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| Max Coltheart |
Since the late 1990s my colleague Robyn Langdon and I, initially in collaboration with Martin Davies and the clinical neuropsychologist Nora Breen, and later in collaboration with various others especially Ryan McKay, have been developing a cognitive-level theory of the genesis of delusions which we call the two-factor theory. Our view is that scientific understanding of any delusional condition has been achieved if the answers to two questions has been discovered. Question 1 is: what caused the idea that is the content of the delusion to first come to the deluded person’s mind? Question 2 is: what caused this idea – a candidate for belief - to be accepted as a belief, rather than rejected, which is what ought to have happened because there is so much evidence against it?
Our theory stems from ideas about delusion put forward by William James in 1890 and Brendan Maher in 1974. Both proposed that delusional beliefs result from the use of intact normal reasoning processes in an attempt to develop hypotheses to explain abnormal experiences that the patient is having. These abnormal experiences correspond to factor 1 in our theory, and we agree with James and Maher that it is the application of normal processes of inference (we suggest it is abductive inference that is used here) that yield the hypotheses that can become delusional beliefs.
Where we depart from James and Maher is in our view that the
hypotheses abductively inferred from the abnormal experiences as attempted
explanations of these experiences will normally be evaluated, and then rejected
because of the strength of the evidence against them. That would prevent these
candidates for belief from becoming actual (delusional) beliefs. Only if a
second factor is also present, an impairment of the belief evaluation system,
will patients fail to reject the hypotheses suggested by the abnormal
experiences. So only when this second factor is present will delusional beliefs
arise. (See Coltheart, Menzies, and Sutton 2009).
Consider the Capgras delusion: the belief that someone
emotionally close to you, often a spouse, has been replaced by a complete
stranger. Haydn Ellis, Andy Young and colleagues showed in 1997 that in
patients with Capgras delusion their autonomic nervous systems do not respond
much more strongly to familiar faces than to unfamiliar faces (much stronger
response when a face is familiar is what is normally seen). So a patient expecting
to have a strong autonomic response when he sees someone who looks exactly like
his wife will not have this experience. What could explain this strange and
unexpected (absence of) experience? Well, suppose that this person was not the
wife but some complete stranger: that hypothesis would explain the absence of
the experience. That’s how James or Maher would explain Capgras delusion using
their one-factor theory. But this explanation can’t be correct, because
patients with damage to ventromedial regions of frontal lobe also do not respond much more strongly
to familiar faces than to unfamiliar faces; yet they are not delusional. They
are able to avoid adopting as a belief the hypothesis “This is not my wife”.
Capgras patients can’t avoid this, and we infer that this is the case because
in the Capgras patients a second factor is present, an impairment of the normal
processes of belief evaluation.
The general form of the analysis illustrated above is one we
have applied to the explanation of a variety of delusions. It runs like this.
First, ask Question 1 (what caused the idea that is the content of the delusion
to first come to the deluded person’s mind?). Hope to identify such a potential
cause. Then seek evidence from the neuropsychological literature for the
existence of patients in whom precisely this cause is present but who are not delusional. Then claim that what distinguishes the
delusional from the nondelusional patients is that the delusional patients have
a second impairment, an impairment of the belief evaluation system; this
impairment prevents them from using evidence that would prevent them from
accepting the belief, i.e. evidence that if used would prevent them from
becoming delusional.
Some independent criterion that would support the claim that
an impairment of the belief evaluation system characterises all patients with
delusions is needed. One approach we have taken here is to point to various
pieces of evidence suggesting an association between an impairment of the
belief evaluation system and damage to the right dorsolateral prefrontal
cortex.
But that’s for another blog post. And so is the topic of hypnotic
induction of delusional belief: we work on that with Amanda Barnier, Rochelle Cox and their hypnosis research group.