Acta Psychiatr Scand 2018: 137: 85–87 © 2017 John Wiley & Sons A/S.
n Wiley & Sons A/S. Published by John Wiley & Sons Ltd
All rights reserved
DOI: 10.1111/acps.12837
Editorial
Thinking fast and slow – in clinical
psychiatry
He walked into my rooms slowly, barely swinging
his arms and showing no light in his eyes in
response to my welcome. Parkinson’s Disease?
Melancholia?
He provided a succinct reason for the appoint-
ment. ‘I developed depression 3 months ago. Just
after my 63rd birthday. Never had it before. My
mother developed depression at exactly the same
age. She needed ECT to get better’.
I undertook a review of his depressive symptoms
before taking a general history covering other pos-
sible diagnostic issues and his personal narrative.
He was clearly depressed, but my primary objec-
tive was to ‘subtype’ his depression. His response
to a set of questions that I have progressively
weighted over the years (e.g. anhedonic and non-
reactive mood, marked anergia, impaired ‘foggy’
concentration, mood and energy worse in morn-
ings) argued for a melancholic depression as a ‘no
brainer’ diagnosis and as a stretched metaphor. I
commenced him on an antidepressant and, at
reviews, his depression had significantly improved
by 2 weeks and fully remitted at 6 weeks. I recom-
mended he remains on the same dose of the medi-
cation in the light of the gravity of his initial
presentation and as he was not experiencing dis-
tinct side-effects.
A year later he returned to say that ‘it’ had
returned in the last fortnight. He again showed dis-
tinct psychomotor retardation and affirmed the
same set of depressive features. Asked about his
medication, he stated that he had stopped it
6 weeks previously. My ‘fast brain’ encouraged me
to state the obvious – melancholia is highly likely
to return if maintenance medication is ceased, and
that he should immediately restart it. However, I
held such censuring back as my ‘slow brain’ kicked
in and I broadened my questioning. Were there
any new symptoms? Well, he had had a disastrous
golf round that week – his swing just didn’t work
at all. Anything else? He had been embarrassed to
drop a grocery bag at the supermarket that morn-
ing. Anything else? Well, yes. He had noticed some
numbness in two fingers in his left hand. Anything
ACTA PSYCHIATRICA SCANDINAVICA
else? Now that he thought about it, there was also
some left-sided facial numbness.
The prescription pad was retracted and instead a
neurology referral form completed. An MRI that
afternoon showed a subdural haemorrhage which
was successfully drained that evening. At review a
fortnight later, he appeared completely normal
and no symptoms of ‘melancholia’ were present.
We both judged that it might be best not to rein-
troduce the antidepressant at that time.
This vignette serves as an introduction to clinical
reasoning and one of its key components: pattern
analysis. Pattern analysis? As medical students, we
marvelled at how a senior physician might in a
minute or two – and perhaps only after absent-
mindedly tapping a kneecap or transiently applying
a stethoscope and asking a brief set of disparate
questions – offer a diagnosis that would be con-
firmed by a definitive laboratory test (or autopsy).
We students, by contrast, might have spent days
interviewing and examining the patient, as well as
poring over textbooks, and remained bothered and
bewildered by our failure to obtain diagnostic clo-
sure. What intuitive art – for it surely was not
science – did our seniors possess? And how might it
be acquired, as it was not listed in our syllabus and
no lecturer ever took us into this arcane world. It
lies at the heart (and perhaps the art) of psychiatry,
reflecting psychiatry’s domains and the absence of
any gold standard laboratory tests.
Malcolm Gladwell (1) proselytized the concept
that it took 10 000 h of deliberate practice to
develop a skill set. In his monograph, ‘Thinking,
Fast and Slow’, Daniel Kahneman noted (2) how
chess masters are able to move down an assembly
line of chess boards slaved over for hours by ama-
teur chess tragics to make rapid and brilliant chess
moves seemingly intuitively. But Kahneman dis-
missed intuition, arguing more for the masters see-
ing each chess board differently, reflecting the
10 000 h of dedicated performance to become
familiar with thousands of configurations and
with each involving arrangements of related
pieces that could defend or threaten each other. In
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Editorial
essence, pattern recognition acquired by repeated
experience.
Of further relevance to clinical reasoning, Kah-
neman distinguished ‘fast’ (or implicit) from ‘slow’
(or explicit) thinking. He detailed how fast think-
ing operates automatically and without voluntary
control, seeks categories or prototypes and looks
to construct the best possible narrative or formula-
tion. Such thinking is, however, gullible, possesses
a bias to believe, neglects ambiguity, and focusses
on existing and supporting evidence rather than
ignoring absent evidence. By contrast, he judged
‘slow’ thinking as intrinsically lazy but that it
can be called on (as an executive control system)
after the fast thinking phase to consider alternate
explanations.
Is one style (i.e. slow or fast thinking) optimal
for psychiatric diagnosis and formulation? I doubt
it. The slow brain would be called on in a psychia-
trist’s early training years and when reliance on
formalised diagnostic criteria may dictate clinical
judgement. Later, after (say) ten thousand hours,
the fast brain may be dominant for some practi-
tioners. The optimal endpoint is more likely to
involve an iterative process, with the ‘fast’ brain
automatically generating a formulation or a diag-
nosis and then the ‘slow’ brain effecting its execu-
tive control system and considering supportive or
alternate explanations. I once asked a number of
psychiatrists as to when they had achieved a crest
in clinical reasoning. Most nominated a peak in
their sixties, paradoxically a time when most prac-
titioners are planning retirement. And so clinical
pattern analysis is not innate, requiring the thou-
sands of hours described by Gladwell. This does
not apply solely to psychiatrists, but is a mature
skill required within many professions: other clini-
cal specialties, chess masters, fire wardens and even
chicken sexers.
Where do I position psychiatric clinical reason-
ing in a decade? As noted earlier, the psychiatric
field lacks laboratory tests for diagnostic clarifica-
tion and this argues for a need to weight clinical
reasoning and refined pattern analysis. However,
most if not all psychiatric diagnoses lack precise or
even clear boundaries, leading to formalised (and
informal) diagnostic categories being of limited
validity, while comorbidity is common. Further-
more, management is not generally simply shaped
by ‘the diagnosis’, but optimally by a formulation
which asks why ‘this patient has presented at this
time with this condition’, and generates a compos-
ite of diagnosis, personal narrative, antecedent
distal and proximal determinants, as well as
personality style. Psychiatric pattern analysis may
then be relevant across limited and formal
86
diagnostic disease groups such as validly diagnos-
ing melancholia or schizophrenia, or say in
differentiating schizophrenia from bipolar disorder
and from schizoaffective disorder. Conversely, it
could well be argued that it is potentially of high
utility in determining whether an individual has a
non-disease condition such as a personality disor-
der and that its application is not limited to the
interpretation of symptoms and signs but from
other sources such as the psychiatrist’s interpreta-
tion of their own counter-transference and other
subjective information.
As the science suggests that clinical pattern anal-
ysis may not be readily ‘teachable’, I doubt that it
will become an undergraduate or postgraduate
course in psychiatry. Are we then left with the
necessity of requiring the psychiatrist (and those in
other clinical fields) to assess thousands of patients
over decades to ensure the ten thousand hours
threshold has been exceeded? Is there not a place
for computer-assisted or machine learning diag-
nostics even if limited to the diagnosis of psychia-
try’s disease states? While such computer
programs have been under development since the
seventies, none have delivered at an acceptable
level. Overviews of the topic still conclude that
computers cannot replace doctors at the bedside.
Computers may just be unable to master the multi-
ple domains that are involved in deriving a valid
diagnosis. For example, diarrhoea is not an imme-
diate clinical signal for a diagnosis of sarcoid of
the hypothalamus, and only a skilled clinician
might wend their way from such a symptom to that
endpoint diagnosis. This suggests that computers
could be designed more to complement clinical rea-
soning than seeking to develop them as definitive
diagnostic tools in and of themselves. Again, how-
ever, the broad domains of psychiatric diagnoses
would suggest that such application might be lim-
ited to a small set of diagnostic categories.
Can we learn from chess? In 1997, IBM’s com-
puter, Deep Blue, beat Garry Kasparov at chess
and since then computers have consistently beaten
chess masters. However, while the chess masters
operate to a pattern analytic approach, computers
operate by judging the best next moves rather than
searching for patterns. Each bring differing ana-
lytic approaches to the table. Currently, the evi-
dence suggests that, to win a chess match, a
computer plus a skilled player will perform better
than either one alone.
Thus, rather than seeking to develop a computer
program that will have diagnostic superiority to an
ace clinical psychiatrist, it may be more important
to develop programs that complement the psychia-
trist’s judgement. For example, the psychiatrist

might diagnose ‘depression’ and then turn to the
computer for subtyping the specific depressive con-
dition. Thus, the computer would assist by deter-
mining whether the depressed patient was most
likely to have a unipolar depression (and, if so, a
biological melancholic or an environmental non-
melancholic disorder) or a bipolar disorder based
on the presence (and absence) of multiple symp-
toms and their weightings. Similarly, the computer
might be programmed to establish the presence or
absence of disordered personality function and, if
affirmed, to generate the particular personality dis-
order ‘type’ or ‘types’. If such programs were to be
developed, then the decision tree computer algo-
rithms might benefit from incorporating the multi-
ple signals (and the signal weightings) acquired by
the clinicians who have laboured thoughtfully at
the relevant coal face for decades. And then, in an
iterative manner, the computer could progressively
refine the signal weightings for patients with – as
against those without a particular diagnosis – and
with such Bayesian calibrations then being applied
to sharpen the diagnostic criteria employed by clin-
icians, and ideally contributing to improving for-
malised diagnostic criteria. In essence, the
computer would provide ‘fast brain’ information
for reflective consideration by the clinician
engaged in a ‘slow brain’ appraisal and review, and
there would be an iterative process between the
clinician and the computer in advancing the key
diagnostic signals and their weightings.
A year later, my patient’s ‘melancholia’ returned
abruptly. A neurology review and repeat MRI
failed to identify any neurological cause, the
Editorial
same antidepressant was reintroduced and his
depression remitted after 5 weeks. He has now pre-
sented the same basic phenomenological pattern
on three occasions but with two differing causes
and with each requiring contrasting management
strategies. To expect a computer to diagnose
melancholia and then exclude the myriad factors
that would have established a diagnosis of
‘pseudo-melancholia’ (and its specific nature)
strikes me as unlikely to be successful; indeed, the
input data required would be enormous and also
dependent on the validity of its reporting.
Thus, clinical reasoning and pattern analysis lie
at the heart of psychiatry. And the injunction
‘Physician know thyself’ challenges us individually
and collectively to consider how best to reap the
riches of the ‘fast’ and our ‘slow’ pieces of our
brains.
Declaration of interest
Nil disclosures reported.
G. Parker1,2
1
School of Psychiatry, University of New South Wales, Sydney,
Australia and
2
Black Dog Institute, Sydney, Australia
E-mail: g.parker@unsw.edu.au
References
1. Gladwell M. Outliers: the story of success. New York: Lit-
tle Brown and Company, 2008.
2. Kahneman D. Thinking, fast and slow. New York: Farrar,
Strauss and Giroux, 2011.
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