Mental health

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Drunk Rats Could Overturn Neurological Orthodoxy

Published by Anonymous (not verified) on Tue, 15/01/2013 - 9:41am in

A form of brain abnormality long regarded as permanent is, in fact, sometimes reversible, according to an unassuming little paper with big implications.

Here's the key data: some rats were given a lot of alcohol for four days (the "binge"), and then allowed to sober up for a week. Before, during and after their rodent Spring Break, they had brain scans. And these revealed something remarkable - the size of the rats' lateral ventricles increased during the binge, but later returned to normal.

Control rats, given lots of sugar instead of alcohol, did not show these changes.

This is really pretty surprising. The ventricles are simply fluid-filled holes in the brain. Increased ventricular size is generally regarded as a sign that the brain is shrinking - less brain, bigger holes - and if the brain is shrinking that must be because cells are dying or at least getting smaller. So bigger ventricles is bad.

Or so we thought... but this study shows that it might not always be true: alcohol reversibly increases ventricular volume over a timescale of days. It does so, the authors say, essentially by drying brain tissue out; like most things, if you dry the brain out, it gets smaller (and the ventricles get bigger) but when the water comes back to the tissues, it expands again.

As you can see here in Figure 2...

Maybe. I admit that just eyeballing this, it looks more like the ventricles are getting brighter, rather than bigger, but I'm not familiar with the details of water scanning. Maybe some readers will know more about it.

If it's true, this is big - maybe it's not just high doses of alcohol that does this. Maybe other drugs or factors can shrink or expand, the ventricles, or even other areas, purely by acting on tissue water regulation, rather than by anything more 'interesting'.

Take the various claims that some psychiatric drugs boost brain volume while others decrease it, just for starters...could they be headed for a watery grave?

Of course, this is in mice - and it might not translate to humans... we need to find out, and I for one am keen to apply for a grant. Here's my draft:

Participants: 8 healthy-livered neuroscientists.
Materials: 1 MRI scanner, 1 crate Jack Daniels.
Methods: Subjects will confer to pick a Designated Operator, who will remain sober. If no volunteers for this role are forthcoming, selection will be randomized by Bottle Spinning. All other participants will consume Jack Daniels ad libitum, and take turns being scanned. Once all Jack Daniels is depleted, participants will continue to be scanned until fully sobered up (defined as when they can successfully spell "amygdalohippocampal").
Instructions to Participants: i) what happens in the magnet, stays in the magnet. ii) If you 'dirty' the scanner, you clean it up. iii) Bottle caps are not MRI safe!

Er... seriously though, someone should check.

ResearchBlogging.orgZahr NM, Mayer D, Rohlfing T, Orduna J, Luong R, Sullivan EV, and Pfefferbaum A (2013). A mechanism of rapidly reversible cerebral ventricular enlargement independent of tissue atrophy. Neuropsychopharmacology  PMID: 23306181

DSM-5: A Ruse By Any Other Name...

Published by Anonymous (not verified) on Sun, 13/01/2013 - 8:45pm in

In psychiatry, "a rose is a rose is a rose" as Gertrude Stein put it. That's according to an editorial in the American Journal of Psychiatry called: The Initial Field Trials of DSM-5: New Blooms and Old Thorns.

Like the authors, I was searching for some petal-based puns to start this piece off, but then I found this "flower with an uncanny resemblance to a MONKEY" which I think does the job quite nicely:
Anyway, the editorial is about the upcoming, controversial fifth revision to the Diagnostic and Statistical Manual (DSM) of the American Psychiatric Association (APA).

A great deal has been written about the DSM-5 over the past few years, as "the rough beast, its hour come round at last / Slouches towards Bethlehem to be born" (see, I can reference early-20th-century poetry too).

But now the talk has moved into a new phase, because the results of the DSM-5 'field trials' are finally out. In these studies, the reliability of the new diagnostic criteria for different psychiatric disorders was measured. The new editorial is a summary and discussion of the field trial data.

Two different psychiatrists assessed each patient, and the agreement between their diagnoses was calculated, as the kappa statistic, where 0 indicates no correlation at all and 1 is perfect.

It turns out that the reliabilities of most DSM-5 disorders were not very good. The majority were around 0.5, which is at best mediocre. These included such pillars of psychiatric diagnosis like schizophrenia, bipolar disorder, and alcoholism.

Others were worse. Depression, had a frankly crap kappa of 0.28, and the new 'Mixed Anxiety-Depressive Disorder' came in at -0.004 (sic). It was completely meaningless.

The American Journal editorial was written by a group of senior DSM-5 team members. I'm sure they wanted to write a triumphant presentation of their work, but in fact the tone is subdued, even apologetic in places:

As for most new endeavours, the end results are mixed, with both positive and disappointing findings...Experienced clinicians have severe reservations about the proposed research diagnostic scheme for personality disorder...like its predecessors, DSM-5 does not accomplish all that it intended, but it marks continued progress for many patients for whom the benefits of diagnoses and treatment were previously unrealized.

Remember: this is the journal published by the organization responsible for the DSM and even they don't much like it.

But the real story is even worse. The previous editions of the DSM also conducted field trials. These trials had a system to describe different kappa values: for example, 0.6-0.8 was 'satisfactory'.

However, the new DSM-5 studies used a different, lower threshold. They simply moved the goalposts, deeming lower kappa values to be good. At one point, they wrote that values of above 0.8 would be 'miraculous' and above 0.6 a 'cause for celebration', yet this wasn't the view of previous DSM developers.

The indispensable 1boringoldman blog has a nice graphic showing the results of the DSM-5 trials, with the kappas graded according to the old vs. the new criteria. As you can see, the grass is greener on the new side.
The fact is that the DSM-5 field trial results are worse than the results from DSM-III, the 1980 version that's served mostly unchanged for 30 years (DSM-IV made fairly modest changes.) The reliabilities have got worse - despite the editorial's claims of 'continued progress'. It's true that the DSM-5 field trials were a lot bigger and conducted rather differently, but still, it's a serious warning sign.

Finally, there was great variability in the results between different hospitals - in other words the reliability scores were not, themselves, reliable. Some institutions achieved much higher kappa values than others, but it's anyone's guess how they managed to do so.

Still, there's great news: the DSM-5 is just a piece of paper (well, a big stack of them). Any psychiatrist is free to ignore it - as the creator of the more reliable DSM-IV (not III, oops) is now urging them to do.

ResearchBlogging.orgFreedman R, Lewis DA, Michels R, Pine DS, Schultz SK, Tamminga CA, Gabbard GO, Gau SS, Javitt DC, Oquendo MA, Shrout PE, Vieta E, and Yager J (2013). The Initial Field Trials of DSM-5: New Blooms and Old Thorns. The American Journal of Psychiatry, 170 (1), 1-5 PMID: 23288382

Smart People Say They're Less Depressed

Published by Anonymous (not verified) on Sat, 12/01/2013 - 8:26pm in

The questionable validity of self-report measures in psychiatry has been the topic of a few recent  posts here at Neuroskeptic.


Now an interesting new study looks at the question in issue from a new angle, asking: what kind of people report feeling more or less depressed? Korean researchers Kim and colleagues found that intelligence and personality variables were both linked to the tendency to self-rate depression more severely.

The study involved 100 patients who'd previously suffered from an episode of depression or mania and who, according to their psychiatrist, had now recovered and were back to normal. Kim et al looked to see what the patient thought about their mood, by getting them to complete the Beck Depression Inventory (BDI) self-report questionnaire.

This was compared to the clinican-administered HAMD scale (another Neuroskeptic favourite) which is meant to be independent of self report.

It turns out that the BDI and HAMD scores were only weakly correlated - with a coefficient of just r=0.32. That's really not very good considering that, in theory, they both measure the same thing: 'depression'. Many people reported being considerably depressed when their clinicians rated them as fine.

But more interestingly, certain characteristics of the patients were correlated with their self-report/clinician-rating discrepancy. Specifically, patients with a lower IQ, who were more impulsive, and less conscientious, tended to self-report more severe depression.

Now, the uncharitable interpretation of these people is that they were just too sloppy to complete the form properly... the uncharitable interpretation of the psychiatrists is that it's their fault for underestimating depression in people less inclined to express themselves in 'the right way'. There's no way to know.

Either way, it's a serious problem because it shows that self-report and observer-report measures of depression aren't just poorly correlated, they're actually measuring different things for different people.

It could be even worse than it appears because the HAMD, although supposedly not a self-report measure, does in fact heavily rely on the patient's cooperation. So a 100% clinician-rated scale might be even further removed from self-report.

ResearchBlogging.orgKim EY, Hwang SS, Lee NY, Kim SH, Lee HJ, Kim YS, and Ahn YM (2012). Intelligence, temperament, and personality are related to over- or under-reporting of affective symptoms by patients with euthymic mood disorder. Journal of affective disorders PMID: 23270973

Artwork During Recovery From Encephalitis

Published by Anonymous (not verified) on Sun, 06/01/2013 - 9:37pm in

I recently wrote about anti-NMDA receptor encephalitis, a neurological disorder that often manifests with psychiatric symptoms, such as depression and hallucinations.

The latest American Journal of Psychiatry features a strange series of four drawings made by a 15 year old girl during an episode of the disease, which presented as psychotic symptoms but later progressed to severe insomnia and epilepsy before it was diagnosed and treated.


"As she gradually recovered we asked her to draw something. She did not know what to draw, so we suggested an animal, such as a dog, but she did not know how to start.

When we told her that a dog has four legs, a tail, two ears, two eyes, and a mouth, she drew an abstract figure that consisted of a head with four legs (A). Her next drawing, of a cat, looked exactly the same, apparently since they share the same basic features.

Two weeks later the dog now looked more recognizable but like a human, standing upright, with two arms and four legs...All body parts were listed beneath the figure in the same color as they were drawn (B).

Two months after the patient was transferred to a local rehabilitation center, the cat was catlike for the first time; it had four legs, was normally proportioned, and was correctly positioned. Colors were used adequately. However, this drawing still looked like one by a primary school child instead of a 15- year-old girl (C).

Finally, after 5 months of rehabilitation her drawing had a normal composition. She still had the urge to write down what she drew, she did not encircle the figures anymore (D)."

ResearchBlogging.orgEsseveld MM, van de Riet EH, Cuypers L, and Schieveld JN (2013). Drawings During Neuropsychiatric Recovery From Anti-NMDA Receptor Encephalitis. The American journal of psychiatry, 170 (1), 21-2 PMID: 23288386

Finally, Hard Evidence Against The "Autism Epidemic"?

Published by Anonymous (not verified) on Sun, 30/12/2012 - 11:56pm in

The idea of an 'autism epidemic' has a lot of people very worried.


No-one disputes that diagnosed rates of autism have increased enormously over the past 15 years or so, around the world. However, other people write it off as essentially a cultural phenomenon: we're getting better at detecting the disorder and more willing to label kids as having it.

I subscribe to the latter view, but there's very little hard evidence for it. To prove that diagnostic changes have occurred, rather than a true increase in autism, you'd have to know what would have happened to today's kids, say, 20 years ago. Would they have been diagnosed? We have no way of knowing. At least not until someone invents a time machine.

However, a new study just out offers a valuable new perspective on the debate: Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence.

According to authors Soumya Mazumdar and colleagues, there's a zone of high autism prevalence in California, areas where kids aged 0-4 years old are more likely to be diagnosed with the condition. The epicentre is L.A.; there's actually three overlapping hotspots centred on Santa Monica, Alhambra and North Hollywood.

In these clusters, autism rates are between 2 and 6 times higher than the rest of the state.

Now an interesting thing about these areas was that they're rich in paediatricians, autism advocacy organizations, and money. In other words, there's better access to health services and probably more awareness of autism. This is suggestive evidence that the reason lots of kids get diagnosed here is about diagnosis, not autism per se.

But the blockbuster result is that children born outside the cluster, who later moved home into one, had a higher chance of getting a diagnosis than those who stayed out. The effect was smaller than for kids born inside the hot zone, but it was significant.

That's also consistent with the idea that the clusters are clusters of diagnosis, not autism.

It's not proof. You could argue that there's some toxic chemical, say, present in the rich parts of L.A. that causes autism, even if you move into the toxic area only at age 3 or 4, and that's been getting worse recently, leading to rising rates.

But it seems a stretch. What's the chemical? And why hypothesize one, when the diagnostic services hypothesis nicely accounts for these findings? As the authors say:

The findings reported in this article do not fully reject the possibility that environmental toxicants drive some of the risk of autism ... since there are a plethora of possible toxicants, it is impossible to falsify all hypotheses that researchers have started to explore.

 ResearchBlogging.orgMazumdar S, Winter A, Liu KY, and Bearman P (2012). Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence. Social Science And Medicine PMID: 23267775

Mental Illness and Crime, Yet Again

Published by Anonymous (not verified) on Sat, 29/12/2012 - 9:32pm in

As if on cue, a major study about the relationship (if any) between mental disorder and crime has appeared just when everyone's talking about that.


Although having said that, people seem to be interested in that issue most of the time nowadays, in the UK at any rate, with schizophrenia topping the list of supposedly scary syndromes.

So - should we be worried?

The new research, from Australian team Morgan et al, surveyed everyone born in the state of Western Australia between 1955 and 1969. About 1.6 million people lived there over the course of the study so this was a big project.

By linking local records of arrests over the period 1985 to 1996 to the database of psychiatric diagnosis, the researchers were able to examine disorder-crime correlations in the entire population - meaning that there was no possibility of bias.

So what happened? Here's some highlights:

  • 32% of psychiatric patients had been arrested at least once. Unfortunately, it's not clear what the rate was in the general population, but that falls into the range of overall arrest rates in most countries.
  • 11% of those arrested had a psychiatric diagnosis. This rose to 20% of arrests for violent offences.
  • 0.8% of suspects had schizophrenia, rising to 1.7% for violent offences.
  • The number of arrests in people without a disorder fell over the period 1985-1996, reflecting the well-known fact that people commit fewer crimes as they get older. However, in psychiatric patients, there was no change over time.
  • For murder, 30% of suspects had a psychiatric history while 3% had a diagnosis of schizophrenia.
  • Both substance abuse and personality disorders were associated with higher arrest rates than schizophrenia, but schizophrenia in turn was higher than depression, anxiety, and other miscellaneous disorders.
  • Although only 1.7% of violent offenders had schizophrenia, those with the disorder were somewhat more likely to involve strangers, and to take place in public places, and less likely to target family and partners.

Overall this confirms that the great majority of crimes, including violent ones, are not committed by people with mental illness, and that your chance of getting 'murdered by a lunatic' is incredibly low. This strikes me as the only statistic that matters to most people.

There's a long-standing debate over whether people with various disorders are more likely to commit crimes than they would be if they didn't have one, the relative risk. While interesting, this is a purely academic question. What the rest of us need to know is the absolute risk, and this is low.

ResearchBlogging.orgMorgan VA, Morgan F, Valuri G, Ferrante A, Castle D, and Jablensky A (2012). A whole-of-population study of the prevalence and patterns of criminal offending in people with schizophrenia and other mental illness. Psychological medicine, 1-12 PMID: 23234722

Religion Rises After Disaster Strikes

Published by Anonymous (not verified) on Thu, 27/12/2012 - 12:37am in


People turn to religion after natural disasters - but it doesn't actually provide much solace.

So say researchers Sibley and Bulbulia, who examined the population of Christchurch, New Zealand, before and after the 2011 earthquake. 185 died and many city landmarks were damaged in the disaster.

The paper, Faith after an Earthquake, opens with a Biblical quote.

Sibley and Bulbulia took advantage of the fact that a longitudinal study of the 'health and values' of the New Zealanders was already underway when the quake struck, and the survey included questionnaires about religious beliefs.

They found that, compared to before the event, residents of the affected Canterbury region were more likely to report becoming religious (8.6%) than of losing their faith (5.3%); in the rest of the country religion declined from 2009 to 2011, so the earthquake-hit area was exceptional.
The authors say:

Philosophers have plausibly argued that natural disasters such as the Christchurch earthquake are rationally incompatible with the existence of an all-powerful, all-loving God, because natural disasters cause pointless suffering to innocents... though faith eroded elsewhere in New Zealand, there was a significant upturn in religious faith among those who experienced the misery of New Zealand's most lethal natural disaster in eighty years.

But did faith help people cope with the disaster?

No - believers reported no better subjective well-being compared to the non-religious, either before or after the earthquake, although those who both lost their faith (apostates) during the period and were personally affected suffered a decline.

What's rather odd about this, however, is that other results showed that apart from the apostates, well-being wasn't affected by the earthquake at all. So it's no surprise that the religious coped no better: the irreligious already coped very well, so there was no room for improvement.

ResearchBlogging.orgSibley, C., and Bulbulia, J. (2012).Faith after an Earthquake: A Longitudinal Study of Religion and Perceived Health before and after the 2011 Christchurch New Zealand Earthquake PLoS ONE, 7 (12) DOI: 10.1371/journal.pone.0049648

When "Mental" Illness Isn't

Published by Anonymous (not verified) on Sat, 22/12/2012 - 10:08pm in

 There's a theory that 'psychiatric diseases' like depression and schizophrenia aren't diseases because they're not diagnosed on the basis of any kind of biological abnormality, but purely on symptoms - unlike 'real' diseases like cancer and AIDS.

Now, in my view there's quite a bit of truth in that - but there's also a serious flaw in the argument. Sometimes, disorders diagnosed on the basis of psychiatric symptoms do turn out to have had a clear biological cause. So the original diagnosis of a psychiatric disease was correct: there was indeed a disease.

This is happening more and more often now because of biomedical advances.

A group of German neurologists and psychiatrists recently wrote about a case of a man diagnosed with bipolar disorder:

In February 2009, a 28-year-old presented to our clinic with a first episode of depression. He reported depressed mood, anhedonia, decreased drive, reduced alertness and concentration. The symptoms responded well to quetiapine 100 mg.

Fourteen months later, a first manic episode with logorrhea [excessive speech], aggressive and disinhibited behavior occurred... it completely remitted after treatment with quetiapine 1000mg. A diagnosis of bipolar I disorder was made.

Two months later, the patient presented with another depressive episode... Despite treatment with quetiapine, aripiprazole, lithium, valproate and escitalopram, the patient did not improve...

So far, seems like a fairly typical case of bipolar. However, it turned out that...

Neurological examination was remarkable for extrapyramidal symptoms with left-sided rigor and bradykinesia [slowed movements]. On initial and concurrent magnetic resonance imaging (MRI), numerous subcortical lesions in the frontal lobes were detected... Screening for autoimmune antibodies detected NMDAR antibodies.

It turned out the guy had autoimmune encephalitis: his body was generating antibodies that blocked the brain's key NMDA receptors; the drug ketamine does that too. Treatment with immunosuppressant drugs was started and he recovered fairly quickly. For a first-hand account of the disease, in which it was also diagnosed as a psychiatric disorder initially, see the recent book Brain On Fire.

Now, let's imagine that this had happened in 1960. What would the guy's story have been then?

He'd have been seen by a psychiatrist and diagnosed with bipolar, just as he was today. Depending on how severe the depression was, and whether or not he had any more episodes, he might well have ended up in a psychiatric hospital.

But he probably wouldn't have been diagnosed with a neurological disorder. He'd have tested negative for all the neurological diseases known at the time. No-one tested for NMDA antibodies back then, because NMDA receptors weren't even discovered until 1981.

It's true that his neurological exam showed a movement disorder (left-sided rigor and bradykinesia)  but this might well have been written off as a side effect of the high dose antipsychotics he was taking, which cause similar movement disorders.

50 years ago this guy, and many others like him, could well have ended up committed to an asylum. 100 years ago, I think it would have been almost certain he'd have been deemed 'insane' and locked up at some point.

If so, some of the people in psychiatric hospitals 50 or 100 years ago will have had this disease - or others. And if we didn't know about anti-NMDA encephalitis until recently, who's to say what we'll discover next?

ResearchBlogging.orgChoe CU, Karamatskos E, Schattling B, Leypoldt F, Liuzzi G, Gerloff C, Friese MA, and Mulert C (2012). A clinical and neurobiological case of IgM NMDA receptor antibody associated encephalitis mimicking bipolar disorder. Psychiatry research PMID: 23246244

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