Research Blogging - Medicine - English

Bright Lights, Cold Bodies - The Near-Death Experience Explained

2013-05-21T08:53:47Z

Last February, Dr. Sam Parnia, an intensive care physician who has been researching near-death experiences for the past 15 years, published his new book ‘Erasing death: The Science That is Rewriting the Boundaries Between Life and Death’. Following the release of that book, Dr. Parnia was interviewed on National Public Radio in the US. It wasn’t so much this interview that sparked my interest, as much as the comments that followed. “It’s hard to believe that this guy is actually a doctor based on the junk he presents here,” commenter ‘Joe MARTYN’ says. And another user, ‘Steven Kay’, adds: “Oh, please.. Not this guy again. Why not interview the last person who claims to have seen the Virgin Mary?” To be fair, many other commenters did appreciate the interview and the work that Dr. Parnia had done. But still, the virulent dismissiveness related to this subject baffled me. Why is research on near-death experiences received with such hostility?...

van Lommel P, van Wees R, Meyers V, & Elfferich I. (2001) Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands. Lancet, 358(9298), 2039-45. PMID: 11755611

Epilepsy Service Organization in Countries with Limited Resources

2013-05-20T13:23:31Z

tumblr: bellapaige88On average, 9.5/1000 population has epilepsy in Low and Middle Income Countries (LAMIC). A research which has resulted in the global campaign against epilepsy has shown, the gap between treatment need and the treatment provision worldwide is approximately 70% [1]. This large ‘treatment gap’, i.e., lack of appropriate treatment for a large number of patients with epilepsy, due to a number of causes including inability to identify cases, inability to deliver adequate treatment, people’s attitudes and perception, availability of anti-epileptic drugs and finally, health policies of individual countries and the priority given to epilepsy. [2]The first step towards narrowing the treatment gap is improving diagnosis. Clinical investigations that help in the diagnosis of epilepsy include electroencephalography (EEG), neuro-imaging techniques such as computed axial tomograpy (CT) and magentic resonance imaging (MRI). Simple blood tests, including haematological, liver and kidney function profiles can reveal treatable causes of epilepsy, such as parasitic infections. Neuropsychological evaluation identifies areas of function and dysfunction. Long term video monitoring can greatly improve the diagnosis of epilepsy. Therapeutic drug monitoring can ensure that patients are receiving optimal doses of medication and can help greatly in avoiding toxicity. However, the availability of investigative procedures varies greatly, from 82.4% for EEG, 70.5% for CT, 45% for therapeutic drug monitoring to only 20.6 % for MRI, 21.7% for long-term video monitoring and in LAMICs. Special investigations of brain function such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) are not available in most LAMIC centres.Epilepsy services in low and middle income countries are almost non-existent and service organization is a challenge. Epilepsy services should be community based and it is important to integrate these services into the primary health care structure to ensure sustainability. The Indian model is one such example, where epilepsy care has been incorporated into programmes for poverty alleviation [3]. Public-private partnerships and non-governmental organizations (NGO) are also important components of the Indian model. [4]The ultimate goal of all workers in the epilepsy field is to improve the quality of the life of people with epilepsy and their families. The prime manner in which this is aimed for is by the provision of good medical care.Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM, & Sander JW (2003). The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60 (9), 1544-5 PMID: 12743252Mbuba CK, Ngugi AK, Newton CR, & Carter JA (2008). The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49 (9), 1491-503 PMID: 18557778 Pal, D., Das, T., & Sengupta, S. (2000). ...

Mbuba CK, Ngugi AK, Newton CR, & Carter JA. (2008) The epilepsy treatment gap in developing countries: a systematic review of the magnitude, causes, and intervention strategies. Epilepsia, 49(9), 1491-503. PMID: 18557778

Pal, D., Das, T., & Sengupta, S. (2000) Case-control and qualitative study of attrition in a community epilepsy programme in rural India. Seizure, 9(2), 119-123. DOI: 10.1053/seiz.1999.0357

Mani KS, Rangan G, Srinivas HV, Srindharan VS, & Subbakrishna DK. (2001) Epilepsy control with phenobarbital or phenytoin in rural south India: the Yelandur study. Lancet, 357(9265), 1316-20. PMID: 11343735

Wang WZ, Wu JZ, Wang DS, Dai XY, Yang B, Wang TP, Yuan CL, Scott RA, Prilipko LL, de Boer HM.... (2003) The prevalence and treatment gap in epilepsy in China: an ILAE/IBE/WHO study. Neurology, 60(9), 1544-5. PMID: 12743252

Sugary Drinks May Increase Risk of Kidney Stones

2013-05-20T13:10:39Z

Staying hydrated is good advice for men who’ve had kidney stones before, but sugar-sweetened sodas and fruit punch may not be the best choice of fluids....

Ferraro, P., Taylor, E., Gambaro, G., & Curhan, G. (2013) Soda and Other Beverages and the Risk of Kidney Stones. Clinical Journal of the American Society of Nephrology. DOI: 10.2215/CJN.11661112

Epidemiology of Childhood Brain Disorders: ADHD and Autism

2013-05-20T11:55:27Z

The U.S. Centers for Disease Control has published a comprehensive summary of the epidemiology of childhood brain disorders in the most recent Morbidity and Mortality Weekly Report.This report produced some sensationalized headlines that up to 20% of children suffer from a mental disorder. However, I was more interested in looking at the prevalence estimates for some of the individual disorders from the report.The report collates data collected from a variety of surveys and data sets including the NHANES, NHIS and the National Survey of Children's Health (NSCH). These surveys typically use parental report to estimate prevalence ratesFor the purposes of this post, I will focus on two childhood brain disorders: attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).The key findings from the report in ADHD include:7.6% of parents reported their child between 3-17 years had received a diagnosis of ADHD in the NHIS8.9% of parents reported their child received a diagnosis of ADHD in the NSCH study9.6% to 12.3% of boys had received a diagnosis of ADHD3.8% to 5.4% of girls had received a diagnosis of ADHDA diagnosis of ADHD was more with older age, in children with health insurance and higher income groupsA diagnosis of ADHD was not related to parental education level The key findings from the report for autism and autism spectrum disorder include:.8% to 1.1% of parents reported their child between 3-17 years had received a diagnosis of autism1.8% of parents reported their child had received a diagnosis of ASDSurveys consisted noted a male predominance with boys having an estimated 3.5 to 4.5 times higher rate of autism and ASD diagnosisAgain having health insurance increased the rate of autism or ASD diagnosis by around two foldAutism and ASD prevalence rates were somewhat higher in the Northeast region of the U.S. and in white, non-Hispanic childrenIn contrast to ADHD, ASD rates were similar across parental income categoriesThe report notes in the discussion section: "Substantial but not insurmountable challenges to surveillance of mental disorders in children exists." They note current methods focus on parental reports and are biased by variability in access to health and mental health providers. The also note the imperfect diagnostic approach to childhood mental disorders and the need for more consistent diagnostic approaches.This report is a good comprehensive summary of what we know about these childhood brain disorders in the United States. Readers with more interest in this topic can access the free full text report in the citation below. In the next two posts, I will summarize key findings in the conduct disorder and affective disorder categories.Photo of clown fish from the Oklahoma Aquarium is from the author's files.Perou R, Bitsko RH, Blumberg SJ, Pastor P, Ghandour RM, Gfroerer JC, Hedden SL, Crosby AE, Visser SN, Schieve LA, Parks SE, Hall JE, Brody D, Simile CM, Thompson WW, Baio J, Avenevoli S, Kogan MD, Huang LN, & Division of Human Development and Disability, National Center on Birth Defects and Developmental Disabilities, CDC, Atlanta, Georgia (2013). Mental health surveillance among children - United States, 2005-2011. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002), 62 (2), 1-35 PMID: 23677130...

Perou R, Bitsko RH, Blumberg SJ, Pastor P, Ghandour RM, Gfroerer JC, Hedden SL, Crosby AE, Visser SN, Schieve LA.... (2013) Mental health surveillance among children - United States, 2005-2011. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002), 62(2), 1-35. PMID: 23677130

Autism, plasma cytokines and siblings

2013-05-20T03:59:00Z

I'm gonna try and be fairly brief in this post on the paper by Valerio Napolioni and colleagues* (open-access) looking at plasma cytokine profiles in cases of autism and their asymptomatic siblings. Brief because (a) the paper is open-access and (b) the participant groups (autism: n=25; sibling controls n=25) were relatively small so one has to be quite careful in extrapolating the findings with any large degree of confidence.Siblings by Paul Klee @ WikiPaintings Just in case you are new to cytokines, we are talking biological signalling and communication, and in particular, the language of inflammation both pro- and anti-inflammatory (see this post).With the autism spectrum conditions in mind, research into cytokines has filled quite a few peer-reviewed papers** from lots of different perspectives (see here and here for example). The main message so far is that it is complicated as per everything about autism and immune function.Despite the quite small participant group, the Napolioni paper does seem to be an important paper for a few reasons:They report no overall difference in cytokine profiles - measuring 40 cytokines - between cases of autism and their asymptomatic siblings. This despite the fact that autism symptoms and total IQ measures were different. That was the paper's headline.But.... "the cytokine/chemokine levels in our subjects did correlate with the quantitative clinical traits" or in other words, certain analysed parameters seemed to match with level of severity of autistic traits as measured by schedules such as VABS and SRS. "IL-1β appears to be the cytokine most involved in the quantitative traits".When looking at the children with autism according to various clinical subgroups - non-verbal, functional gastrointestinal (GI) issues, history of regression, history of allergies - a few correlations were noted. So, children who were non-verbal seemed to show higher levels of cytokines such as IL-10, one of the more anti-inflammatory cytokines. Children with accompanying GI issues seemed to show higher levels of more pro-inflammatory cytokines like IL-1β and IL-6 compared with those without GI problems. Reported regression as part and parcel of symptom onset also seemed to show some correlation with specific cytokines too.As the authors point out correlation does not imply causation. Such that just because they reported connections between cytokines and functioning and other factors does not necessarily mean that these observations are causative of autism (or anything else). That being said, as I hinted before, this is not the first time that cytokines and their connection to immune function have been discussed in the autism research literature (see yet another example of this here***); many correlations in similar directions makes for some interesting discussions at least.That headline that children with autism and their siblings did not significantly differ in their cytokine profile carries a few possibilities for interpretation. The authors suggest that this could be evidence of "an ‘autism endophenotype’ that expands immune dysfunction to family members who are seemingly unaffected by the core symptoms of autism". One might also say the same thing about the Gondalia paper**** on gut bacteria in cases of autism and siblings (see here).Assuming that the broader autism phenotype (BAP) does not come into play here, one might speculate that (a) cytokine profiles are not related to the presence of autism, or (b) that the manifestation of autism, some autism, is representative of cytokine involvement but in addition to other factors in terms of the affected sibling - "when an environmental stress (for example, prenatal exposure to environmental toxins, viral and bacterial infections, parental microchimerism, etc.) occurs during development". This last point takes me back to that 1971 John Money study on the appearance of familial autoimmune related conditions 'round about' the presence of autism and a similar correlation. Part of a predisposition to autism?I note from Figure 4 of the paper, that when it came to summarising the various associations across the groups (and sub-groups), quite a few of the very significant differences seemed to be due to differences in IQ, which was tested using the Stanford-Binet Intelligence Scales (fifth edition). Aside from previous messages of caution on the use of this measure in autism research*****, one has to wonder whether this might be a more pertinent variable when it comes to cytokines and autism. I don't know enough about cytokine profiles in intellectual disability in children for example, to make any novel claims about this, but certainly intellectual development has been mentioned in the research literature with certain cytokines in mind******.OK I said I would try and be brief with this post and have failed miserably. The Napolioni paper has though been worth it though for the potential insights that it might provide into the complex world of cytokines and immune function in relation to the presentation of autism.To close, and following yet more 'we'll win it next year' commentary with regards to the UK entry in the event that is the Eurovision Song Content, might I suggest a group for your serious consideration as a contender next year?-----------* Napolioni V. et al. Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder. Journal of Neuroinflammation 2013; 10: 38.** Goines PE. & Ashwood P. Cytokine dysregulation in autism spectrum disorders (ASD): Possible role of the environment. Neurotoxicol Teratol. 2013; 36: 67-81.*** Ricci S. et al. Altered cytokine and BDNF levels in autism spectrum disorder. Neurotox Res. April 2013.**** Gondalia SV. et al. Molecular characterisation of gastrointestinal microbiota of children with autism (with and without gastrointestinal dysfunction) and their neurotypical siblings. Autism Research. 2012; 5: 419-427.***** Coolican J. et al. Brief report: data on the Stanford-Binet Intelligence Scales (5th ed.) in children with autism spectrum disorder. J Autism Dev Disord. 2008; 38: 190-197.****** von Ehrenstein OS. et al. Child intellectual development in relation to cytokine levels in umbilical cord blood. Am J Epidemiol. 2012; 175: 1191-1199. ----------...

Napolioni V, Ober-Reynolds B, Szelinger S, Corneveaux JJ, Pawlowski T, Ober-Reynolds S, Kirwan J, Persico AM, Melmed RD, Craig DW.... (2013) Plasma cytokine profiling in sibling pairs discordant for autism spectrum disorder. Journal of neuroinflammation, 38. PMID: 23497090

Do Hyaluronic Acid Injections Reduce Biomarkers of Collagen Degradation?

2013-05-20T00:04:00Z

Take Home Message: Hyaluronic acid injections decrease factors related to collagen degradation. Some blood tests may differentiate responders and nonresponders to these injections. Knee osteoarthritis, one of the leading causes of disability, has no cure and current treatments commonly involve medications to decrease inflammation and pain. Hyaluronic acid (HA) injections have become a popular form of treatment for knee osteoarthritis. However, the mechanism of action has yet to be determined. Therefore, the authors examined serum biomarkers of collagen breakdown (Coll2-1 and Coll2-1 NO2) in 45 patients with various stages of knee osteoarthritis before (-15 days), at the time of injection, and following treatment (30 and 90 days) with HA injections....

Henrotin Y, Chevalier X, Deberg M, Balblanc JC, Richette P, Mulleman D, Maillet B, Rannou F, Piroth C, Mathieu P.... (2013) Early decrease of serum biomarkers of type II collagen degradation (Coll2-1) and joint inflammation (Coll2-1 NO2 ) by hyaluronic acid intra-articular injections in patients with knee osteoarthritis: A research study part of the Biovisco study. Journal of Orthopaedic Research, 31(6), 901-7. PMID: 23423846

Blood magic: old blood ages the young

2013-05-19T23:52:07Z

“Our ancient countess was refused her desires will To bathe in pure fresh blood She’d peasant virgins killed Elizabeth, in the chasm where was my soul Forever young, Elizabeth Bathorii in the castle of your death You’re still alive, Elizabeth” -“Elizabeth”, Ghost As folklore has it, Elizabeth Bathorii, Countess of Hungary, often bathed in […]...

Villeda SA, Luo J, Mosher KI, Zou B, Britschgi M, Bieri G, Stan TM, Fainberg N, Ding Z, Eggel A.... (2011) The ageing systemic milieu negatively regulates neurogenesis and cognitive function. Nature, 477(7362), 90-4. PMID: 21886162

Loffredo FS, Steinhauser ML, Jay SM, Gannon J, Pancoast JR, Yalamanchi P, Sinha M, Dall'osso C, Khong D, Shadrach JL.... (2013) Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell, 153(4), 828-39. PMID: 23663781

Zhang G, Li J, Purkayastha S, Tang Y, Zhang H, Yin Y, Li B, Liu G, & Cai D. (2013) Hypothalamic programming of systemic ageing involving IKK-β, NF-κB and GnRH. Nature, 497(7448), 211-6. PMID: 23636330

‘Is ‘cloning’ mad, bad and dangerous?’ – an argument revisited

2013-05-18T14:10:15Z

Is 'cloning' appropriate terminology for somatic cell nuclear transfer derivation of human embryonic stem cells?...

Tachibana, M., Amato, P., Sparman, M., Gutierrez, N., Tippner-Hedges, R., Ma, H., Kang, E., Fulati, A., Lee, H., Sritanaudomchai, H.... (2013) Human Embryonic Stem Cells Derived by Somatic Cell Nuclear Transfer. Cell. DOI: 10.1016/j.cell.2013.05.006

Why Psychology 101 Should Be Evolutionary Psychology

2013-05-18T11:40:39Z

In two recent posts, I have referenced a relatively-average psychologist (again, this psychologist need not bear any resemblance to any particular person, living or dead). I found this relatively-average psychologist to be severely handicapped in their ability to think about … Continue reading →...

Smallegange, R., van Gemert, G., van de Vegte-Bolmer, M., Gezan, S., Takken, W., Sauerwein, R., & Logan, J. (2013) Malaria Infected Mosquitoes Express Enhanced Attraction to Human Odor. PLoS ONE, 8(5). DOI: 10.1371/journal.pone.0063602

Darth DSM-5 and autism

2013-05-18T05:33:00Z

Blue Harvest @ Wikipedia @ Family GuyI need to create a suitable atmosphere for this post, so try this music for size and think Blue Harvest...Right. The wait is over. The discussions / arguments / objections / agreements are all confined to history. Drum roll, spotlight centre-stage... enter DSM-5 and into unknown territory we all go, particularly with autism, sorry.. autism spectrum disorders (ASDs) in mind.As you can see from the link above to the new diagnostic guidelines from the American Psychiatric Association (APA) the diagnosis of autism has, as was widely anticipated, changed somewhat to encompass quite a few adaptations (see this previous post).I'm not saying too much more on this at the present time, bearing in mind 'spectrum' is a word which seems to get more of a mention in this revision of the DSM; and not just with autism in mind (see here and here*).Obviously things aren't going to just change overnight with DSM-5 as it is eventally rolled out. Clinicians will need to learn some new diagnostic brushstrokes. Remember too that DSM is only one part of the diagnostic manuals currently in use (although even ICD is subject to revision in coming years already mentioning something called Social Reciprocity Disorder?). That being said, the implications of DSM-5 on issues like the autism numbers game - same as what happened across previous versions - are probably going to be subject to some pretty intense scrutiny over the coming years.Don't also be under any disillusion that the new changes are going to herald any giant leaps forward in autism research anytime soon. Interestingly, Dr Tom Insel, head of the US National Institute of Mental Health (NIMH) was recently quoted as saying that "NIMH will be re-orienting its research away from DSM categories", reported also by other authors** (open-access). In other words, even with the fresh smell of new DSM in the air, a new 'nosology' is already planned.To close, Peter 'Han Solo' Griffin on TIE fighters... dan-dan-da-dan, da-da-dan-dan-dan...---------* Adam D. Mental health: on the spectrum. Nature. 2013; 496: 416-418.** Lai M-C. et al. Subgrouping the autism “spectrum": reflections on DSM-5. PLoS Biol. 2013; 11: e1001544.----------Lai M-C, Lombardo MV, Chakrabarti B, & Baron-Cohen S (2013). Subgrouping the Autism “Spectrum": Reflections on DSM-5 PLoS Biology...

Lai M-C, Lombardo MV, Chakrabarti B, & Baron-Cohen S. (2013) Subgrouping the Autism “Spectrum": Reflections on DSM-5. PLoS Biology. info:/