The British Journal of Psychiatry (2011)
198, 323–327
Correspondence
Edited by Kiriakos Xenitidis and
Colin Campbell
I have no such moment to offer. But brilliant folk like Lawrie and
his colleagues have that tradition and they perhaps raise the
chances that such scientific inspiration can help us once again.
1
Contents
&
The classification of psychosis
&
An unjust review
&
Theories on the evolutionary persistence
of psychosis
&
Don Quixote and Sancho Panza: folie à deux?
&
The benefits of an active control arm
Lawrie SM, Hall J, McIntosh AM, Owens DGC, Johnstone EC. The ‘continuum
of psychosis’: scientifically unproven and clinically impractical. Br J Psychiatry
2010; 197: 423–5.
2
Tyrer P. From the Editor’s desk. Br J Psychiatry 2010: 197: 508.
3
Rose SPR. The biology of the future and the future of biology. Perspect Biol
Med 44: 473–84.
4
Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, ‘Just the facts’: what
we know in 2008. Part 1: Overview. Schizophr Res 2008; 100: 4–19.
Peter J. Gordon, Consultant in Old Age Psychiatry, Forth Valley NHS, Stirling, UK.
Email: [email protected]
doi: 10.1192/bjp.198.4.323
The classification of psychosis
Lawrie et al’s editorial on the ‘continuum of psychosis’ is timely
and welcome.1 I see this debate two ways: as a doctor needing
order to help ease suffering, I agree that it is better, for the time
being, to keep existing diagnostic categories of psychiatric
disorder, however imperfect they may be. As a patient, I of course
want care, but I also want to be understood. Many psychiatrists
now consider that too much of life is branded ‘disorder’: in this,
none of us diminishes the reality of suffering, but we do look
for better ways of explaining it. Certain scientists may hate this
– but people’s lives do have narrative. I think we underestimate
humankind if we say that we cannot accept symptom-based
descriptions of suffering. I hope I am not wrong to suggest that
most of the treatments used today to improve mental health are
not disease specific, but rather act on either mood, thought or
both.
Nevertheless, I agree that the cry for a spectrum approach to
psychosis is premature and it does not fit with my experience of
so many troubled lives encountered. Peter Tyrer is correct to raise
the potential problems, both clinical and pragmatic, of premature
abandonment of current diagnostic classifications.2 However,
there remains a need to reconsider the neo-Kraepelinian model,
if only to bring greater alignment with the technology that Lawrie
et al hope will be to our greater mental good. It is my belief that,
under the present classification system, neurobiological research
cannot fully address complexity. My own view is that we have
given too much attention to what Steven Rose3 has termed
‘neurogenetic determinism’ rather than applying biological
research to life (we should not risk losing the baby with the bath
water, however dirty).
I would contest the presentation of the neurobiology literature
as presented by Lawrie et al in the opening paragraph of their
editorial. I would also contest the claim, attributed to a paper
by Tandon et al,4 that ‘advances in our understanding of aetiology
and pathogenesis [of psychosis are] based on highly replicable
neurobiological differences’. I have read that paper several times,
but found, for all the studies and indeed all the words, neither
one simple biomarker of any utility nor indeed anything even
approaching specificity. Perhaps we should ask why this may be?
Could it be that categories, clinically practicable, and needed for
now, do not match the complex epigenesis of psychosis?
In concluding, I would suggest that we do not forget history.
James Clerk Maxwell was bold enough to stop looking for matter
and to consider the energy fields that now govern our lives and,
indeed, technology that has been to our collective good. Do we
need another Maxwell moment, scientifically brilliant, religion
free, willing to see matters as simple as possible, but not simpler?
Lawrie and colleagues urge us not to reject the current categorical
classification system prematurely.1 I wish to add to the argument
that a categorical system is more likely to be internationally useful.
More than 80% of mental illness occurs in middle- and lowincome countries.2 Much of the world’s mental illness is seen in
overstretched clinics, by practitioners who treat up to 100 patients
a day and often have had no training in psychiatry since medical
or nursing school. Administering the rating scales necessary for a
dimensional system may be possible in high-income countries, but
is difficult or impossible elsewhere. The categorical classification
system can be used quickly by someone with relatively little
training. There is also the problem of translating and validating
the rating scales into hundreds of languages. Most published
research currently uses the same categorical system, which means
that it is useful to doctors all over the world. If the research were
to refer only to a dimensional system, then it would not be useful
in settings where it is impossible to administer the rating scales.
The categorical system gives more people access to evidence-based
treatment than any dimensional system would. A classification
system that is going to be used all over the world needs to be
simple and robust across healthcare systems, languages and
cultures, and this is just as important as how closely it resembles
the truth.
1
Lawrie SM, Hall J, McIntosh AM, Owens DGC, Johnstone EC. The ‘continuum
of psychosis’: scientifically unproven and clinically impractical. Br J Psychiatry
2010; 197: 423–5.
2
World Health Organization. Disease and injury regional estimates
for 2004. WHO (http://www.who.int/healthinfo/global_burden_disease/
estimates_regional/en/index.html).
Wendy D. Shoesmith, Senior Lecturer in Psychiatry, University Malaysia Sabah, Kota
Kinabalu, Malaysia. Email: [email protected]
doi: 10.1192/bjp.198.4.323a
As psychologists who have long researched and argued for a
dimensional view of psychosis, we would like to comment on
Lawrie et al’s editorial.1 We are surprised that the authors pay
no attention – with one exception – to the psychological literature.
If they had done so they would know that considerable evidence
supporting the continuum view has accrued over many decades.
The one psychologist they do cite – the late Paul Meehl – is an
unfortunate choice. Quite apart from the fact that it is unclear
to us how Meehl’s taxonomic (categorical) approach actually helps
their case, the authors ought to be aware that the theory is now on
the wane. A more viable alternative is what we have termed a ‘fully
dimensional’ theory that is capable of encompassing more of the
323
Correspondence
known facts about psychosis, including the clear dimensionality of
the risk of illness and the likely form of the heritability underpinning this, coupled with the notion of discontinuity to recognise
the break in behaviour and psychological state that occurs when
vulnerability translates into clinical symptoms. Importantly, the
model also recognises something that Lawrie et al entirely ignore
– the fact that psychotic traits can have a healthy expression that
takes the individual outside the domain of psychiatric judgement.
Of course, many questions remain, such as how to deal with
the overlap between schizophrenic and affective expressions of
psychosis, explain the underlying biological mechanisms of these
disorders, and incorporate into our thinking how expressions of
vulnerability can vary from sick to benign. However, answers to
these questions will not make dimensionality go away, for it is part
of the essence of human variability (of which psychosis is one
form).
On the practical front, these ideas admittedly make for a
messy picture that is inconvenient for clinicians seeking a neat
solution to diagnostic issues. But psychiatry does itself no favours
by ignoring them and retreating (yet again) behind the ramparts
of its traditional mode of thinking. Fortunately, as Lawrie et al will
be aware, their profession actually has moved forward in recent
years towards an attempt to find ways of integrating both
dimensional and categorical perspectives into its future diagnostic
systems. Our plea is that, in doing so, it becomes an even more
‘psychologically informed’ psychiatry.
Gordon Claridge, Professor of Abnormal Psychology (retired), Department
of Experimental Psychology, University of Oxford, Oxford, UK, email:
[email protected]; Neus Barrantes-Vidal, Professor, Clinical
and Health Psychology, Universitat Autònoma de Barcelona, and Research
Consultant, Sant Pere Claver – Fundació Sanitària, Barcelona, Spain
doi: 10.1192/bjp.198.4.323b
Authors’ reply:
We thank Drs Gordon and Shoesmith for their
interest in our editorial, their complimentary remarks and their
considered responses to what we said. Dr Gordon repeats our call
to avoid prematurely abandoning categories or dimensions, and
highlights the lack of known diagnostic biomarkers for psychosis,
either as a whole or for current subtypes. Tandon et al1 did not
really consider this, quite reasonably, as their review focuses on
what is known about the aetiology and pathogenesis of
schizophrenia. As we have clarified in a forthcoming review,2
the lack of known biomarkers for psychosis (whether as categories
or continua) is at least partly because the right sort of studies to
find them have only rarely been done and reported in this light.
The relevant populations need to be studied and then the results
analysed according to the principles of clinical epidemiology
(or evidence-based medicine), to extract the potential clinical
significance for individuals of statistically significant abnormalities
evident in groups of patients. Thus, for example, if one wished to
identify specific diagnostic markers of schizophrenia that have
clinical utility, a (preferably large) representative population of
people in their first episode would need to be assembled, and
predictive values and/or likelihood ratios calculated for the value
of potential markers of schizophrenia as opposed to, say, bipolar
disorder. Despite the paucity of studies, there are already a
few well-replicated large differences between people with
schizophrenia and healthy controls, which may also distinguish
them from those with bipolar disorder.2 Not all of these require
high-tech investigations. Simple clinical measures of neurodevelopmental aberration such as neurological soft signs, and even
historical measures such as early social difficulties, are common in
people who go on to develop schizophrenia but may not be in
324
those with bipolar disorder. These already influence clinical
decision-making but in an informal and rather haphazard fashion.
The optimal method of eliciting and using such information needs
further investigation, as outlined above and in our review.2
Dr Shoesmith is absolutely right to remind us that any
resource-intensive diagnostic procedure is going to be much less
practical in less well-developed health services. This is of course
an immediate and quite possibly fatal problem for any system
requiring multiple ratings on continua and could be even more
so if, for example, magnetic resonance imaging of the brain/mind
turns out to be diagnostically valuable – as we suspect it might.2 In
the long run, whatever turns out to be the best conceptual
approach to psychosis for the maximal benefit of patients, and
whether or not this has to be pioneered in leading clinical
research centres, the process of formalising our diagnostic
and therapeutic judgements will bring a much-needed and
long-overdue re-engagement of psychiatry with the rest of
medicine.
We are also grateful for the opportunity to respond to the
letter from Professors Claridge and Barrantes-Vidal, especially
those of us who after more than four decades still remember
Professor Claridge’s excellent and provocative teaching on, and
seminal contributions to, the field of schizotypal cognitions,
beginning as they did more than 30 years before this area became
fashionable. We cite Paul Meehl as he is one of the very few
commentators on diagnosis in psychiatry, whether psychologists
or psychiatrists, to have offered a testable hypothesis that would
allow one to make an informed decision about whether a
categorical or continuous approach might be more valid. We
recognise that there have been several alternative proposals to
handling the complexity of psychosis, but very few of these have
been tested in practice. To clarify our position, we are not opposed
to continuous measures, be they psychological trait or cognitive
test scores or brain imaging variables, nor are we particularly in
favour of the status quo or hybrid models. We are simply arguing
that any proposals to change our diagnostic approach to
psychosis, which has survived to this day for some quite good
reasons, should be based on data and therefore built on evidence
rather than fashion or because something looks good on paper.
We would very enthusiastically support, for example, a trial that
tested the efficacy of one or more treatments on one or more
continua of psychosis severity. Having said that, however, even
if that trial generated informative results for clinical practice,
any resulting practical system would of necessity have to include
thresholds for treatment and would thereby create categories. As
we said, continua may or may not be more valid than categories
of psychosis, but clinical decisions require choices between
alternative courses of action.
1
Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, ‘Just the facts’: what
we know in 2008. Part 1: Overview. Schizophr Res 2008; 100: 4–19.
2
Lawrie SM, Olabi B, Hall J, McIntosh AM. Do we have any solid evidence of
clinical utility about the pathophysiology of schizophrenia? World Psychiatry
2011; in press.
Stephen M. Lawrie (email: [email protected]), J. Hall, A. M. McIntosh,
D. G. C. Owens, E. C. Johnstone, Division of Psychiatry, Royal Edinburgh Hospital,
Morningside, Edinburgh EH10 5HF, UK.
doi: 10.1192/bjp.198.4.324
An unjust review
In his review of my book Fiction’s Madness,1 Beveridge comments
on my omission of Laurence Sterne’s Tristram Shandy in
discussing the history of the novel form.2 On fictional
development in the 1950s, Hawthorn3 pointedly excludes Tristram
Correspondence
Shandy as anticipating the novel and I made plain that the
(postmodern) changes I observed ‘came into common usage in
Europe and the Unites States in the last three decades or so’
(Hawthorn: p. 62). To negate (my) differentiating modernist
fiction from the 1950s postmodernist ‘shift’ might make good
criticism if not merely advanced as opinion.
On my text choices being idiosyncratic, I acknowledged this
inevitability (p. vi) before providing choices of others as a balance,
including David Goldberg. But this was ignored and readers left
with assumptions of my eccentricity.
I did not identify psychoanalysis as a dominant force in the
1930s. I asserted its significance as an interest in Freudianism, in
the 1920s, with ‘think-tanks’ involving John Rickman, Lionel
Penrose, A. G. Tansley and John Bowlby, who qualified medically
in the 1930s. This interest persisted into the 1950s, some medical
superintendents being conversant with psychoanalysis whose
emergent tensions, in psychiatry, I addressed in my chapter on
Pat Barker’s Regeneration.4
On Kafka’s Metamorphosis being a short story: I quote
acclaimed literary critic Harold Bloom:5 ‘Considering the origins
of this great short novel, The Metamorphosis’ (p. 65).
In effect, your reviewer ignored most of my book, opting
for points of little intellectual interest. As for my (perceived)
disparaging remarks about psychiatry ‘throughout the book’, my
critical take on psychiatrists Dr Yealland (Chapter 3) and Dr
Weir-Mitchell (Chapter 5) stemmed from fiction. My ‘disparaging
comments’ were exceptionally sporadic but their effect clearly
outweighed the rest of my text.
It is false that I ‘dismiss’ Nietzsche, Socrates and Foucault.
I critically quoted Foucault thus: ‘Shall we try reason: to my mind
nothing could be more futile’ (p. 66). I attributed only to Socrates
that he was Plato’s mouthpiece and placed my take on Nietzsche
within Hesse’s Steppenwolf and Richard III.
In general, the review was ill-considered, selectively dismissive
and factually inaccurate.
1
Clarke L. Fiction’s Madness. PCCS Books, 2010.
2
Beveridge A. Fiction’s Madness. Br J Psychiatry 2010; 197: 337–8.
3
Hawthorn J. Studying the Novel (4th edn). Bloomsbury Academic, 2001.
4
Barker P. Regeneration. Viking Press, 1991.
5
Bloom H. Bloom’s Guides: The Metamorphosis. Chelsea House, 2007.
Liam Clarke, Reader in Mental Health, University of Brighton, 49 Darley Road,
Eastbourne BN20 1EN, UK. Email: [email protected]
doi: 10.1192/bjp.198.4.324a
Author’s reply: I would like to make the following points. First,
in referring to Laurence Sterne’s Tristram Shandy, which is
regarded by most commentators as a novel, I was challenging
the author’s contention that: ‘From the eighteenth century
through to the nineteenth, novels were realist by nature [ . . . ]
from the 1950s, however, novels began to move in mysterious
ways. Suddenly ‘‘Multivoiced’’ narratives, unreliable narrators,
allegories, genre dodging, satire, and allusiveness [ . . . ] became
the order of the day’ (Clarke,1 pp. 11–12). Sterne’s Tristram
Shandy, written in the 18th century, and James Hoggs’ The Private
Memoirs and Confessions of a Justified Sinner, written in 1824,
experiment with the genre and with the notion of the unreliable
narrator. Indeed, Clarke himself (p. 17) cites Ford Madox Ford’s
1915 novel The Good Soldier as representing a good example of
an unreliable narrator.
Second, in his letter the author states that he did not identify
psychoanalysis as a dominant force in the 1930s, but in his book
he writes: ‘Psychoanalysis was a major force in English psychiatry
during the 1930s’ (p. 150).
Third, as regards disparaging remarks about psychiatry, the
quote about the smugness of male psychiatrists comes directly
from the author, not from a novel. Elsewhere we find other critical
remarks. Commenting on psychiatric training the author states:
‘three years of preparation for membership of the Royal College
of Psychiatrists [ . . . ] requires not a whit of training in interpersonal relations, little of self-reflection, or what it means to be
human. Such diversions might inhibit the self-assuredness
provided by a medical model of madness. Alternatively, of course,
the hyped confidence may simply compensate for the
psychiatrists’ self-perceived fragility compared with the knowledge
basis and status of other medical specialities’ (p. 147).
Finally, with reference to a dismissive approach to major
thinkers, the author discusses what he calls ‘Socrates’ infamous
claim that no one can knowingly do wrong’, and concludes:
‘Perhaps Socrates got it wrong’ (p. 156). He writes that ‘Although
Nietzsche’s Superman (Ubermensch) was realised most horrifically,
in our own time, by the Nazis, the impulse to stomp on others
continues’ (p. 136). He also observes: ‘Foucault foolishly suggests
abandoning rationality itself ’ (p. 186).
Allan Beveridge, Queen Margaret Hospital, Whitefield Road, Dunfermline KY12 0SU,
UK. Email: [email protected]
doi: 10.1192/bjp.198.4.325
Theories on the evolutionary persistence of psychosis
We note that the Darwinian models of psychosis reviewed by
Kelleher et al1 in their editorial were all variants of the ‘costly
by-product’ evolutionary model whereby an adaptive neurobiological system that enhances fitness in the vast majority of
the population generates the risk of error in a small minority,
resulting in psychosis (including schizophrenia). Burns2 identified
the frontotemporal and frontoparietal cortical connections of the
social brain, whereas Crow3 proposed that the dysregulation
occurs in the language centres.
We wish to propose a different and entirely environmental
Darwinian formulation for the non-affective psychoses based on
an ‘environmental mismatch’ model. We have explained
elsewhere4 that, although we agree with Burns’ proposal regarding
locating the dysregulation and dysconnectivity within the social
brain, we contend that the aetiology of the dysregulation relates
to the effects of the novel post-Neolithic social environment.
Although the susceptibility to non-affective psychosis, including
schizophrenia, is likely to be ancient, the schizophrenic and the
non-affective psychosis phenotype did not manifest itself until
very recently in our species’ history. In other words, the risk of
these disorders lay dormant and did not become evident until
the post-Neolithic period.
Hence, we have proposed a reformulation of the social brain
theory of schizophrenia and contend that schizophrenia (and
the non-affective psychoses) are novel human phenomena that
arose following the establishment of large permanent human
settlements that accompanied the advent of agriculture and the
abandonment of the hunter–gatherer way of life. We have
contended that the blurring of the demarcation between in-group
and out-group membership and living in close proximity to
strangers is a stressor that can lead to perturbation in the
development of the social brain in vulnerable individuals,
resulting in the syndrome of schizophrenia. Hence, according to
our formulation, schizophrenia is the result of a mismatch
between the post-Neolithic human social environment and the
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Correspondence
possible future research involving those who have the non-clinical
psychosis phenotype, it is important for people working in
mental health services to remember that not all those they
encounter with symptoms are ill. For those that are unwell, there
will be other aspects of their existence that are positive and that
may be life-enhancing for them and those around them. They
should be encouraged to develop these aspects of themselves as
part of their long-term recovery, in addition to the treatment
and support they receive from health services, carers and friends.
design of the social brain. We highlight the importance of the
distinction between in-group and out-group membership that lies
at the heart of intergroup conflict, violence and xenophobia. Our
hypothesis (the out-group intolerance hypothesis) provides an
explanation for the disparities in the prevalence of schizophrenia
across the world and for the higher risk of this condition
among immigrants and city dwellers. We propose that our
hypothesis can account for a range of disparate epidemiological
and other findings regarding schizophrenia that have thus far
defied explanation by other theories, including the Darwinian
by-product formulations reviewed by Kelleher et al.
1
Kelleher I, Jenner JA, Cannon M. Psychotic symptoms in the general
population – an evolutionary perspective. Br J Psychiatry 2010; 197: 167–9.
1
Kelleher I, Jenner JA, Cannon M. Psychotic symptoms in the general
population – an evolutionary perspective. Br J Psychiatry 2010; 197: 167–9.
2
Claridge G (ed). Schizotypy: Implications for Illness and Health. Oxford
University Press, 1997.
2
Burns JKP. An evolutionary theory of schizophrenia: cortical connectivity,
metarepresentation, and the social brain. Behav Brain Sci 2004; 27: 831–55.
3
Nettle D. Schizotypy and mental health amongst poets, visual artists, and
mathematicians. J Res Pers 2006; 40: 876–90.
3
Crow TJ. Is schizophrenia the price that Homo sapiens pays for language?
Schizophr Res 1997; 28: 127–41.
4
Nettle D, Clegg H. Creativity, schizotypy and mating success. Proc Roy Soc B:
Biol Sci 2006; 273: 611–5.
4
Abed R, Abbas M. A reformulation of the social brain theory for
schizophrenia: the case for outgroup intolerance. Perspect Biol Med 2011;
in press.
Riadh Abed, Consultant Psychiatrist and Medical Director, Rotherham, Doncaster
and South Humber NHS Mental Health Foundation Trust, St Catherine’s Hospital,
Doncaster DN4 8QN, UK, email: [email protected]; Mohammed Abbas,
Consultant Psychiatrist, Bradgate Mental Health Unit, Leicester, UK
Marcia Willis, Locum Consultant, Child and Adolescent Psychiatrist, Brent Child and
Family Clinic, Warranty House, Dudden Hill Lane, Neasden, London NW10 1DD, UK.
Email: [email protected]
doi: 10.1192/bjp.198.4.326
doi: 10.1192/bjp.198.4.325a
Don Quixote and Sancho Panza: folie à deux?
Kelleher et al1 note the significant prevalence of non-clinical
psychotic symptoms in the general population and discuss some
hypotheses regarding its evolutionary survival. One theory not
mentioned by them or those who have so far responded is a trait
known as schizotypy. While accepting that to some degree the
whole topic is rich with speculation, I suggest that schizotypy
may be the missing piece in the puzzle. What follows is necessarily
a brief summary of some of the relevant literature.
Differing from both schizotypal and schizoid personality
disorders, schizotypy2 is a heritable trait associated with an
increased likelihood of creativity and of religious or mystical
experiences. Importantly for this discussion, schizotypy also
appears to be necessary but not sufficient for the development
of schizophrenia, although not all those with schizotypy develop
psychotic illnesses.
The four key dimensions of schizotypy are unusual
experiences (which may be considered to be related to positive
symptoms), cognitive disorganisation (related to thought
disorder), introverted anhedonia (related to social withdrawal
and depression) and impulsive non-conformity. This last is related
to some of the disturbed behaviour, such as aggression and selfharm, seen in a range of psychiatric illnesses, including psychosis.
Regarding creativity, additional research by Nettle3 suggests
that different dimensions of schizotypy are associated with
different types of creativity. Nettle & Clegg further find that
schizotypy is associated with increased ‘evolutionary fitness’
due to a greater number of sexual partners (and therefore
offspring) in those with the unusual experience and impulsive
non-conformity dimensions of the trait.4 In those with the former
but not the latter dimension, the relationship with mating success
is mediated by creativity. Nettle & Clegg have proposed that
schizotypal traits, which in this case may be a proxy for some
non-clinical psychotic symptoms, have therefore persisted because
their potential negative effects are offset by enhanced mating
success.
Regardless of the outcome of the search to understand the
persistence of psychotic symptoms in human beings and of
326
Martins de Barros & Busatto Filho date the first report in fiction
of folie à deux to the Brazilian author Machado de Assis in 1879.1
I submit that the first fictional account of ‘shared delusions’ was
by Miguel de Cervantes over 250 years before. Cervantes wrote
Don Quixote de la Mancha in or around 1604, publishing the first
part in 1605 and the second, a decade later.
In Don Quixote, the eponymous hero, we have a domineering
and voluble fantasist driven ‘out of his wits’ by the undue
influence of books of chivalry: ‘He so buried himself in his books
that he spent the nights reading from twilight till day break and
the days from dawn till dark; and so from little sleep and much
reading, his brain dried up and he lost his wits.’2 His character
is steeped in rich descriptions of grandiloquent and persecutory
delusions, polymorphic hallucinations and cognitive blunting.
Sancho Panza, his squire, whom he enlists as his companion for
his travels, is described as ‘an honest man – if a poor man can
be called honest – but without much salt in his brain-pan’.2
So we have a dominant Don Quixote, who has lost his reason,
and a submissive, not so bright Sancho Panza, thrown together
through much of their travels, creating a situation ripe for the
development of folie à deux. And indeed we see a slow erosion
of reason in Sancho Panza. He initially displays some resistance
and skepticism to Don Quixote’s delusions about windmills being
monstrous giants or St Benedict’s monks being a crew of wicked
and diabolical ‘perfidious scoundrels’. But he increasingly becomes
convinced of the veracity of Don Quixote’s beliefs. One example
should suffice, the example of the balsam of Fierabras. This is a
concoction that Don Quixote claims he can make on the cheap.
He tells Sancho Panza, ‘If ever you see me cut through the middle
in some battle [ . . . ] you have only to take the part of my body
that has fallen to the ground and place it neatly and cunningly,
before the blood congeals, on to the half that is still in the saddle,
taking special care to make them fit exactly. Then you must give
me just two drops of this balsam to drink and, you will see, I shall
be as sound as an apple.’2 Sancho replies, ‘If that is so, from now
on I renounce the governorship of the promised isle, and all I want
in payment for all my good services is for your worship to give me
the recipe for that marvelous liquor.’2
Correspondence
By the end, Sancho Panza’s descent into these fantastic
delusions is complete. So much so that at his death bed, when
Don Quixote regains a measure of lucidity and tries to persuade
Sancho to see reason, Sancho Panza is completely insightless
and unamenable.
We are not witness to the effect of the separation of Sancho
Panza from Don Quixote, as the story ends before it. But apart
from that, the description of folie à deux is complete in this wonderfully told tale.
1
de Barros DM, Filho GB. First fictional report of folie à deux. Br J Psychiatry
2011; 198: 30.
2
de Cervantes M. Don Quixote (trans JM Cohen). Penguin, 1950.
Vijay Kumar, Consultant Psychiatrist in Old Age Psychiatry, Cheshire and Wirral
Partnership NHS Foundation Trust, Jocelyn Solly House, Macclesfield, UK. Email:
[email protected]
efficacy of oral atypical antipsychotics with that of intramuscular
typicals and produced mean changes in rating scale scores similar
to those in Lesem et al’s paper, on similar timescales.3
When alternative treatments exist, placebo-controlled trials are
appropriate if the target condition is characterised by a high
placebo-response rate or a high relapse, remission or spontaneous
resolution rate, or if existing therapies are partially effective or
have high side-effect rates.4 Inclusion of an active control arm
to the trial would have added to the number of patients required
in each arm, but would have provided valuable information on the
tolerability and efficacy of the inhaled or oral medication.
1
Lesem MD, Tran-Johnson TK, Riesenberg RA, Feifel D, Allen MH, Fishman R,
et al. Rapid acute treatment of agitation in individuals with schizophrenia:
multicentre, randomised, placebo-controlled study of inhaled loxapine. Br J
Psychiatry 2011; 198: 51–8.
2
Yildiz A, Sachs G, Turgay A. Pharmacological management of agitation in
emergency settings. Emerg Med J 2003; 20: 339–46.
3
Lim HK, Kim JJ, Pae CU, Lee CU, Lee C, Paik IH. Comparison of risperidone
orodispersible tablet and intramuscular haloperidol in the treatment
of acute psychotic agitation: a randomized open, prospective study.
Neuropsychobiology 2010; 62: 81–6.
4
Emanuel EJ, Miller FG. The ethics of placebo controlled trials – a middle
ground. N Engl J Med 2001; 345: 915–9.
doi: 10.1192/bjp.198.4.326a
The benefits of an active control arm
Lesem et al1 highlight the importance of rapid and safe treatment
of agitation, indicating the delayed onset of action associated with
intramuscular injection. They make no reference to the time from
oral medication administration to onset of effect. However, the
combination of oral atypical antipsychotics, with or without
benzodiazepines, is well described.2 Small trials have compared the
Andy R. Shepherd, CT1 Trainee, Greater Manchester West Mental Health Trust.
Email: [email protected]
doi: 10.1192/bjp.198.4.327
Corrections
Mental disorders and termination of education in high-income
and low- and middle-income countries: epidemiological study.
BJP, 194, 411–417. The following funding source was omitted
from the start of the list on p. 416: US National Institute of Mental
Health – Mental Health Burden Study (contract number
HHSN271200700030C).
The man behind Philippe Pinel: Jean-Baptiste Pussin (1746–
1811). BJP, 198, 241. The DOI for this item is: 10.1192/
bjp.198.3.241a. The online version has been corrected in deviation
from print and in accordance with this correction.
doi: 10.1192/bjp.198.4.327a
327
Theories on the evolutionary persistence of psychosis
Riadh Abed and Mohammed Abbas
BJP 2011, 198:325-326.
Access the most recent version at DOI: 10.1192/bjp.198.4.325a
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