Whilst it is legitimate to search by key words it still means you ought to read the abstract itself and then if you have decided it is of relevance to attempt the whole paper itself. That is where most people fall down, they will post a list of citations supposedly in support of the argument, having failed to consider counter citations (which any good rhetorician needs to look at as well in order to prepare ones own counter arguments as to why they are not felt to support the data one is defending.

   One of the things you are taught as a post grad is how to read papers properly and to consider that abstracts are not the be all and end all, as there are good abstracts and bad abstracts, and mostly they tell you nothing about the methodology or not enough to be able to mount a proper critique.

   Of course we all get sloppy, opinionated and biased, to the extent that we will prejudge that if a paper is coming from such and such a name, who has little reputation preceding of well argued papers then we are more likely to pass it over, especially when it is coming from the bad science brigade.

   The new flim flammery though is to make it appear that those more respected authors who we trust are saying the opposite of what we expect them too, witness the way the Geiers jumped on the semi-legitimate science of the double barrelled one to support there unsustainable quackery.

   Well this is what RAJ and those other Trolls who cut there teeth on the ASA newsgroup do, because all they have to do is misdirect and fool enough people to look authoratative in whatever they are saying, it’s trickery worthy of Derren Brown the charlatans charlatan isn’t it? Absolutely classic.

   You will notice I am doing it myself by my own magisterial pronouncement seen in the phrase “semi-legitimate science of the double barreled one” therein lies my own bias, but I have to say that not in a long time have I found him convincing in the least, and won’t until he takes off those monotropic spectacles of his and starts being objective again.

   At least I can take the piss out of myself eh, this pot is shining himself with brillo :)

7. 
   Laurentius Rex
   November 5th, 2009
   02:44:27

   Whoops that is what comes from being up too late, commented on the wrong blog there gonna have to copy and paste it back where it belongs.

8. 
   Stephanie
   November 5th, 2009
   16:54:34

   Thank you for this paragraph: “Individuals familiar with autism may be aware that dyslexia can also co-occur with autism and therefore may be wondering how the two conditions can be the “same” and “different”. In the new 2009 paper, this concern is addressed, saying that while autism and classic dyslexia are anatomical opposites, the underlying neurobiology of either extreme can cause a disability in reading. Therefore, while classic dyslexia is due to increased long-range/decreased short-range neural connections, the dyslexia associated with autism is due to increases in short-range/decreases in long-range white matter fibers. Since autism and dyslexia are still currently defined by behavioral criteria, this explains how it’s possible to have similar behavioral traits and divergent anatomies.”

   Both mine and my husband’s sides of the family have a history of dyslexia, but our children are the only ones with autism diagnoses. Now our youngest is starting to write and he’s showing signs of dyslexia. It’s not a spelling thing, because he can spell the words out right with letter blocks, but when he writes his “s” and “p” they get flip-flopped.

   Could you recommend a good means to access the 2009 article?

9. 
   Emily L. Williams
   November 5th, 2009
   17:45:10

   I haven’t had a chance to read through all the comments thoroughly, but will do so this evening. Just to say that “in press” means the article has been accepted and cleared as is. The above articles are also currently available online so they are considered “published”, although you do need a subscription to the journals in order to see them. But I can send copies of any of the cited work to anyone interested. Just email me. :) elwill08@louisville.edu

   ~Emily…

10. 
    Lynda
    November 5th, 2009
    18:08:32

    It would be interesting to look at people with Autism who were early readers. My son read at two. At six he could “decode” at the sixth grade level, but couldn’t comprehend. At about 10 he read a book in Spanish out loud which was upside down and viewed in a mirror. I use to tell people his condition was the exact opposite of dislexia.

11. 
    Laurentius Rex
    November 5th, 2009
    18:38:38

    Ah Emily, it seems then that different publications have different degrees of meaning when they use the term “in press” my misunderstanding.

    Still I suppose some neurological oddity just drives me to be suspicious of Dr Casanova, because I did not find his much vaunted discovery of micro columns to be that convincing, and until I see further evidence on that I now regard him with some suspicion.

    In press or published, it still requires further independant studies to back it up, though of course it does indicate a line of research that others might like to pursue in order to see if they can.

    In the cause of skepticism I submit myself to the same rigourous analysis and declare the probable reason I have a belief that there is some underlying connection somewhere (be it the opposites thery expressed here or actually anatomical similarity) between dyslexia and autism is my own anecdotal observations, and hey if what you see around you, primed for co-incidence, or whatever if it is good enough for the mercurians, I will have a stab at it myself.

    Or I could put it another way and say that quite possibly dyslexia (as behaviouraly defined as you quote) is also a broad church with many roads to rome, as already is believed to be the case with alternative but non contradictory neurological findings for auditory based dyslexia, visual dyslexia etc, which are as hotly disputed in the dyslexia fora as all our theries of autism are.

12. 
    Leila
    November 5th, 2009
    19:15:43

    Lynda, my son is the same way – hyperlexic, so it makes sense that the brain works the opposite way from dyslexia.

13. 
    Emily L. Williams
    November 5th, 2009
    19:49:41

    To Lynda and Leila:

    Based on this theory, hyperlexia and the dyslexia associated with autism would have more in common with one another than an “average reader” not associated with autism or with classic dyslexia. You’re familiar with the idea that genius and madness are not all that different? Well, this is a somewhat similar concept—not to be calling anyone “mad” of course. ;) But it all has to do with Signal-to-Noise ratios (SNR) in the brain. An increase in the short-range connections will refine the signal of a given stimulus. However, if the signals are increased so much, then those signals all end up becoming a mishmosh of incomprehensible background noise. In the case of hyperlexia, which can either be defined as a savant ability in phoneme decoding OR an increase in the same plus better overall reading/comprehension skills (depending on who you talk to and which paper you read), an increase in such ability would be a refinement of the stimulus signal but not to the point it actually turns the stimuli into incomprehensible noise. In point, a refinement of signal actually makes them BETTER at decoding phonemes. In the case of autistic dyslexia, the signals become so great that it all just becomes noise and phonemic decoding is lost. So you have hyperlexia, and if you tweak that signal up just a bit more, you have an autistic form of dyslexia.

    In theory, autism is characterized by increased overall signal, whereas dyslexia has increased noise. BUT in autism SO much signal can occur that it becomes noise anyways. Which is, theoretically, how both autism and the syndrome of classic dyslexia can share that common trait(s). Hopefully that makes some sense and I haven’t confused you.

    To Laurentius Rex:

    To my knowledge, “in press” is used once an article has been accepted for publication as is. It will continue to be called “in press” even once it’s published online. Once the hard copy of the publication is available, it is no longer considered “in press”. If a researcher wishes to cite any of their work which is either unpublished or not in press, they will say “unpublished data” or something to that extent. Although I’m not overly familiar with ALL the different types of citation styles and each journal does tend to have their own variation. But that’s a quirk of the publishing companies and not of the researchers themselves.

    As for needing more research, there is always the need. Which is why Manny Casanova continues researching. As do I. However, his work so far (histochemistry, functional imaging, computer modeling, rTMS clinical trials & electrophysiology) fits in perfectly with the overarching theory and provides further confirmation. And while you’re obviously familiar with at least some of his work, I have the feeling, Laurentius, based on your comments, that you’ve not read very much of it or have read it but not understood aspects of it. In which case, if I can be of any assistance to you, either in providing more materials (electronic forms of his published articles, chapters, or symposiums) or in explaining any concepts which have remained unclear to you, I’d be more than happy to help. Just let me know.

    And I do understand your concern about the reputation of Medical Hypotheses. However, since I am a newer author (I’m first author on the above publication) and Manny was attempting to get hypothesis paper published in a different journal, our selection was few. Plus it was just easier and faster to get it published in MH, so we chose that. If you’re concerned about the journal’s reputability, then I’d like to point out that while this paper is an extended review of the theory, he has already presented this theory in abbreviated form in other articles of his in more reputable journals.

    ~Emily…

14. 
    Laurentius Rex
    November 6th, 2009
    00:36:05

    It is true I have not paid a lot of attention to Dr Casanova’s papers they are a bit off piste to me, I can’t read everything and I try to control my curiosity somewhat by concentrating on papers that are in some way relevant to my particular furrow in the field. If for instance you read every paper that was included in the abstracts book from each years IMFAR you would be reading from here to eternity and I am not talking about the novel here.

    In so far as my main interest lies, it lies in papers that have relevance to my hypothesis that there is something different in Autistic visual perception, though I have neither the funding nor the right connections to investigate that with pans and scans, much though I would like to at some stage. I have to work in an altogether more round about way, and use my mind to substitute somewhat for the reliance on machinery.

    The problem is whichever way, when you start correlating results, if the study sizes are small, and you don’t look very hard for all the confounding factors, basic psychology trumps the numbers game and can lead you to use statisitical tests that generate significance and reject those that don’t, and to round up the numbers when it favours you and down when it doesn’t and not even know what you are doing. It is even worse when you give it over to the number crunching that surrounds scanning, I have lost the paper that I was looking for about how unreliable this can be because of the maths involved, but it did lead me to look twice at putting too much faith in the dark glass you look through. I look out at the world through my spectacles, and I see a strange smudge there, is it there or is it a speck of dirt on my glasses if you see what I mean.

    Charles Bonnet syndrome :) beware the brains ability to fabricate something out of chaos, its the reason we are so good at percieving objects from the background in the first place, but hey turn up the gain and yes you are reading the noise not signal.

    When things start to fit too closely that is when the strongest doubts ought to enter, to be sure you are not inadvertently trimming the ends of those jigsaw pieces to make them fit so neatly like the train of clues in a Dan Brown novel.

15. 
    Emily L. Williams
    November 6th, 2009
    03:46:33

    To Laurentius:

    I understand about funneling your reading energy into materials more relevant to your area(s) of interest. But if you haven’t read through the materials on connectivity and minicolumns (which are not relegated to Manny Casanova’s work but have been researched by other scientists as well), then I’m confused as to why you have criticisms. Except that it sounds like you feel the above doesn’t mesh with your own hypothesis regarding vision in autism. In which case, if you truly think the concepts are in opposition to one another, even though you admit to lacking a firm grasp on the research I’ve made reference to, then we’ll simply have to agree to disagree. :)

    If you are ever interested in reading up on minicolumns and local connectivity in autism, I can point you towards some review papers as opposed to data articles. They would give a better overview.

    ~Emily…

16. 
    dr treg
    November 6th, 2009
    11:29:58

    To Laurentius
    This short, simple video might help you understand more about some of the proposed structural models of autism according to different scientists – i.e. is autism a mini-columnopathy, synaps-opathy or dendropathy (dendritis)? Of course it might be all three.
    http://www.youtube.com/watch?v=5rvyCUc2TC0
    It is also interesting that the OP quotes the Journal of Medical Hypothesis but in a previous article ridicules the same journal for not being peer-reviewed. It seems the OP`s views depend on which way the wind is blowing.

17. 
    Emily L. Williams
    November 6th, 2009
    17:12:49

    Sullivan said: “Sometime I need to communicate with Dr. Cassanova. He has done some interesting work. However some of his early descriptions of TMS (in the press, not papers) were questionable, talking about reversing magnetic regions in the brain with TMS. The more recent interviews I’ve read have not mentioned those theories.”

    Sorry, I completely missed this. The early media descriptions of the rTMS trials were confusing, mainly because it’s a science that the media doesn’t grasp well. Nor do I pretend to be an electrophysiologist. However, the idea is based on the functional behavior of minicolumns in autism, wherein the lateral inhibition of those units is inadequate to keep information from essentially “spilling over” into neighboring minicolumns. This fits well with the increased seizure risk in autism, sensory issues, etc. In order to improve the lateral inhibition, the team has targeted a particular kind of GABAergic interneuron call a Double Bouquet cell. Normally, these provide lateral inhibition but in the case of autism, while they may be functioning normally, are inadequate for the increased excitation. rTMS used at low frequencies can actually preferentially target these double bouquet cells, increasing lateral inhibition and helping to contain the excitation within the minicolumn.

    Because it takes time to run clinical trials, the rTMS data is still largely unpublished. The unpublished results, however, are HIGHLY promising and participants and families-of have been giving very positive feedback concerning reduction in social anxieties, etc.

    So the rTMS trials are still going very strong. But it just takes time to do the trials, analyze the data, and finally publish it. Which is why it’s been a number of years since the media first reported on the rTMS here.

18. 
    passionlessDrone
    November 6th, 2009
    20:33:49

    Hi Emily Williams –
    I was intrigued by what I read concerning rTMS at the time it was reported, but got overwhelmed reading other stuff and it slipped off my radar. I appreciate very much your description above.

    I’m curious as to the (proposed) mechanism by which rTMS provides persistent changes. Would you be willing to into more depth here? I would also be curious as to your thoughts as to similarities between this and the use of neurofeedback.

    – pD

19. 
    Emily L. Williams
    November 6th, 2009
    22:16:45

    Hi, pD. I would love to go into as much detail as you like, except that electrophysiology is definitely not my area and so I can give you some basic overviews of the approach as I understand it but I’m afraid I can’t go any deeper than that.

    TMS is separated into two types: high-frequency and low-frequency. High-freq TMS has most often been used and is the method associated with increased seizure risk. Low-freq TMS, the TMS utilized in the University of Louisville rTMS trials, is not associated with any kinds of increased risks.

    The cortex is comprised of many types of cells, one important cell type being excitatory pyramidal neurons, named because of the triangular shape of their cell bodies. These cells are lined in vertical columns in the cortex and seem to have the capacity to act as single functional units, hence the focus on the minicolumn rather than at a single cellular level. Interspersed among these columns are inhibitory cells known as interneurons. As you can probably guess, these interneurons have the capacity to inhibit/refine the excitatory signals coming from the pyramidal cells. One particular type of interneuron that is the focus of these rTMS trials is the Double Bouquet cell. These cells lie between minicolumns, providing a shower curtain of inhibition so that when one column fires, the DB cells have the capability of preventing one minicolumn from triggering the firing of its neighbor.

    Research suggests that autism is characterized by hyperexcitability of these minicolumns, which increases the risk that the signal within a column will overcome the lateral inhibition and spill out into neighboring columns. Low-frequency TMS can specifically target the DB cells based on Faraday’s Law, because of the perpendicular arrangement of these DB cells to the surface of the brain (any physicists reading I’m sure can give a better synopsis of this effect in general physics, so feel welcome to interject). The rTMS, due to the perpendicular arrangement of the DB cells to the cortex’s surface, triggers firing of those DB cells, increasing the inhibitory power. With enough treatments, plasticity sets in and the rewiring occurs to reduce the lateral “spillage”.

    Regarding persistent changes, the results are still fairly new and I honestly don’t know how long they’ve performed follow-up assessments as to the permanence of the behavioral changes; I’ll have to get back to you on that. However, if the results are based largely on plasticity, then there is always the potential to revert to pre-study behaviors. However, one hope would be that the changes persist, not necessarily due to the rTMS directly but for natural learning to take over and for improvements to continue. E.g., some individuals have reported more desire for socialization and have become more involved; just the act of involving themselves more in social settings should also promote learning and hopefully a continued decrease in social anxiety and related issues.

    As for similarities between rTMS and neurofeedback, I’m afraid I am not familiar with the related materials so can’t really say anything in regards to that.

    ~Emily…

20. 
    passionlessDrone
    November 9th, 2009
    18:29:57

    Hi Emily –
    I appreciate you taking the time to respond to me. I came up with a couple more questions, would you be willing to entertain me?

    High-freq TMS has most often been used and is the method associated with increased seizure risk. Low-freq TMS, the TMS utilized in the University of Louisville rTMS trials, is not associated with any kinds of increased risks.

    This is very intriguing to me. Considering our particular population of interest has high concordance with epilepsy, I’d imagine you are treading carefully. Are pre / post eegs being used in your research to determine if the treatment is having normalizing, or denormalizing effects?

    Considering that what we are trying to do is increase inhibitory signals, I’m really struggling to see a dose relationship that has the effect of increased seizure risk; presumably via decreased inhibition. Do you have any thoughts on that?

    The rTMS, due to the perpendicular arrangement of the DB cells to the cortex’s surface, triggers firing of those DB cells, increasing the inhibitory power. With enough treatments, plasticity sets in and the rewiring occurs to reduce the lateral “spillage”.

    Hm. Can you go into detail (or point me to good links) as towards the ‘wrong wiring’ that is believed to be being ‘fixed’ by rTMS? I did a little bit of reading regarding minicolumn findings in autism that seemed to speak towards a reduction in size, what I read indicated that this structural component was entirely set prenatally. I can see how finding a way to improve inhibitory signals from your existing DB cells might help, but I guess this doesn’t fit into my view of fixing bad wiring so much as making efficient wiring more efficient.

    As for similarities between rTMS and neurofeedback, I’m afraid I am not familiar with the related materials so can’t really say anything in regards to that.

    We investigated it some a while back; the claim is that it is more of a passive means for changing brain function. Essentially the patient is given EEGs, shown a video game / program, and ‘rewarded’ visually for thinking in the ‘right’ way. The video slows down / stops if it detects brain waves in ‘bad’ frequencies. The idea is, if you practice thinking ‘right’ for more time, your brain gets used to it, and getting immediate visual feedback helps to guide your concentration in this regard. There are several studies showing changes in EEGs following neurofeedback training.

    I was very skeptical initially, but when I tried on the electrodes and let my mind wander, it definitely had an effect on the videos being displayed. As far as a relationship to rTMS and neurofeedback, I was thinking rTMS would be more of an aggressive means to modify brain function, while neurofeedback is more passive. I was never able to get anyone to try to tell me, chemically, what they thought the mechanism of action in neurofeedback might be.

    I appreciate you taking comments from the masses.

    – pD

21. 
    daedalus2u
    November 9th, 2009
    19:02:29

    pd, there are (at least) two types of connectivity, actual connectivity (the actual connections made via axons and synapses), where there are ~10^4 actual connections per neuron. On average only one of these connections can be active. In other words the average number of “downstream” neurons that fires has to be ~1. If it is less then 1, then the avalanche of neuronal activity extinguishes. If it is greater than 1, then the avalanche of neuronal activity increases exponentially until it saturates in a seizure.

    What regulates the number of downstream neurons firing is the functional connectivity. That is obviously regulated in real time, but how and in what ways is not very well known. Changes in functional connectivity are what are observed in fMRI BOLD. Activity in certain brain areas increases (n greater than 1) and then decreases (n less than 1). That change in activity is highly coupled to blood flow, such that the changes in hemoglobin levels measured by fMRI BOLD are used as a one to one surrogate for actual brain activity. What regulates that blood flow is nitric oxide, and I think that it is NO that also regulates the functional connectivity.

    Changes in actual connectivity (i.e. neuronal remodeling) requires time for nerves to extend axons and form synapses and so change the neuroanatomy. Acute changes in behavior are likely not due to changes in neuroanatomy (because there isn’t enough time for neuronal remodeling to occur) but more likely due to changes in the regulation of functional connectivity. A very slight change in the number of downstream nerves firing per upstream nerve could have a very large impact on brain function.

    The average is 1 out of 10,000 or so. Changing that number to 1.1 out of 10,000 or 0.9 out of 10,000 would have a very large impact once the avalanche expands (or contracts) exponentially, but would be very hard to measure. The brain doesn’t really have a synchronous clock, but if it did, then a couple hundred cycles at n = 1.1 would saturate the whole brain (unless there was feedback which stopped it (which there is)). Similarly at n = 0.9 the whole brain would go quiet in a similar amount of time.

22. 
    Emily L. Williams
    November 9th, 2009
    19:27:26

    Will hopefully answer more of this later that daedalus hasn’t already touched on. But just to say that high-frequency TMS is associated with increased seizure risk, whereas low-frequency TMS can potentially decrease the risk of seizures and has been used to some success in focal neocortical epilepsies. It’s the latter, low-freq TMS, which this study has been using. So your confusion as to how a method associated with increased seizure risk could possibly offer relief in autism is well founded. But it’s the other form, low-freq, that we’re using that’s associated with decreased seizure risk.

    ~Emily…

23. 
    passionlessDrone
    December 1st, 2009
    18:39:20

    Hello friends –
    I saw this hit pubmed today and thought I’d post a link.

    Low-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Affects Event-Related Potential Measures of Novelty Processing in Autism.

    Emily – would you like to step in and give some more details on this study? Or, alternatively, how would you feel about sending an interested, but cash strapped enthusiast a copy? passionlessdrone@yahoo.com

    – pD

24. 
    Emily L. Williams
    December 2nd, 2009
    02:17:55

    Hi, passionless. Unfortunately I’ve not been involved in the electrophysiology side of the team’s research and so I’m afraid I’m going to have to leave that to Manny to reply. But I will let him know of your interest, see if I can herd him over here, and perhaps he can also provide you with a copy of the manuscript (although since it’s a new publication and ahead of print, I’m not absolutely certain he himself has a presentable copy).

    ~Emily…

25. 
    Manuel
    December 2nd, 2009
    14:51:14

    Hi Passionless,

    We have been using electrophysiological measurements for outcome in our trial. Most other trials use neurobehaviroal screening techniques which exclude lower functioning patients from participating including my own grandson. My intent is to have representative results for the whole population of ASD patients.

    TMS appears to have positive effects in autism. Our first study circumscribed itself to the effects of TMS on the brain. The last publication surveyed the effects of TMS on a neural network having to do with novelty processing. Again results have been positive. It is baby steps, studying the results of TMS by itself and then under different environmental conditions.

    If anybody is interested I can send a copy of the galley proofs’ pdf. Send me an email at m0casa02@louisville.edu.

    Best regards,

    Manuel

26. 
    passionlessDrone
    December 2nd, 2009
    15:19:01

    Hi Manuel Cassanova –
    Thank you for your kind and rapid response. I’ve send you an email regarding the manuscript. Hopefully I’ll be able to glean something from it.

    Though you are most likely aware of this study, just yesterday I ran into a write up of another study that used TMS to investigate trust and/or reputation. I know that a few months ago when a couple of TMS related news releases were floating around the autismphere there was some skepticism towards the mechanism of TMS, so I thought I’d post it here.

    How to lose friends and alienate people by disrupting the brain

    Thanks again for stopping by and responding to my post.

    – pD

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