Tuesday, 11 June 2019

Factor One, Familiarity and Frontal Cortex

In this post, Phil Corlett, Associate Professor of Psychiatry at Yale School of Medicine, discusses some of the ideas in his paper ‘Factor one, familiarity and frontal cortex: a challenge to the two-factor theory of delusions’ recently published in the Journal of Cognitive Neuropsychiatry.

Over recent years, Imperfect Cognitions has become the premier hub and outlet for work on the neurobiology and cognitive psychology of delusions. It has featured my work on aberrant prediction error and delusions in schizophrenia (Corlett et al., 2007), and work that conceptually replicates it (Kaplan et al., 2016). There has been work, also highlighted on the blog, from neurological patients that suggest instead that a 2-factor explanation of delusions may be more appropriate (Darby et al., 2017), although that work was not conclusive (McKay and Furl, 2017).

It has all garnered much interest. Partly because delusions inherently fascinating, I think, and partly because the arguments being waged have clinical import as well as more broad appeal – they are about our beliefs, which we all cherish and often find hard to relinquish. These debates also factor on how best to map the mind and brain. Whilst the debate is about delusions, it has more wide-ranging implications.

Recently I uncovered something in the literature which I believe undermines the 2-factor theory of delusions (Davies et al., 2001, Coltheart, 2010, Coltheart et al., 2011). I believe this discovery warrants our consideration, and, my own reflection has led me to raise four objections to the factor theory of delusions. Two of those are about the control cases who are a foundational for the 2-factor theory of Capgras delusion (the flagship of the 2-factor explanatory fleet). 

One further objection is about the evidence base when it comes to other monothematic delusions. And a final objection is with regards to how we ought to map-mind to brain, whether encapsulated modularity obtains when it comes to belief and perception. If beliefs do alter perception, that is a problem for 2-factor theory.

Briefly, 2-factor theory was devised to explain the monothematic delusions that arise following traumatic brain injury, such as Capgras (that a loved one, familiar conspecific or object has been replaced by an imposter that looks the same but does not feel the same). The 2-Factor explanation holds that people experience the lack of familiarity for their loved one (Factor 1) and they adopt the belief that they are an imposter because they have a belief evaluation deficit (Factor 2) (Davies et al., 2001, Coltheart, 2010, Coltheart et al., 2011)

It is argued that a second factor is necessary because there exist neuropsychological patients who lack familiarity responses to familiar faces, but do not have delusions (Tranel et al., 1995) – these people are the focus of my update. Their familiarity response is usually operationalized as changes in their skin conductance to famous faces like Marilyn Monroe or Margaret Thatcher. Since they lack these changes, but do not have delusions, 2-factor theorists suggest a second, delusion-generating factor is needed.

2-factor theory is based on the observation that these cases all have circumscribed damage in bilateral ventromedial prefrontal cortex (Tranel et al., 1995). People with neurological delusions usually have additional damage to dorsolateral prefrontal cortex, often on the right (Davies et al., 2001, Coltheart, 2010, Coltheart et al., 2011).

2-factor theory for Capgras then suggests that vmPFC damage subtends Factor 1 (the loss of familiarity response to familiar faces, so ‘That doesn’t feel like my wife’) and rDLPFC damage underlies Factor 2 (inappropriately adopting the belief that my wife is an imposter) (Davies et al., 2001, Coltheart, 2010, Coltheart et al., 2011).

In reviewing the literature, I recently discovered a paper by Damasio and Tranel (Tranel and Damasio, 1994) that reports more about those 4 cases. I learned that the 4 cases who lack familiarity responses to familiar faces and have vmPFC damage have:

  1. More extensive damage – including to dorsolateral prefrontal cortex and right dorsolateral prefrontal cortex in particular (Tranel and Damasio, 1994)
  2. Have more extensive skin conductance changes beyond familiar faces – they lack a response to almost all psychologically salient visual stimuli (Tranel and Damasio, 1994).
Thus, my first two objections to 2-factor theory:
  1. rDLPFC damage is not sufficient for belief evaluation dysfunction as claimed by 2-factor theorists
  2. The cases on which Factor 1 is predicated do not have a specific enough deficit to determine the Capgras delusion content. Since the 4 cases lack arousal responses to all kinds of salient stimuli.
Taken together, these two points call for a re-appraisal and of 2-factor theory. At the very least, they ought not to be called VMPFC controls. If they do not share the same SCR deficit as Capgras patients, then they ought not serve as the logical basis for demanding a second deficit in belief evaluation.

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