Autism: a spectrum, dimensions or clusters? How about a multi-dimensional cluster of spectrums?

A write-up (see here) of the paper by Hyunsik Kim and colleagues [1] was the initial impetus for formulating this blog post, but it quickly escalated into something a little larger when the findings from Frank Duffy & Heidelise Als [2] also popped up.

The question at hand: how should one conceptualise autism? Is it truly a spectrum as per the Lorna Wing proposition, or is it something a trifle more complicated? As per the title of this post, should we perhaps be thinking about autism as some sort of "multi-dimensional cluster of spectrums?" I'll come back to that idea shortly.

Well, it's not for me to make definitive conclusions on this blog. Science rarely, if at all, provides an absolute 'truth' but rather the probability that something is approaching truth. Such a notion goes double when you consider the singular label of autism and the huge heterogeneity that it encompasses. There are no easy answers and probably little or no truths.

Starting with the Kim paper (including some notable names such as the surname 'Gadow') and the name of the research game was modelling, modelling in a computational sense. So: "The sample comprised 3,825 youth, who were consecutive referrals to a university developmental disabilities or child psychiatric outpatient clinic." The CASI-4R - formulated by Prof. Gadow - was the schedule administered, which includes "an ASD [autism spectrum disorder] symptom rating scale" among other things. Some nifty statistics were applied to the data and the initial findings were 'tested' on a further group of over 2500 children.

Results: "Based on comparison of 44 different models, results indicated that the ASD symptom phenotype is best conceptualized as multi-dimensional versus a categorical or categorical-dimensional hybrid construct." And the dimensions mentioned in that 'multi-dimensional' statement? Well, lucky for us they were something familiar: "social interaction, communication, and repetitive behaving."

Then to the Duffy/Als paper (again, these authors are no stranger to autism research) and a similar starting point: "The authors postulate that the broad definition of an omnibus 'spectrum disorder' may inhibit delineation of meaningful clinical correlations." Indeed, very familiar (see here). The conclusion: "evidence that an objectively defined, EEG [electroencephalogram] based brain measure may be helpful in illuminating the autism spectrum versus subgroups (clusters) question." The tool used by Duffy/Als in their study was something called NbClust "specifically designed to provide an objective means, i.e. independent of investigator choice, to identify the ‘optimal’ cluster number within a population." Said tool was applied to EEG data derived from 400 participants diagnosed with an ASD. Statistics and more statistics applied to the data revealed that: "430 subjects diagnosed as being on the autism “spectrum” and represented by 40 EEG coherence factors..., fell into two distinct clusters." These autism spectrum clusters differed from each other and importantly, from "554 subject neuro-typical control group subjects, not involved in the clustering process." Interesting results but an unfortunate use of the term 'neurotypical' (see here). Duffy & Als conclude that their data support a view whereby "autism disorder should not be seen as a continuous spectrum." So Kim & Duffy/Als arrive at similar conclusions: a singular 'spectrum' idea of autism is probably not the best way of conceptualising the essence of the label.

I would perhaps add in a little more evidence for the idea that 'multi-dimensional clusters of spectrums' is a potentially better fit. I used the words 'spectrums' (plural) because there is a growing body of evidence to support the idea of more than one 'type' of autism. I say that from the perspective of evidence for autism being 'acquired' under several different circumstances (e.g. accompanying inborn errors of metabolism, linked to exposure to certain infections or diseases, etc). There's also evidence that clinical profiles under the umbrella term autism are not uniform (e.g. regressive autism, the so-called 'optimal outcomers', differing developmental trajectories, etc). And when one looks at something like the success (or not) of intervention, it's plain to see that there is no universally shared genetics and/or biology of autism in the singular either (see here and see here for examples). Add in the idea that autism rarely appears in a diagnostic vacuum (see here) and that said comorbidity might 'cluster' in some subgroups of autism (see here), and I hope you can see why 'plural' might be a good addition to any attempt to re-conceptualise autism: spectrum, dimension, tapestry, cluster or however you think it should be defined...

Oh, and since we're on the topic of trying to conceptualise autism, a new book out recently has been reviewed in Nature (see here). It talks about how "conclusive findings about sex-linked brain differences have failed to materialize" which is particularly apt in relation to previous talk about 'extreme male brains' as a way of conceptualising [some] autism (see here). One quote I particularly liked from the review is this one: "The brain is no more gendered than the liver or kidneys or heart."

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[1] Kim H. et al. Quantifying the Optimal Structure of the Autism Phenotype: A Comprehensive Comparison of Dimensional, Categorical, and Hybrid Models. J Am Acad Child Adolesc Psychiatry. 2018 Oct 29. pii: S0890-8567(18)31894-X.

[2] Duffy FH. & Als H. Autism, spectrum or clusters? An EEG coherence study. BMC Neurol. 2019 Feb 14;19(1):27.

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EEG abnormalities and "high functioning" autism

I'm not a great fan of the term 'functioning' when it comes to autism (see here) hence the quote marks around high-functioning in the title of this post. Yes, I understand the message that it's trying to convey and that we don't have viable alternatives at the moment. It just however seems a little sweeping in terms of 'generalised' describing and labelling of people...

No mind. Today I'd like to bring the paper by Özdem Ertürk Çetin and colleagues [1] to your attention and the observation that their results "support the fact that EEG abnormalities are observed at a higher rate also in ASD [autism spectrum disorder] with a better functionality." EEG - electroencephalographic or electroencephalogram - refers to the recording of electrical activity in the brain. Although in small amounts, our cells use electrical signals to message each other; said activity in the brain can be picked up and recorded using some rather sensitive equipment. EEGs are the method of choice when it comes to investigating epilepsy or related seizure disorders (such conditions are epitomised by abnormal electrical activity between cells).

The connection between autism and epilepsy / seizure disorder is one that has persisted for many years (see here); even now to the point where research is starting to talk about autism / autistic traits being a feature of some cases of epilepsy (see here). Quite a bit of the research looking at autism and epilepsy has tended to suggest that epilepsy may be a little more over-represented for those towards the more severe end of the autism spectrum (i.e. in relation to presentation of symptoms and the presence of some degree of learning / intellectual disability). The Ertürk Çetin findings report that even in those with described 'better functionality' there may be disturbances in relation to the measurement of EEGs.

Looking for "the presence of EEG abnormalities in sixteen children diagnosed with high-functioning ASD" researchers reported that whilst none of the participants had clinical seizures (the overt expression of epilepsy) "5 patients (31.3%) were detected to have EEG abnormalities." Bearing in mind the quite small participant numbers and the fact that no control groups (asymptomatic or otherwise) were included for comparisons, this is quite an important finding. I agree with the authors when they say that: "The potential impact of EEG abnormalities on cognition and behavior, and the risk of epilepsy should be considered during long-term follow-up of these patients." In other words, whenever a diagnosis of autism or ASD is received, one should always consider the possibility that a heightened risk of epilepsy / seizure / abnormal EEG patterns might also be a feature of presentation irrespective of "functioning" status.

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[1] Ertürk Çetin Ö. et al. EEG abnormalities and long term seizure outcome in high functioning autism. Acta Neurol Belg. 2017 Apr 26.

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Ertürk Çetin Ö, Korkmaz B, Alev G, & Demirbilek V (2017). EEG abnormalities and long term seizure outcome in high functioning autism. Acta neurologica Belgica PMID: 28447214

Is coeliac disease an aetiological factor in paediatric nonsyndromic intellectual disability?

In answer to the question posed in the title of this post on whether coeliac disease (CD) might show some connection to intellectual (learning) disability, 'probably not' is the finding reported by Taner Sezer and colleagues [1].

Researchers initially looked at "serum levels of tissue transglutaminase antibody and total IgA" in over 230 children diagnosed with nonsyndromic intellectual disability compared with about the same number of asymptomatic controls. Nonsyndromic intellectual disability by the way, is "defined by the presence of intellectual disability as the sole clinical feature" according to other sources [2]. They reported that "3 patients in the nonsyndromic intellectual disability group (5.45%) and 1 in the control group (0.41%) had positive serum tissue transglutaminase antibody." But when it came to the diagnosis of CD only 1 patient who had nonsyndromic intellectual disability fulfilled the gold-standard criteria of "Duodenal biopsy confirmed celiac disease."

The authors conclude by saying that the: "screening test for celiac disease should not be necessary as a part of the management of mild and moderate nonsyndromic intellectual disability." But further: "cases of severe nonsyndromic intellectual disability could be examined for celiac disease."

These are important data but as you may imagine, I'm minded to suggest that there may be other issues that require further attention. First, and in keeping with a recurrent theme on this blog, CD has a hallowed place in the whole 'gluten affects health' arena as the archetypal gluten-linked autoimmune condition. In recent years however, we've been introduced to the concept of a wider spectrum of issues with gluten not necessarily CD and not necessarily other gluten-related ills such as wheat allergy: non-coeliac gluten sensitivity (NCGS). I know there are ums-and-ahs about how real NCGS is and what constitutes diagnostic criteria (see here) but I'm of the opinion that we need to look at this wider concept with much greater assiduity.

Second, and allied to the idea that CD might not be the be-all-and-end-all of gluten issues is the idea that the serology of CD but not the histology might show some connection to behaviour. I say this with the Ludvigsson paper in mind (see here) and what it might mean for autism, a label that shares quite a bit of overlap with learning disability (see here).

Finally, I do find it interesting that whilst Sezer et al suggest that population-wide screening for CD should not be carried out for nonsyndromic intellectual disability they do suggest that specific cases might warrant further investigation. Drawing on the data from research on Down's syndrome for example, manifesting intellectual disability and carrying something of quite an elevated risk of CD (see here), it is evident that there may in some cases be a heightened risk of CD or other gluten-related issues co-occurring within this population. If one also considers that a gluten-free diet (the primary tool to manage CD) might also show some effect on EEG findings (see here) bearing in mind the connection between EEG findings, epilepsy / seizure-type disorders and intellectual disability [3], it's also not beyond the realms of possibility that further relationships might be noted with continued investigations in this area.

Music: The Libertines - What A Waster.

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[1] Sezer T. et al. Is Celiac Disease an Etiological Factor in Children with Nonsyndromic Intellectual Disability? J Child Neurol. 2015 Jun 15. pii: 0883073815589759.

[2] Kaufman L. et al. The genetic basis of non-syndromic intellectual disability: a review. Journal of neurodevelopmental disorders. 2010;2(4):182-209.

[3] Robertson J. et al. Prevalence of epilepsy among people with intellectual disabilities: A systematic review. Seizure. 2015 Jul;29:46-62.

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Sezer T, Balcı O, Özçay F, Bayraktar N, & Alehan F (2015). Is Celiac Disease an Etiological Factor in Children with Nonsyndromic Intellectual Disability? Journal of child neurology PMID: 26078418

Gluten-free diet affecting EEG findings?

Acknowledging that a certain 'jolly' person with a beard wearing a red suit will be visiting a few homes across the globe quite soon (the only time of the year that most people would let a stranger enter their home via a chimney) I want to briefly direct your attention to the paper by Parisi and colleagues [1] talking about how in "the presence of unexplained EEG abnormalities and/or other neurological disorders/SDB [sleep disordered breathing] an atypical or silent CD [coeliac disease] should also be taken into account."

Merry Christmas.

One sentence in particular took my attention: "After 6 months of GFD [gluten-free diet] headache disappeared in 72% of children and EEG abnormalities in 78%" based on examination of a small participant group (N=19) "with a new biopsy-proven celiac disease (CD) diagnosis."

Coeliac disease (CD), gluten and EEG abnormalities is something I'm actually quite interested in. As per my previous musings, I'm not expert on the dark art that is EEG (see here) but I am interested in how EEG findings might relate to CD and in particular, the suggestion that CD might also have a neurological effect for some (see here). The idea that embarking on a gluten-free diet (the primary intervention for CD) might 'correct' unusual EEG patterns and/or their clinical signs is by no means a new one as per studies such as the one from Diaconu and colleagues [2] talking about the use of the diet and a 'favourable course' when it came to migraine and epilepsy.

Hopefully without too much speculation or controversy, the possibility that a gluten-free diet might impact on EEG issues and/or epilepsy outside of CD has also cropped up in my own research. My dabbling in the science of gluten-free diets for cases of autism (stress on 'cases' [3]) has led me to hear some individual instances where the diet seemed to accompany positive changes to the presentation of seizures in cases of autism [4]. I've talked about individual cases documented in the research literature where a gluten-free diet might have been part and parcel of seizure control in relation to autism (see here), also as a segment of the regime known as a ketogenic diet (see here). One of the studies which I think is missing from the body of research looking at dietary intervention in autism (some autism, perhaps some autism falling into that non-coeliac gluten sensitivity category) is whether impacting on 'unusual' EEG patterns might be something to look at when it comes to gluten removal...

Merry Christmas! And the usual 'best seasonal song ever' link... The Pogues and Kirsty MacColl.

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[1] Parisi P. et al. Role of the gluten-free diet on neurological-EEG findings and sleep disordered breathing in children with celiac disease. Seizure. 2014 Oct 6. pii: S1059-1311(14)00267-2.

[2] Diaconu G. et al. Celiac disease with neurologic manifestations in children. Rev Med Chir Soc Med Nat Iasi. 2013 Jan-Mar;117(1):88-94.

[3] Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. 2014 Oct 14:1-6.

[4] Whiteley P. et al. Gluten- and casein-free dietary intervention for autism spectrum conditions. Front Hum Neurosci. 2013 Jan 4;6:344.

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Parisi P, Pietropaoli N, Ferretti A, Nenna R, Mastrogiorgio G, Del Pozzo M, Principessa L, Bonamico M, & Villa MP (2014). Role of the gluten-free diet on neurological-EEG findings and sleep disordered breathing in children with celiac disease. Seizure PMID: 25457448

Mind-body exercise and self-control in autism?

Despite knowing a little something about the discipline of psychology and in particular, it's varied success/failure (delete as appropriate) when applied to a complicated condition like autism, I'll admit that I do have some difficulty in grasping certain ideas and concepts which make up the psychological research landscape.

Yin yang? @ Wikipedia 

Take for example the concept of mindfulness, which is definitely starting to be another 'big thing' when it comes to psychology stressing how the mind might be able to influence all manner of things including several physical 'frailties'. It's fascinating to me how something as simple as glorified meditation might be able to do so much.

A good example of mindfulness at work was seen in Dr Michael Mosley's recent BBC Horizon venture on 'The Truth About Personality'. Wherein the 5:2 diet (see here) was replaced by some interesting discussion on how we could all become much happier and less anxious through mindfulness and an interesting technique called cognitive bias modification (CBM). Aside from making an important mention of the concept of epigenetics and how we should be looking at the function of the genome as well as its structure, it was interesting to see Dr Mosley report some benefit from the interventions at the end of the program, measured also via more objective means over and above his subjective 'I feel better' sentiments.

This very long-winded introduction brings me to the topic of today's post on a mind-body exercise regime and autism following the publication of a study by Agnes Chan and colleagues* (open-access) who reported some success from their Chan-based mind-body exercise program on self-control (see here for the trial registration). The SFARI blog has also recently posted about this study (see here).

Before heading into the paper I should point out that this is not the first time that this type of program has been talked about with autism in mind. For example, I stumbled across this paper** by the same authorship group which talked about some potential effects from "a Shaolin-medicine-based dietary modification" which talked about removing foods which "will generate excessive internal heat and adversely affect the temper and cognitive functions" to include "ginger, garlic, green onion, spicy foods, eggs, meat, and fish". I don't really want to comment on the hows and whys of 'excessive internal heat' on autism in this post so will leave it there for now and allow readers to draw their own conclusions. I might also add that I've talked Chinese medicine and autism before on this blog as per the 'Jedi' massage (see here, lightsaber not required).

OK back to the Chan-based mind-body exercise program on self-control. The program is based on the practice of Nei Yang Gong and essentially includes "sets of slow movements that emphasize smooth, gentle, and calm movements". The authors suggest that these movement help with self-awareness and mental self-control but can also help in the reduction of stress (something all too familiar where autism is mentioned). They add that it is a slightly different program from just mindfulness and mediation. There are plenty of videos on the web illustrating the types of movements it includes.

The authors randomly allocated 46 children diagnosed with an autism spectrum condition to either the Chan-based mind-body exercise program under analysis or something called progressive muscle relaxation although only 20 kids in each trial arm completed the four-week study. Alongside measuring neuropsychological functioning, authors also ATECd the kids to pick up parent-reported behaviour changes and looked at event-related EEG results during "an inhibitory control test, namely, the Go/No-Go task".

The results: "the autistic children in the experimental group showed better self-control than those in the control group after the one-month intervention" based on the results of the neuropsychological tests. Analysis of the ATEC scores however were not so clean-cut as both groups were reported to show [variable] positive changes on the subscales (the experimental group generally however showing a more pronounced positive effect). The authors do note that when it came to looking at specific issues such as temper outbursts "the experimental group reported a significantly greater reduction" over the control group. Oh and did I mention that there were some changes on the EEG too? (bearing in mind my considerable non-expertise when it comes to this dark art).

OK, I know its tempting to look at this paper and its results and start to criticise based on things like the lack of blinding to group allocation / intervention regime and the use of the ATEC (but wait a minute...). There was also, for example, no treatment as usual group included in the study you might say. But just hold on a minute, when it comes to ascertaining medication in relation to autism and other conditions for example, on more than one occasion there has been criticism that researchers have been too over-reliant on drug vs. nothing (or placebo) over drug A vs. drug B. At least the authors in this study were able to say that their program was better than just muscle relaxation techniques. Perhaps the next study to be done would be comparing their program with something more pharmacological?

Likewise in our modern Western medical system which we all love, it is perhaps easy to rather disparagingly talk about things like 'internal heat' whilst carrying that little smirk on our faces as if 'we know better'. I don't know enough about Chinese medicine to say whether this is something real and tangible or just some ancient hand-me-down. All I can see is that the authors have made an attempt to (experimentally) bring their expertise to bear on a group of people who are probably more prone than most to issues with things like self-control and anxiety. And if it worked, well, it worked. That and I assume the fact that once one has been trained in the ways of Nei Yang Gong, it's probably going to be something that can done quite easily and certainly quite affordably in the longer term (probably also with minimum side effects I would imagine).

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* Chan AS. et al. A Chinese Mind-Body Exercise Improves Self-Control of Children with Autism: A Randomized Controlled Trial. PLoS ONE. 2013; 8(7): e68184. doi:10.1371/journal.pone.0068184

** Chan AS. et al. A chan dietary intervention enhances executive functions and anterior cingulate activity in autism spectrum disorders: a randomized controlled trial. Evid Based Complement Alternat Med. 2012;2012:262136. doi: 10.1155/2012/262136.

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Agnes S. Chan (2013). A Chinese Mind-Body Exercise Improves Self-Control of Children with Autism: A Randomized Controlled Trial PLoS ONE DOI: 10.1371/journal.pone.0068184

Functional connectivity, NAC & schizophrenia

I promise that I am not getting obsessed with N-acetyl-cysteine (NAC) nor am I moving my focus from autism research to schizophrenia research despite recent posts. It just so happened that I stumbled upon this paper by Carmeli and colleagues* (full-text) recently and the needle on my interest-o-meter started to register something potentially important.

Indeed, there were several things about this paper which just made it seem right to comment on it: the use of that dark art, EEGs, the small participant group with schizophrenia, the NAC thing and the tie-up with glutathione. My previous posts on the potential for overlap between schizophrenia and autism and the significantly over-represented paper discussion serve as reminders that although discrete conditions, the words 'cut from the same cloth' in a biochemical sense might not necessarily be an inappropriate saying.

The paper is available to all but a summary:

• N-acetyl-cysteine (NAC) was given to participants diagnosed with DSM-IV schizophrenia (N=11) in a randomised, double-blind, crossover protocol for 60 days, followed by placebo for another 60 days (or vice versa). Yes, you saw right, the trial only included 11 participants which dropped to 8 participants when all was said and done. Having said that, this group (I think) were involved in a larger trial of NAC and schizophrenia undertaken by some of the authors.
• Resting EEGs were carried out at baseline, 2 months (treatment cross-over point) and 4 months (study end). I am not an EEG Jedi Master so an easy description I cannot give [said in best Yoda voice] of what was done aside from pasting from the article: "..whole-head topography of the multivariate phase synchronization (MPS) for 128-channel resting-state EEGs". I think this means that neural synchrony was a big part of the analysis but don't quote me on that.
• After some statistical wizardry, the results suggested that NAC supplementation seemed to affect EEG synchronisation in a couple of brain areas and despite the small participant numbers, the results seemed to be fairly similar across individual participants at least in relation to a few of those brain areas. From a behavioural perspective, the results also seemed to tie into other findings of issues with executive functions and attention noted in people with schizophrenia.

Despite the small sample size, these are interesting findings. Interesting because of the implications for schizophrenia and brain function which kinda follows on from the recently discussed study on schizophrenia and dietary intervention from a few years back. I know synchronisation is not the same as cerebral blood flow, but the link is the suggestion that at least some of the brain findings in schizophrenia might, just might, be functional rather than just structural and hence partially reversible in the same way that pharmacotherapy such as neuroleptics are used. A similar thing also to what Dr Michael Merzenich discussed in this recent piece in Nature on neuroplasticity and brain training. I would hasten to add that I am reserving judgement on the schizophrenia - brain training link until more substantial evidence is forthcoming.

As to the involvement of NAC and glutathione in schizophrenia, well this paper by Olivia Dean and colleagues** (full-text) seems to sum it up quite well. That and a post by Dr Deans with a rather appropriate title (I have a NAC for that). I also think back to the study looking at possible biomarkers for schizophrenia and their finding of issues with cystine (the dimer of cysteine) and can't help but think that there might be something crucial there which really should be looked at with greater assiduity.

* Carmeli C. et al. Glutathione precursor N-acetyl-cysteine modulates EEG synchronization in schizophrenia patients: a double-blind, randomized, placebo-controlled trial. PLoS ONE. February 2012.
DOI: 10.1371/journal.pone.0029341

** Dean O. et al. N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action. Journal of Psychiatry & Neuroscience. 2011; 36: 78-86.
DOI: 10.1503/jpn.100057

EEGs and autism and a few other conditions

Science fascinates many people including me. I love the complexity of it, the technology behind it, the sheer enormity of it. The hospital and laboratory scenes of everyone's favourite unpronounceable physician, Dr Hfuhruhurr, kinda sum up science: flashing lights, bubbling test tubes, 'the cranial screwtop method' and brains [and the words 'get that cat out of here']. During my very earliest days in research, one area of brain science was always a marvel to me: conducting and interpreting electroencephalograms (EEGs).

I have never been physically present during an EEG but have had the opportunity to look as some of the raw data produced and it fascinated me. What is perhaps so interesting is that a person, suitably trained, can look at the various squiggles of an EEG and determine the presence of an epileptic seizure and also, depending on the activity of the EEG, diagnose different types of seizure even pointing to differing epilepsy-related conditions. I know of at least one physician who is skilled in this dark art. Yes, the Force is indeed strong with them.

I talked about epilepsy and autism in a previous post, although not specifically discussing the use of EEGs. When looking at the literature about autism and EEGs, there are quite a few interesting points to note about things like the comorbidity of abnormal EEG results and the presence of epilepsy in some cases of autism. Also are the various suggestions that EEGs might serve as a potential objective early marker of autism and possibly a few other things. Mmm, we will see.

The study at the centre of this post was published in BMC Medicine by Bosl and colleagues* a few months back (full-text available here). The suggestion was that a statistical algorithm applied to EEG results might be able to classify very young children as either typical developers or as being at-risk for developing an autism spectrum condition. The results whilst small-scale made a few media waves along the lines of 'it will change the field, if this works' (comment made by one of the study authors).

Of course autism, and the various issues around it, is never so straight forward. Guaranteed that with every giant claim about diagnosis, treatment, aetiology, etc. an opposing view will always emerge, and like a classical opera, scientific battle breaks out ('no you can't, yes I can'). In the case of Bosl and colleagues it was this paper** which appeared in the same journal a few weeks later, questioning some of the claims suggested. The main crux of the criticism seems to be about the use of high-risk at population levels vs. high-risk at an individual level.

Fair's fair there is an author response to the criticism of their paper, available full-text here. They do offer some explanation for why they chose to record and report their results as they did. Credit also to them in highlighting why the media took so much interest in the story: novel medical research + lots of public interest + practical implications = a good story.

Its not just autism that is getting the EEG-biomarker treatment; so is Chronic Fatigue Syndrome (CFS) with the publication of this paper (again full-text) by Duffy and colleagues*** published in BMC Neurology. There hasn't been time for a formal scientific criticism of Duffy's paper but I'm sure it will come eventually. I have to say that the sample size included in this recent CFS paper is pretty big: 70 patients with well-defined CFS, 24 with depression, 148 with general fatigue and 390 asymptomatic controls. With a large sample size comes greater study power and hence greater predictive value. Indeed Duffy and colleagues are talking about nearly 90% of unmedicated women with CFS and over 90% of controls being correctly classified using their method.

As an outsider looking in on the world of EEG use and research, I have to say that I am intrigued by the possibilities of EEG-derived biomarkers even if only as part of a suite of investigations. Aside from the fact that EEGs are fairly inexpensive to do and importantly not invasive like the recent data on motor skills, I would like to think that the electrical activity of our brains, or rather their patterns of activity, are just waiting to be decoded in much the same way as the analysis of any other genetic or biological system might hide various secrets about our human condition. At the very least, EEGs might provide a window on the effectiveness of interventions targeting the brain as exampled here with the antidepressant treatment response.

To end, Dr Hfuhruhurr imparts his pearls of medical wisdom.

* Bosl W. et al. EEG complexity as a biomarker for autism spectrum disorder risk. BMC Medicine. February 2011.

** Griffin R. & Westbury C. Infant EEG activity as a biomarker for autism: a promising approach or a false promise? BMC Medicine. May 2011.

*** Duffy FH. et al. EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients-A case control study. BMC Neurology. July 2011.