Thursday, 29 September 2016

The Adult Psychiatric Morbidity Survey (APMS) 2014 and autism

They've finally arrived. The results of the English Adult Psychiatric Morbidity Survey 2014 have been published by NHS Digital (yes, our Nation's healthcare services has a digital arm) and when it comes to autism (adult autism 18 years+), some rather peculiar statistics have been produced.

OK, for those who want/need a quick heads-up on all-things Adult Psychiatric Morbidity Survey (APMS), I'll refer you to a previous post I wrote covering this prevalence survey with autism in mind (see here). APMS provides estimates of the numbers of various mental health diagnoses among adults living in private households in England.

The 2014 data report some key facts, not least that: "One in three adults aged 16-74 (37 per cent) with conditions such as anxiety or depression, surveyed in England, were accessing mental health treatment, in 2014." This figure is an increase on the 2007 APMS data (24%). There are also some other important data derived from the 2014 survey too with regards to sex differences in relation to "common mental disorder (CMD)" in diagnosis and in symptoms. Lessons need to be learned.

It is however with autism in mind (see here for the section covering autism), that I'm concentrating on in this post and the observation that: "The estimated prevalence of autism in 2014, using the threshold of a score of 10 on the ADOS [autism diagnostic observation schedule] to indicate a positive case, was 0.7% of the adult population in England (equivalent to a rate of 7 per thousand). The estimated prevalence of autism in the 2007 data (1.0%) was similar to the 2014 estimate; with largely overlapping confidence intervals." A separate 'additional notes' document accompanies the APMS 2014 autism findings (see here).

1% in 2007 and 0.7% in 2014? Accepting that when it comes to prevalence estimates there is always a degree of 'error' expected (as per the comment on 'overlapping confidence intervals') I'm a little bit puzzled by this latest data and the idea that the figures are described as 'similar'. Puzzled because as well as suggesting that adult autism prevalence estimates might have actually dipped between the years, the authors note that their search of 3 quite populous areas of England ("Leicestershire, Lambeth and Sheffield") across both the 2007 and 2014 data combined only found "31 participants identified with autism."

So what's going on with the APMS and autism?

A question indeed and I assume that the 'combining' of the 2007 and 2014 datasets reveals quite a bit more than just the very small number of participants identified in the studies. I have to say that my brow is furrowing a little at the sight of the Autism Spectrum Quotient (AQ) as retaining an 'autism screener' role in the APMS 2014. If I've learned anything about the AQ in recent times it is that whilst measuring something, it may not be a particularly great exclusive screen for autism (see here). Even the authors attached to the APMS 2014 autism data have said so [1]: "The AQ-20 was only a weak predictor of ADOS-4 cases." I've also mentioned about the ADOS module situation and the whys and wherefores with APMS in mind in that previous post on the topic (see here again).

So we're left with a quandary. The much heralded '1% of adults may have autism' statistic is replaced by a lower value (with appropriate caveats on confidence intervals) of 0.8% when the APMS 2007 and 2014 data are combined. Is this a true reflection of adult autism in England in recent times? How does this tally with the suggestion that child and adolescent rates of autism are on the increase as per that seen in other parts of the UK (see here)?

Or, are the processes pertinent to estimating adult autism used by the APMS not really cutting the statistical/methodological mustard?

Which one is it?

----------

[1] Brugha TS. et al. Validating two survey methods for identifying cases of autism spectrum disorder among adults in the community. Psychol Med. 2012 Mar;42(3):647-56.

----------

ResearchBlogging.org Brugha TS, McManus S, Smith J, Scott FJ, Meltzer H, Purdon S, Berney T, Tantam D, Robinson J, Radley J, & Bankart J (2012). Validating two survey methods for identifying cases of autism spectrum disorder among adults in the community. Psychological medicine, 42 (3), 647-56 PMID: 21798110

On "socially successful elementary school-aged children with autism"

"School-based interventions should address malleable factors such as the number of peer connections and received friendships that predict the best social outcomes for children with ASD [autism spectrum disorder]."

So said the study findings reported by Jill Locke and colleagues [1] looking at "the stable (unlikely to change) and malleable (changeable) characteristics of socially successful children with ASD."

Mindful that the phrase 'socially successful children' is perhaps not one that I'm particularly enamoured with, and certainly not one that necessarily opens the doors to 'successful' academic outcomes in childhood for example (see here), the Locke paper makes for interesting reading.

Looking at nearly 150 "elementary-aged children with ASD" authors listed a number of factors linked to 'playground peer engagement' and 'social network salience ' a.k.a playing with other children in the school yard and "inclusion in informal peer groups." The severity of autistic symptoms was unsurprisingly a key feature as was those numbers of 'peer connections' and 'received friendships'.

What do these results mean? Well, minus sweeping generalisations, there may be some pretty easy ways that 'social outcomes' can be positively influenced for at least some children on the autism spectrum; not least one important variable: friends. Yes, a shocker I know.

I've used the term 'easy ways' and 'friends' in that previous sentence to denote how [sometimes] complicated and expensive/resource intensive interventions to 'increase social outcomes' when it comes to the label of autism really might not be the most effective use of resources. I however understand that friends, real friends, are not just something that can be magically produced on demand and that also friendships, whilst in the end generally worthwhile, are not without their own stresses and strains (some of which might be even more stressful and strainful(!) for a child on the autism spectrum).

One approach that does seem to be finding some favour in the peer-reviewed domain at least is that of employing a buddy system. The findings reported by Laushey & Heflin [2] whilst not without their methodological issues, provide some important assertions that a peer buddy approach might be something for schools to consider for some pupils with autism. I know some people might argue that a buddy is not the same as a friend but I'm not one of the them: opportunity (not necessity) is the mother of invention. Visit most schools (at least in here in the UK) and you will see similar arrangements being made for pupils whether diagnosed with autism or not. That and use of 'buddy/friendship stops' in certain parts of the playground and you'll see how important socialisation is viewed for all school pupils.

I'm also a greater believer that sport and exercise can be an important part of inclusion practices when it comes to autism - something equally applicable to school. Y'know, those team games that help build and forge important bonds between children particularly when it comes to competitive team games, also introducing the important concept of 'belonging'. I appreciate that finding the right sport is important in terms of likes/dislikes and ability but there are quite a few options out there. Indeed, drilling further down into the concept of 'belonging', one can perhaps see how even at elementary school age, finding your social niche can open up a whole world of new friends/associates thus implying that school clubs (e.g. Lego club, ICT club) might also be an important intervention tool too.

I don't want to come across too formulaic or mechanical when it comes to how to improve social outcomes for children on the autism spectrum because there is not one-size-fits-all 'flowchart' to this issue. Appreciating also that some children on the autism spectrum might not necessarily want to be 'social butterflies' there has to be some indication from the child as to the extent of their wants and wishes when it comes to social interaction also taken into account.

I should also remind readers that when it comes to friendships, children can be a rather fickle bunch...

----------

[1] Locke J. et al. Characteristics of socially successful elementary school-aged children with autism. J Child Psychol Psychiatry. 2016 Sep 13.

[2] Laushey KM. & Heflin LJ. Enhancing social skills of kindergarten children with autism through the training of multiple peers as tutors. J Autism Dev Disord. 2000 Jun;30(3):183-93.

----------

ResearchBlogging.org Locke J, Williams J, Shih W, & Kasari C (2016). Characteristics of socially successful elementary school-aged children with autism. Journal of child psychology and psychiatry, and allied disciplines PMID: 27620949

Wednesday, 28 September 2016

Postural tachycardia syndrome and gluten?

Please use your full stops wisely.
I believe that this is the first time that I've talked about postural tachycardia syndrome (PoTS) on this blog as I bring to your attention some rather intriguing findings reported by Hugo Penny and colleagues [1] on how PoTS and gluten-related disorders might not be unstrange diagnostic bedfellows.

PoTS by the way, describes symptoms where standing upright / sitting down induces dizziness, fainting and other symptoms. As well as being quite prevalent in a certain condition called Ehlers-Danlos syndrome (see here), PoTS is also described fairly frequently in cases of chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) too.

Describing how "patients with postural tachycardia syndrome (PoTS) were placing themselves on a gluten-free diet without medical consultation" the authorship team (mentioned previously on this blog) residing in the great city of Sheffield decided to look-see whether there may be underlying medical reasons why such gluten-free moves seemed to be used in cases of PoTS. They screened their 100 participants with PoTS "for gluten sensitivity, related symptoms and dietary habits" as well as assessing for coeliac disease, the archetypal gluten-related autoimmune condition.

Results: compared with a couple of control groups numbering in total above 1500 local participants, coeliac disease (CD) seemed to be more common in the PoTS groups - "serology and biopsy-proven coeliac disease." Alongside: "PoTS patients also had a higher prevalence of self-reported gluten sensitivity... compared with age-matched and sex-matched controls." The authors conclude that there may be more to see when it comes to the presence of classical and non-classical gluten-related disorders in relation to PoTS.

This is potentially important stuff. Accepting that outside of the immediate dizziness and fainting symptoms associated with PoTS there may be other 'gastrointestinal' involvement [2] the intriguing idea that [certain] symptoms might be to some degree alleviated by use of a dietary change is worthy of greater inspection. Indeed, set within the context of an associated diagnostic label, orthostatic intolerance, where an upright posture provokes related symptoms, also being potentially linked to gastrointestinal issues [3] one has an interesting template as to how gut and brain might show some important links. That a gluten-free diet will most likely target both gut and brain (yes, it might) provides plenty of food for thought as to possible mechanisms.

I'm also pretty interested in the growing research base looking at a possible autoimmune component to at least some cases of PoTS [4]. I know this takes us into some 'brow-furrowing' areas of peer-reviewed science [5] (indeed, complicated science) but the potential importance of cases of autoimmune PoTS intersecting with cases of autoimmune coeliac disease provides yet another example of how birds of an autoimmune feather tend to flock together (see here). The implication being that cases of PoTS should perhaps be screened for CD and other autoimmune disease/features and perhaps treated accordingly, offers some new directions for research and clinical practice.

And just in case you are still convinced that use of a gluten-free diet outside of CD is all bunk, the worm still continues to turn...

To close, 'Shatner's Bassoon'. That is all.

----------

[1] Penny HA. et al. Is there a relationship between gluten sensitivity and postural tachycardia syndrome? Eur J Gastroenterol Hepatol. 2016 Sep 7.

[2] Wang LB. et al. Gastrointestinal dysfunction in postural tachycardia syndrome. J Neurol Sci. 2015 Dec 15;359(1-2):193-6.

[3] Sullivan SD. et al. Gastrointestinal symptoms associated with orthostatic intolerance. J Pediatr Gastroenterol Nutr. 2005 Apr;40(4):425-8.

[4] Thieben MJ. et al. Postural orthostatic tachycardia syndrome: the Mayo clinic experience. Mayo Clin Proc. 2007 Mar;82(3):308-13.

[5] Blitshteyn S. & Brook J. Postural tachycardia syndrome (POTS) with anti-NMDA receptor antibodies after human papillomavirus vaccination. Immunol Res. 2016 Aug 25.

----------

ResearchBlogging.org Penny, H., Aziz, I., Ferrar, M., Atkinson, J., Hoggard, N., Hadjivassiliou, M., West, J., & Sanders, D. (2016). Is there a relationship between gluten sensitivity and postural tachycardia syndrome? European Journal of Gastroenterology & Hepatology DOI: 10.1097/MEG.0000000000000740

Tuesday, 27 September 2016

Neurotensin, intestinal inflammation and autism?

"Elevated peripheral pro-NT [neurotensin] levels reflect more severe forms of active celiac disease, indicating a potential role of NT in intestinal inflammation."

The suggestion, from Caroline Montén and colleagues [1], that the neuropeptide called neurotensin might play a role in paediatric coeliac disease is an interesting one that caught my eye recently. Interesting not only because of the potential implications for the archetypal 'gluten-causing' autoimmune condition called coeliac disease, but also because neurotensin might have some rather important links to [some] autism too [2].

OK, a quick recap is perhaps useful. Neurotensin when it comes to autism typically means one name, Theoharis Theoharides, he of mast cells fame (see here). The idea is that neurotensin (NT) is, among other things, quite a 'potent trigger' of mast cells and when activated these mast cells can release their inner contents that include quite a few substances linked to allergic inflammation. At least some of the talk linking 'inflammation' and autism might include a role for mast cells [3]  and so hey presto, a potentially important chain of biological events might therefore be linked.

Going back to the original Montén paper on NT and coeliac (celiac) disease, researchers set about investigating "if plasma pro-NT levels correlated with the degree of intestinal mucosal damage and tissue transglutaminase autoantibody (tTGA) levels in children with celiac disease." They did find elevated levels of one of the NT precursor fragments in a coeliac disease group (n=96) compared with controls (n=89) and there did seem to be something of a possible connection between pro-NT levels and tTGA. On these basis, they concluded that NT might indeed be linked to the intestinal inflammation noted in cases of coeliac disease. Mast cells might also be important to coeliac disease too according to recent findings.

Accepting that coeliac disease is not autism (even though in some individual cases they may be linked [4]), there are a few further studies that might be required on this topic with autism in mind. As I've already mentioned, inflammation - particularly inflammation of the gastrointestinal (GI) tract - is not something unheard of in autism research/practice circles (see here). I know furrowed brows can be associated with this area of discussion but I'm talking about peer-reviewed science not anecdote and speculation. One might for example, see an investigation whereby those with autism and GI-related issues (including an inflammatory component) might be more closely inspected for something like NT to see if it is something important. You could even include those potentially falling into the grey area of non-coeliac gluten sensitivity (NCGS) if you so wished (see here). Given also related findings for some on the autism spectrum in relation to tTGA too (see here) and the possibility of another link there with NT, some brave research team might also wish to inspect this parameter. I might also suggest that looking at gut motility patterns in relation to NT levels could be another area ripe for further investigation with autism in mind (see here) given some previous discussions on the effects of NT.

Just a few suggestions for how a little more work in this area might prove illuminating.

Insofar as what to do about a possible link between NT and autism, well someone it seems has already started that conversation [5] and discussions are seemingly continuing in the peer-reviewed domain [6]...

----------

[1] Montén C. et al. Role of pro-neurotensin as marker of paediatric celiac disease. Clin Exp Immunol. 2016 Sep 10.

[2] Angelidou A. et al. Neurotensin is increased in serum of young children with autistic disorder. J Neuroinflammation. 2010 Aug 23;7:48.

[3] Theoharides TC. et al. Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders. Transl Psychiatry. 2016 Jun 28;6(6):e844.

[4] Genuis SJ. & Bouchard TP. Celiac disease presenting as autism. J Child Neurol. 2010 Jan;25(1):114-9.

[5] Ghanizadeh A. Targeting neurotensin as a potential novel approach for the treatment of autism. Journal of Neuroinflammation. 2010; 7:58.

[6] Patel AB. et al. Neurotensin stimulates sortilin and mTOR in human microglia inhibitable by methoxyluteolin, a potential therapeutic target for autism. Proc Natl Acad Sci U S A. 2016 Sep 23. pii: 201604992.

----------

ResearchBlogging.org Montén C, Torinsson Naluai Å, & Agardh D (2016). Role of pro-neurotensin as marker of paediatric celiac disease. Clinical and experimental immunology PMID: 27612962

Monday, 26 September 2016

On HERV-H, autism, ADHD and methylphenidate?

Today's post is a bit of a mash-up including two paper: the first from Emanuela  Balestrieri and colleagues [1] (open-access available here) talking about "increased HERV-H [Human Endogenous Retroviruses - H] transcriptional activity in all autistic patients" included in their cohort (author's words not mine) and the second from D'Agati and colleagues [2] (open-access available here) describing "the reduction of HERV-H expression and the significant improvement of ADHD [attention-deficit hyperactivity disorder] symptoms after 6 months of methylphenidate treatment."

Taken together, both papers provide some potentially important information on how those fossil viruses that litter the human genome might not be as redundant as we might have first thought. Also how some of the commonly used medications to treat/manage certain psychiatric labels might have quite a few more effects than those listed on the package insert. A shocker indeed.

I've covered HERVs a few times on this blog in relation to quite a few labels (see here and see here and see here). If you've clicked on that first link, you'll know that this is not the first time that Balestrieri et al have talked about HERVs with autism in mind [2]. On that first occasion, they even went as far as proposing that "HERV-H expression be explored in larger samples of individuals with autism spectrum in order to determine its utility as a novel biological trait of this complex disorder." This time around "the transcriptional activity of three human endogenous retrovirus (HERV) families, in peripheral blood mononuclear cells (PBMCs)" was examined in 30 children diagnosed with autism spectrum disorder (ASD) and 30 asypmtomatic controls. Quantitative real-time PCR was the analytical weapon of choice, as "transcriptional levels of env of HERV families were quantitatively evaluated." As I've already mentioned, HERV-H expression showed some interesting trends compared to the not-autism controls. The authors note that this data from Albanian children is pretty much the same as what they found in Italian children diagnosed with autism.

The D'Agati findings - also including Balestrieri on the authorship list - although discussing a case report on what happened to HERV-H expression following use of methlyphenidate (MPH) in relation to ADHD, might also have some implications for [some] autism. Reiterating that this was a case report where both before and after HERV-H expression levels were measured, it potentially offers a road map for how HERV-H expression might be 'affected' by the use of certain medicines. Yes, I know that researchers only measured one variable (HERV-H) and one variable/measurement does not a link make. But given the quite significant overlap between ADHD and autism (see here) and the insinuation that over-expression of HERV-H might not necessarily be a 'good thing', one could see how further [independent] studies might be informative in this area.

Although slightly complicated by the fact that we are only beginning to realise how important HERVs might be to things like stem cells for example or even potentially being involved in the process of genetic deletion (see here), what is becoming clear is that these fossil viruses might be something to watch when it comes to health and wellbeing at different times of development. I've tried not to be too enthusiastic about HERVs and autism / ADHD / other (delete as appropriate) on this blog given our lack of understanding on any connection, specifically the hows and whys of any effect on either aetiology or symptoms. But it is getting harder not to wonder what role these and other mobile elements might play in development and behaviour, particularly in the context of HERVs being implicated in autoimmunity [3] (yes, that might also show a connection to some autism) and a possible role for the still emerging science of epigenetics in both HERV expression [4] and also [some] autism. There is lots more research to be done on this topic.

----------

[1] Balestrieri E. et al. Transcriptional activity of human endogenous retrovirus in Albanian children with autism spectrum disorders. New Microbiol. 2016 Sep;39(3):228-31.

[2] D'Agati E. et al. First evidence of HERV-H transcriptional activity reduction after methylphenidate treatment in a young boy with ADHD. New Microbiol. 2016 Sep;39(3):237-9.

[3] Tugnet N. et al. Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link? The Open Rheumatology Journal. 2013;7:13-21.

[4] Lavie L. et al. CpG methylation directly regulates transcriptional activity of the human endogenous retrovirus family HERV-K(HML-2). J Virol. 2005 Jan;79(2):876-83.

----------

ResearchBlogging.org Balestrieri E, Cipriani C, Matteucci C, Capodicasa N, Pilika A, Korca I, Sorrentino R, Argaw-Denboba A, Bucci I, Miele MT, Coniglio A, Alessandrelli R, & Sinibaldi Vallebona P (2016). Transcriptional activity of human endogenous retrovirus in Albanian children with autism spectrum disorders. The new microbiologica, 39 (3), 228-31 PMID: 27602423


ResearchBlogging.org D'Agati E, Pitzianti M, Balestrieri E, Matteucci C, Sinibaldi Vallebona P, & Pasini A (2016). First evidence of HERV-H transcriptional activity reduction after methylphenidate treatment in a young boy with ADHD. The new microbiologica, 39 (3), 237-9 PMID: 27602426

Saturday, 24 September 2016

Correcting ophthalmic problems in autism

'Does Correction of Strabismus Improve Quality of Life in Children with Autism Spectrum Disorder?' went the title of the paper by Pinar Ozer and colleagues [1]. Yes, it may very well do was the answer (but with certain caveats and the requirement for a lot more research in this area).

Strabismus, a condition where the eyes don't line up in the same direction, can sometime have some quite noticeable effects on a person's vision and indeed, has been linked to various other non-vision related symptoms and outcomes.

Ozer et al looked to identify "the impact of optical or surgical correction of the strabismus on the child using a questionnaire for parents." The published research of this team has been previously discussed on this blog (see here) with ophthalmic findings in mind, and the requirement for quite a few more resources to be put into eye examinations when autism is diagnosed (see here). This time around they were discussing what happens when such eye issues are resolved.

I'm not completely convinced that the Ozer findings this time around reporting 'significant improvements' in areas of "psychosocial interactions" is as it stands, a methodologically firm finding just pertinent to autism. Although no expert on strabismus, from what I gather, the 'cosmetic' side of the condition can have some far-reaching effects on 'psychosocial' functions. I daresay that such effects would be just as prevalent in autism as they are in the general population and hence, correction would likely have similar outcomes.

I am more open to the idea that if strabismus is affecting vision, as in causing something like blurred or double vision, correction of the issue may in some cases have some important 'effects' in relation to autism. Accepting that structural issues with the eye are not necessarily the same as or causative of visual perceptual issues that seem to crop up quite often in the autism research arena, it is not outside the realms of possibility that something like strabismus could be part and parcel of visual effects for some people.

I suppose to reiterate, screening for structural eye/vision issues when it comes to autism remains a pretty important area.

To close, karate gradings for one of my brood today and this is what they will be attempting...

----------

[1] Ozer PA. et al. Does Correction of Strabismus Improve Quality of Life in Children with Autism Spectrum Disorder: Results of a Parent Survey by Ophthalmologists. Semin Ophthalmol. 2016 Sep 6:1-6.

----------

ResearchBlogging.org Ozer PA, Kabatas EU, Bicer BK, Bodur S, & Kurtul BE (2016). Does Correction of Strabismus Improve Quality of Life in Children with Autism Spectrum Disorder: Results of a Parent Survey by Ophthalmologists. Seminars in ophthalmology, 1-6 PMID: 27599387

Friday, 23 September 2016

Epilepsy and systemic autoimmune diseases: birds of a feather?

A couple of years back on this blog I talked about some rather intriguing research suggesting that epilepsy and autoimmune disease might not be unstrange diagnostic bedfellows (see here) and that a "potential role of autoimmunity must be given due consideration in epilepsy." [1]

Today, I'm continuing that research theme as the findings from Zhang Lin and colleagues [2] caught my eye concluding that: "There is an association between epilepsy and SAD [systemic autoimmune diseases], which was shown to be stronger at a young age."

Relying on that rather important methodological tool called a meta-analysis, where various study findings are lumped together and conclusions (hopefully) derived from the whole, Lin et al included data from some 25 studies where epilepsy and SAD had been examined together "which included 10,972 patients with epilepsy (PWE) and 2,618,637 patients with SAD."

Aside from those with epilepsy showing "more than a 2.5-fold increased risk of SAD" the authors also observed the opposite too: "patients with SAD were also shown to have a more than 2.5-fold increased risk of epilepsy." When it came to specifics, those diagnosed with epilepsy were observed to show "a 2.6-fold increased risk of celiac disease" and those "patients with systemic lupus erythematosus had a 4.5-fold increased risk of epilepsy."

I remain intrigued about this topic. Appreciating that within the peer-reviewed literature there is such a thing as autoimmune epilepsy [3] and that even in cases of epilepsy seemingly without the autoimmune encephalitis element to it, there may be antibodies to neuronal tissue involved [4], there are perhaps some further important clinical studies to be done in this area. It is for example, not uncommon to see more than one autoimmune condition appearing at the same time (see here) as various autoimmune overlaps have been noted in the quite voluminous science literature on this topic. The implications perhaps being that if one could find some of the 'causes' behind such autoimmune issues (be that related to molecular mimicry or the presence of a superantigen for examples) one may potentially be able to treat/manage quite a few conditions.

Wearing my autism research blogging hat and extending the possibility of an 'autism link' discussed on my previous post on this topic, I'd like to think there may be some scope for further inquiry with autism in mind too. Not only because epilepsy is one of the prime comorbidites attached to a diagnosis of autism (see here) but also that for some people on the autism spectrum, autoimmunity is also potentially something to contend with (see here). Should we therefore be so surprised at the possibility that autism, epilepsy and autoimmunity could form an important clinical triad for some?

And with full caveats in action about not giving medical or clinical advice on this blog, there is a body of evidence out there supporting immunotherapy for certain types of epilepsy [5] where other interventions have failed. Mmm, I also wonder...

----------

[1] Ong MS. et al. Population-level evidence for an autoimmune etiology of epilepsy. JAMA Neurol. 2014 May;71(5):569-74.

[2] Lin Z. et al. Association between epilepsy and systemic autoimmune diseases: A meta-analysis. Seizure. 2016 Aug 23;41:160-166.

[3] Britton J. Autoimmune epilepsy. Handb Clin Neurol. 2016;133:219-45.

[4] Wright S. et al. Neuronal antibodies in pediatric epilepsy: Clinical features and long-term outcomes of a historical cohort not treated with immunotherapy. Epilepsia. 2016 May;57(5):823-31.

[5] Bello-Espinosa LE. et al. Efficacy of intravenous immunoglobulin in a cohort of children with drug-resistant epilepsy. Pediatr Neurol. 2015 May;52(5):509-16.

----------

ResearchBlogging.org Lin Z, Si Q, & Xiaoyi Z (2016). Association between epilepsy and systemic autoimmune diseases: A meta-analysis. Seizure, 41, 160-166 PMID: 27592469