ABSTRACT
Corlett (Corlett, P. (this issue). Factor one, familiarity and frontal cortex: A challenge to the two-factor theory of delusions. Cognitive Neuropsychiatry) provides a robust critique of the two-factor theory of delusions. The heart of his critique is two challenges he derives from a paper by Tranel and Damasio (Tranel, D., & Damasio, H. (1994). Neuroanatomical correlates of electrodermal skin conductance responses. Psychophysiology, 31(5), 427–438), who illuminate the autonomic responses and brain damage of four patients often cited in support of the two-factor theory of Capgras delusion. I defend the two-factor theory against Corlett’s two key challenges, arguing that his first challenge has been previously addressed, and that his second challenge is overstated. In my view, these challenges do not negate the two-factor account. Nevertheless, two-factor theorists – and computational psychiatrists – should continue to devise and test falsifiable predictions of their respective theories.
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Notes
1. The authors of one prevalence study estimate that about 30 million Americans suffer from tinnitus (Kochkin, Tyler, & Born, Citation2011).
2. Many others have invoked an analogy between resistance to false data (e.g., “fake news”) and biological resistance (e.g., Cook, Lewandowsky, & Ecker, Citation2017; Kucharski, Citation2016; McGuire, Citation1964; Roozenbeek & van der Linden, Citation2018).
3. As an aside, it’s worth noting that these are not really two independent, mutually reinforcing challenges. On the contrary, Corlett’s first challenge – if successful – somewhat undermines his second. After all, if the Tranel et al. (Citation1995) patients don’t actually have the first factor for Capgras delusion (as Corlett alleges), then it hardly matters whether they have the second factor or not – either way, we would not expect them to have Capgras delusion.
4. “[T]he evidence seems clear that damage to right frontal cortex is associated with the presence of delusional belief, and even that the specific region of right frontal cortex that is critical here is rLPFC – and possibly an even more specific region, rDLPFC” (Coltheart et al., Citation2018, p. 237, my emphasis).
5. Ironically, this more specific prediction is based, in part, on Corlett’s own work (Corlett et al., Citation2007).
6. Turner et al. (Citation2017) contrast a case of medication-induced non-delusional déjà vu (“I was a little freaked out when I watched TV as I felt I was watching repeats, although I knew I wasn’t”; Kalra, Chancellor, & Zeman, Citation2007, p. 312) with their own case of déjà vecu (“Everyone says ‘you only think you’ve seen it before’. But I’ll swear black and blue that I have seen it before.”; Turner et al., Citation2017, p. 144).
7. To return to the bees-in-the-head case, it’s worth noting that whereas the most common cause of tinnitus is cochlear damage, the Danvers patient with the bees delusion was thought to have a condition entailing direct mechanical stimulation of auditory cortex (see Maher, Citation1988). Her resulting auditory experience may well have been more intense than the sounds experienced by the average sufferer of tinnitus.
8. Individuals with Frégoli delusion believe that strangers in their environment are actually familiar people in disguise (see Langdon, Connaughton, & Coltheart, Citation2014). Corlett notes that “the control condition (the vmPFC case equivalent) for Fregoli [has not] been identified”. There are, however, non-delusional individuals with intact face recognition who report an abnormal feeling of familiarity for unknown faces (e.g., Vuilleumier, Mohr, Valenza, Wetzel, & Landis, Citation2003; Negro et al., Citation2015).
9. Corlett also suggests confirming that Capgras patients have deficient autonomic responses to personally familiar faces (“a dearth of responding to famous people is not enough”), but there is already evidence they do (Brighetti, Bonifacci, Borlimi, & Ottaviani, Citation2007).