Monday, January 30, 2017

Meyerian history and examination in psychiatry

I mentioned the article about One hundred years of psychiatry at Johns Hopkins in my previous post. The article focuses on how Adolf Meyer developed an organised approach for history taking and mental state examination in psychiatry, which became standard in the US. It was taken over by the Maudsley Hospital in the UK, again becoming standard (see previous post and my review of most recent edition of The Maudsley handbook of practical psychiatry). However, as the article points out, the "meyerian history and examination ... is little used in the United States today as it is often judged to be too time-consuming".

The clinican comes to a formulation at the end of the history and examination, of which a differential psychiatric diagnosis is merely one element. Some may see formulation as more opposed to psychiatric diagnosis (see previous post), but formulation should, as the article says, summarise "the story focusing on the salience of the problems and context - how has the problem developed, interrupted, and/or distorted the patient's life trajectory".

The article discusses why psychiatry does not focus on the meyerian history and examination in a comprehensive and systematic way, and is, therefore, not as patient-centred as it should be (see previous post). One reason is that too many influential psychiatrists are research-based, rather than being involved in routine clinical care settings. Today's medicine doesn't teach a broad enough basis "for knowing our patients and partnering with them in patient care". Meyer made these methods explicit. This is a "truly personalized medicine, distinct from the ongoing extension of the disease model at a molecular level, which is commonly referred to as individualised or precision medicine" (see eg. previous posts The gap between neural circuits and understanding people and Psychiatric research folly).

Critiquing the neuro-turn

Roger Cooter has an article on why the neuro-turn in popular and academic culture needs to be taken seriously. I tend to regard it as 'neo-phrenological phantasy' (eg. see  previous post), but Roger cautions against being "so lightly dismissive". The neuro-turn may be affecting how we view ourselves. Furthermore, it seems to be beyond criticism, or, as Roger puts it, "the neuro-turn stymies ... its own critique".

As an example, another recent paper I have read is about One hundred years of psychiatry at Johns Hopkins. Whilst discussing the heritage of Adolf Meyer and Paul McHugh for current american psychiatry, it suggests that, "One happy byproduct of current research is that ... the competitive jousting between the 'biological' and psychological' ...[has] dissipated". It goes on:-
It has proven difficult to maintain such debates when research now shows the human brain responding robustly to all manner of psychological, pharmacological, and stimulatory interventions.
So, I've been wasting my time trying to encourage this debate! Studies that literally 'light up the brain' have shut down the argument.

Roger describes the attractions of an ahistorical, posthumanist worldview, which may help to mediate neoliberal politics. At least he concludes that critique is even more "vital and urgent". So, maybe I need to keep going.

Monday, January 16, 2017

Is schizophrenia associated with brain volume changes independently of medication?

Further to my previous post, I have been looking at the 2010 study by Jo Moncrieff & Jonathan Leo on the effects of antipsychotic drugs on brain volume. I had not looked at this study before my previous post and perhaps I was being unfair concluding there needed to be more systematic review of brain scan studies of patients with psychosis or schizophrenia prior to them receiving antipsychotic drugs, because Jo and Jonathan have already done it. In her book, The Bitterest Pills, Jo mentioned this joint paper, which was published by Robin Murray, as editor of Psychological Medicine, "despite opposition from most of the five referees" (p.157).

The authors managed to find 21 "drug-naive" studies published between 1995 and April 2009 of patients who had had no more than 4 weeks of antipsychotic treatment. They conclude:-
Most studies of drug-naive patients examined here did not report or detect differences in total brain volume, global grey-matter volume or CSF volumes between patients and controls, including three studies of untreated patients with long-term illness. These results are particularly remarkable, given the difficulty of selecting a comparable control group in these studies. The results suggest that the brain changes found in some first-episode studies may also be attributable to drug treatment, especially because some studies suggest that structural changes may occur after only short periods of treatment.
They reinforced this conclusion in response to correspondence:-
As we showed in our systematic review, a large majority of studies with drug-naive patients with psychosis or schizophrenia have not found any differences in global brain or grey-matter volumes, or in total CSF or ventricular volumes between patients and controls (Moncrieff & Leo, 2010). Although some of these studies reported differences in the volumes of specific structures, such as the thalamus and the caudate nuclei, others found no differences and multiple testing suggests some of the results may be false positives.
I'm left wondering exactly what the evidence is for Robin Murray's view, mentioned in my previous post, that "subtle brain changes [are] present at onset of schizophrenia".

Modern resurgence of biomedical psychiatry may be totally based on an artefact

As Robin Murray mentioned in his article discussed in a previous post, a 1976 paper by Eve Johnstone, Tim Crow et al showing cerebral ventricular enlargement in chronic schizophrenia "kickstarted the huge and ongoing endeavour of neuroimaging in psychosis". This finding was seen as validating the "view that schizophrenia was a neurodegenerative disorder".

As I've mentioned before (see previous post), it was this paper that also produced the remarkable change in the position of E. Fuller Torrey from being Szaszian to a biomedical advocate of forced psychiatric treatment. From his point of view, psychiatry stopped "groping in the dark" from this 1976 point in time (see my book extract). This meant he no longer doubted that schizophrenia is a brain disease.

However, the general acceptance over recent years that antipsychotic medication can reduce brain volume (eg. see previous post) has led to a rethink, exemplified by Robin Murray's article. The cerebral atrophy demonstrated by Johnstone et al (1976) was almost certainly due to antipsychotic medication, at least mainly, and was not an indication that schizophrenia is a brain disease. Johnstone et al were wanting to make out that schizophrenia led to a dementing illness, as they found a significant association of increased ventricular size with measures of cognitive impairment. But any cognitive impairment in schizophrenia is functional not organic, so the whole basis of the paper was flawed. And, its misinterpretation has misled a whole generation of psychiatric researchers.

I've always argued that any difference in ventricular volume may be non-specific rather than due to schizophrenia (see my article). As with any statistical association, a causal connection is not necessarily implied. The brain is a dynamic, not static, organ and ventricular enlargement can change over time affected by confounding variables, such as nutrition and hydration. In fact, ventricular enlargement can also be found in other psychiatric conditions, such as bipolar disorder.

Furthermore, like Robin Murray, maybe I have underestimated the effects of antipsychotic medication. As I said in my book review of The Bitterest Pills, Jo Moncrieff "makes a stronger case than even I was aware of for ventricular enlargement in schizophrenia being a drug-induced phenomenon". Robin, even though he accepts that "high-dose antipsychotics contribute ... to the subsequent 'progressive' changes", still believes there are "subtle brain changes present at onset of schizophrenia". But Jo shows (p. 158) that the interpretation of the results of studies of antipsychotic-naive patients are not clear cut, with inconsistency about the area of the brain identified. Some studies have not reported any difference in global brain volumes in patients prior to them receiving antipsychotic drugs, even though they may have been unwell for many years.

There does, at least, seem to be a need for a proper review of studies of brain scans of patients with psychosis or schizophrenia prior to them receiving antipsychotic drugs. If the Johnstone et al (1976) study is really the reason for the modern resurgence of biomedical psychiatry, its conclusion that cerebral ventricles are enlarged in schizophrenia may be totally based on an artefact.

Monday, January 09, 2017

Constructing a psychiatric future

I'm not sure if Nassir Ghaemi's letter to a medical student about choosing psychiatry as a speciality (see Medscape article) is another acknowledgement of mistakes in his career, like that of Robin Murray (see previous post). He says that DSM is "inherently unscientific" and psychiatric diagnoses are social constructions. From his point of view, psychiatry has pretended diagnoses are scientific facts. As he says, "This has been proven a lie, but we are unwilling to admit our self-deception". He seems to be saying it took him two decades to realise this.

I have several times mentioned the spat I had with Ghaemi when I reviewed one of his books (eg. see previous post). As I said in my review, he was one of the psychiatrists at the forefront of promoting bipolar depression, which I guess he now realises he helped to construct.

Actually, I don't think he needs to be quite so disillusioned about the prospects for psychiatry. It just needs to accept its inherent uncertainty (eg. see previous post).

Sunday, January 01, 2017

Rethinking antipsychotic medication

In a comment on my previous post about his article, Robin Murray has highlighted what he calls critical psychiatry's "scepticism about the unthinking advocacy of prophylactic antipsychotics". I think he has in mind a BJPsych article, which discuses the lack of evidence for long-term effectiveness of antipsychotic medication and expresses concern about antipsychotics causing a decrease in cortical volume and dopamine receptor supersensitivity, besides having side effects on physical health. I suspect this article was written in response to Jo Moncrieff's questioning of the need to rethink antipsychotic maintenance treatment (see her article).

Critical psychiatry has always emphasised discontinuation effects from psychotropic medication. Personally I have always pointed to the importance of psychological aspects in discontinuation. Many of the posts on this blog have been about antidepressant discontinuation (eg. see previous post) but the same principles apply to antipsychotic discontinuation. Removing a drug which is thought to have been beneficial is likely to produce a nocebo response.

A difference between antipsychotic and antidepressant discontinuation is the clear evidence for the development of dopamine receptor supersensitivity. Physical effects may therefore be important but it is not clear to me that dopamine supersensitivity is responsible for antipsychotic discontinuation problems. Certainly tardive dyskinesia can be made worse by antipsychotic discontinuation, which is a physical effect, but dopamine supersensitivity may merely be significant for motor rather than psychological symptoms.

I have also always been cautious about the argument that 'antipsychotics should not be used because they cause brain damage' (see previous post). Actually this effect has always been clear, at least for traditional neuroleptics, because of the potential irreversibility of tardive dyskinesia.

Anyway, I'm glad Robin is now recognising the much neglected research question about whether people who manage to deal with their problems without medication may actually do better in the long-term.

Reassessing sociopsychobiological psychiatry

In a BJPsych article, Will Davies & Rebecca Roache (2017) identify a philosophical research programme for reconceptualising George Engel's biopsychosocial paradigm. I have always argued that Engel's biopsychosocial model and, before that, Adolf Meyer's psychobiology are the historical bases for critical psychiatry (eg. see previous post and my article).

Like me, Davies & Roache recognise the value of the biopsychosocial model and disagree with Nassir Ghaemi, who rejects it. I do not totally agree with them, though, that Engel did not try and provide details about how his model should work but this was primarily in relation to psychosomatic disorders. Yet, they are right, as is Ghaemi, about the eclectic way in which the model is used in current practice which is why I prefer the term 'sociopsychobiological' (see previous post). There have also been other recent attempts to reconsider the biopsychosocial model (see another previous post).

Still, their philosophical perspective is welcome. Critical psychiatry, as does the biopsychosocial model, has ontological, epistemological and moral implications for psychiatric diagnosis and treatment. These are practical implications, for example for the Reseach Domain Criteria (RDoC) project mentioned by Davies & Roache (see eg. previous post). These philosophical issues require more rigorous scrutiny.