Two-factor Theory of Monothematic Delusions: Deficient, Adequate or Successful? Numerous theories have been developed to account for the formation of monothematic delusions, however the two-factor theory arguably provides the most complete explanation. This essay initially outlines definitions and gives a brief background for monothematic delusions and the two-factor theory, followed by a synopsis of Maher’s one-factor theory with its supporting evidence and associated problems. A summary of the two-factor theory is then presented in terms of the role of the first and second factor, showing how the second factor solves some of the problems that arise from a one-factor theory. Possibilities for the specific form of the second factor are then discussed along with the associated problems of each; attribution biases, data gathering biases, and impairment to the belief evaluation system.
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The latter is shown to be the most supportable option, though the remaining issues of the ‘monothematicity problem’ and the ‘appreciation for implausibility problem’ are discussed. It is concluded that the two-factor theory most satisfactorily accounts for monothematic delusion formation, however more empirical proof is required before this theory can be said to be successful. Though the definition is often debated, for the purpose of this essay it is sufficient to say that delusions are “false beliefs based on incorrect inference about external reality that persist despite evidence to the contrary”.
Delusions can be categorized in numerous ways, however the relevant division here is between monothematic and polythematic delusions. Polythematic delusions have more than one theme and often involve an interrelated system of beliefs.2 Monthematic delusions are limited to a single belief, generally somewhat detached from the rest of a person’s beliefs, leaving their cognitive abilities otherwise unaffected. 3 Both one and two-factor theories are ‘bottom-up’ approaches to delusion formation.
This means the direction of causation is from experience to belief; a cognitive defect leads to a perceived unusual experience which prompts the formation of a hypothesis to explain the experience, and when endorsed this hypothesis becomes a delusional belief.4 In order to evaluate delusion occurrence theories, there are several questions to address: where the content of the delusion comes from; why a patient will favour an implausible hypothesis over a more plausible one; why a delusion only forms around a single idea or belief and not many; and why a delusional belief is maintained despite counter-evidence.
One-factor theories, such as Maher’s, maintain that a perceived unusual experience is sufficient for the formation of a delusional belief. Two-factor theories maintain that an unusual experience is only one aspect and a second factor is required to fully satisfy the above questions. Initially, in order to adequately evaluate the two-factor theory, it is necessary to compare it to Maher’s one-factor theory. Maher argues that delusions occur as a result of normal cognition following an unusual event.
The implausibility of the delusional hypothesis formed is understandable considering the strangeness of the event it must explain. 6 In essence, Maher sees delusions as false beliefs that arise from normal reasoning and cognition succeeding an unusual experience. 7 Maher concedes it is possible for people to have unusual experiences without developing delusions, suggesting something additional is required for a delusion to form.8 He suggests the unusual experience must be intense, prolonged or frequently repeated to prompt a delusion.9 As evidence for Maher’s account, it must be shown that the origins of monothematic delusions can be found in perceived unusual experiences. Indeed, evidence suggests Capgras delusion (that a relative has been replaced with an imposter) stems from an inability to distinguish between familiar and unfamiliar faces, as a result of a cognitive defect.10 Similarly another delusion, mirrored-self misidentification (not recognising ones own reflection), results from patients either having a deficit in face processing or from losing the ability to interact fluently with mirrors.
11 Numerous other perceptual irregularities have been discovered in other delusions which support Maher’s account in this respect, as can be seen in Davies et al (2001) table 2.12 Gerrans argues that although Maher’s account may explain why delusional hypotheses are formed, it does not explain why they are maintained despite counterevidence.13 Additionally, Garety and Freeman present evidence to suggest delusional patients exhibit reasoning and attribution biases, thus do not undertake normal reasoning processes when forming delusions as Maher suggests. Maher’s explanation also implies that anyone suffering from a cognitive abnormality causing unusual perceptual experiences should develop a delusion.
However there are cases of people whose brain damage prevents familiar faces from evoking the expected autonomic nervous system responses who do not develop Capgras delusion. 15 Davies et al, proponents of a two-factor theory, agree with Maher’s concession that a second factor is needed to explain why some people with certain damage develop delusions and others do not. However they do not agree that this second factor is related to the duration or intensity of the unusual experience.16 This view is supported by an experiment by Cahill et al which had deluded and non-deluded subjects listen to a distorted version of their own voice through headphones, resulting in deluded patients tending to identify the voice as another’s, whereas non-deluded subjects identified it as their own.
This runs contra to Maher’s account as it demonstrates that delusional beliefs do not result from normal reasoning and cognitive processes; otherwise both groups would have come to the same conclusion. Coltheart outlines the first factor of the two-factor theory as a ‘neuropsychological impairment’, differing from patient to patient, that causes the patient to receive false data in the form of a perceived unusual experience, with the subsequent delusional belief being formed to explain that experience.18 In general terms, the first factor accounts for the delusion’s content, whereas the second factor accounts for why it is adopted and maintained in spite of counterevidence.19 The two factor theory is congruent with Maher’s explanation inasmuch as a delusional hypothesis is generated in order to explain a perceived unusual experience which occurs due to a perceptual deficit, but adds a second factor to explain, as Stone and Young state, why the hypothesis is adopted and maintained as a belief.
The specific form of this second factor is also debated; attribution biases and data gathering biases are put forward by some, however a defective belief evaluation system is the most likely candidate. An attribution bias refers to what people attribute actions to; how they explain why things happen.21 One kind of explanation will generally be favoured over another. For instance, if a person has a deficit in face processing with a bias towards attributing negative events to the external world, this may result in Capgras delusion whereas Cotards (the belief that one is dead) may result from an internalising bias.22 Davies et al argue against attribution biases as the second factor, stating that such biases are present in the non-deluded population also. 23 I believe this point is invalid as it is only when a bias is coupled with a neuropsychological anomaly and unusual event that a delusion arises.
However there is other evidence against attribution biases as the second factor, as although they might explain why an unusual experience results in a delusional hypothesis, they do not adequately account for why the hypothesis is maintained as a belief despite counterevidence. Additionally, not all patients with Capgras delusion, for instance, have an external bias for negative events; some in fact have the opposite.24 A similar bias, data gathering, is also a potential second factor. There is evidence to suggest that people with delusions do not give appropriate consideration to alternative explanations, and that while not completely irrational, they do have a penchant for jumping to conclusions without sufficient evidence.
Notwithstanding, it should be noted that although people with delusions do not actively seek additional evidence, if it is presented they are able to make adequate judgments. 26 In this sense, Maher could be somewhat correct in that deluded patients do not present with abnormal reasoning abilities but rather an abnormality in how they treat evidence.
However, this bias encounters the same problem as an attribution bias, in that it may explain why a delusional hypothesis is initially generated, but not why it is maintained. The third, and most plausible, possibility is a second neuropsychological deficit; one in a person’s belief evaluation system. Coltheart discusses evidence that this is associated with damage to the right lateral prefrontal cortex.27 It can be described as a person losing the ability to adequately reject a hypothesis when evidence is presented against it or it does not concur with their other beliefs and experiences.28 This impairment is the same in all people with monothematic delusions and may explain why a person adopts and maintains a delusional hypothesis, possibly even why they continue to hold the belief in the face of counterevidence (as they are simply unable to process the evidence correctly).
It does however raise several other questions which must be addressed in order to evaluate the success of the theory in accounting for why monothematic delusions occur. The first of two main issues is the monothematicity problem; if patients suffer from such a deficit, why is it they do not adopt other unusual beliefs? The second is that, if patients cannot adequately evaluate their beliefs, how is it that some can appreciate their implausibility? Coltheart et al present a possible solution for the monothematicity problem; that the belief evaluation system is damaged but not destroyed.30 This is evidenced by some patients who suffer from somatoparaphrenia (the denial that a patient’s left limbs are their own) as a result of a right hemisphere stroke, being temporarily cured of their delusion by administration of cold water to the left external auditory canal to stimulate the brain’s right hemisphere.
This shows that although impaired, the belief evaluation system can still function correctly on occasion, thus for a delusional belief to occur, the unusual experience must be consistently present; as when a Capgras patient lacks the appropriate autonomic response every time they look at their spouse. Coltheart would add that in addition to the continuous or repetitious presence of the unusual experience, there must also be a lack of any (equally persistent) counterevidence. A damaged belief evaluation system cannot continually dismiss the delusional belief when continually being supplied by (perceived) evidence in its favour.
The next problem to address is how some patients can appreciate the implausibility of their delusion, even understanding why others reject the belief, and yet still not reject it themselves. If these people really did suffer from an impaired belief evaluation system, this kind of reasoning should not be possible. Davies et al best address this problem with reference to the pre-potent doxastic response, the process that transitions experience to belief.33 If there is this response, a person takes their experience to be veridical automatically, however most people can suspend this response in order to make a more thorough examination of a situation.
They argue that what occurs in delusional patients is a “failure to inhibit a pre-potent doxastic response” thus meaning a person will immediately take any experience as veridical.34 As such, the aforementioned impairment to the belief evaluation system is argued here to be a failure to inhibit this response. If this were the case, the patient would be unable to properly evaluate hypotheses they generated themselves, but would be able to do so for hypotheses generated by others; thus the appreciation of implausibility problem is apparently solved. However this explanation does not seem entirely satisfactory, as it again encounters the monothematicity problem.
If delusional patients suffer from an inability to inhibit their pre-potent doxastic response, surely this would lead to any perceptual experience being taken as veridical and thus more than one delusional belief should be formed. I would suggest this account requires additional clarification, similar to the belief evaluation system being impaired but not destroyed. Although an isolated unusual experience may lead to an initial delusional belief being formed, if the experience does not recur the belief will be discarded when it is re-evaluated. Only if the unusual experience is continuously or repeatedly present is it impossible for the pre-potent doxastic response to be inhibited sufficiently to allow closer evaluation of the delusional belief. This is somewhat in accordance with Hohwy and Rosenberg’s account, though they assert that the failure to inhibit the pre-potent doxastic response occurs only in specific circumstances.
They state this response ensures people take experiences as veridical unless they are not in accordance with other beliefs.36 The belief is then subjected to further reality testing in which all the senses are employed. If this closer examination is not able to discredit the belief (as occurs in delusions due to the perceptual anomaly presenting the person with false data) then the belief is taken as veridical.
Essentially, they argue that reality testing inhibits the pre-potent doxastic response but if that fails then nothing else can inhibit it. However, unless the continuity and/or repetition of an unusual experience is taken into account, as is the damaged as opposed to abolished ability to inhibit the response, then we again face the problem that a single unusual event could cause the formation of a delusional belief as further ‘reality testing’ is not always possible, especially if the experience is unlikely to be repeated. Thus I would not entirely accept their interpretation, and prefer to say the ability to inhibit the response is simply impaired and functioning correctly only intermittently.
The two-factor theory, as outlined above, attempts to solve several problems encountered with one-factor models. The first factor required for the formation of a delusional belief is a neuropsychological anomaly that leads to a perceived unusual experience, prompting the formation of an explanatory hypothesis. In this respect I would agree with Maher’s argument that it is largely the strangeness of the experience that leads to the formation of a delusional hypothesis rather than a more plausible one. I would also tend to agree that the ‘structural coherence’ and ‘internal consistency’ of the delusional hypothesis, as termed by Maher, corresponds to the individual person’s intelligence, culture, religion, social background and so on.37 Langdon and Coltheart express a similar sentiment, stating that the type of hypothesis formed will depend on personal causal preferences as well as attributional biases.
This allows that following the same perceptual anomaly, not all people will develop a delusion and those who do will not all develop the same one. Though still imperfect, the most sustainable form of the second factor is an impairment of a person’s belief evaluation system in the form of a failure to inhibit the pre-potent doxastic response, rendering an individual incapable of adequately assessing evidence when evaluating a hypothesis.
An impaired rather than destroyed system accounts for why a delusional belief is only formed around a solitary idea or theme as the unusual experience must be continuously or repeatedly present. This constant reinforcement of the delusion does not allow the damaged system to ever adequately evaluate the hypothesis. A failure to inhibit a pre-potent doxastic response also accounts for why some patients cannot properly evaluate their own hypothesis but can do so with those of others and thus can have an appreciation for their own delusion’s implausibility.
In principle, the two-factor theory as outlined presents an adequate explanation for delusion formation and maintenance, however it is not without its problems. Although it is suggested that the first factor may have something to do with damage to the right lateral prefrontal cortex, it is also acknowledged that that impairment differs from patient to patient. A similar problem arises with the second deficit resulting in a failure to inhibit the pre-potent doxastic response; perhaps the result of the impairment is understood, but likewise not its biological form. Additionally, there is equal supposition about the actual cognitive process that transforms experience to belief.
As such, the two-factor theory relies on cognitive processes that are ill-understood, and on mental deficits that are almost equally obscure. The argument for the two-factor theory would be bolstered substantially if there were a significant number of documented cases of people with the same ‘phenomenology and neuroetiology’, where some develop a delusional belief and others do not.40 It is understandable however why there is a paucity of such documentation as patients with no symptoms would not become known to clinicians. It can thus be concluded only that the two-factor theory provides a plausible account of why monothematic delusions occur, yet it cannot be called truly successful until the cognitive processes of belief formation, and the mental deficit involved are better understood.
American Psychiatric Association, Diagnostic Statistical Manual of Mental Disorders, Fourth edition, Text Revision (DSM-IV-TR), 2000 Cahill, C. & Frith, C., False perceptions or false beliefs? Hallucinations and delusions in schizophrenia, in P. W. Halligan & J. C. Marshall (Eds), Method in madness, Hove: Psychology Press, 1996, pp. 267-291. Cahill, C. & Frith, C., False perceptions or false beliefs? Hallucinations and delusions in schizophrenia, in P. W. Halligan & J. C. Marshall (Eds), Method in madness, Hove:
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Reality Testing and Delusions of Alien Control, Mind & Language, Vol. 20 No. 2 April 2005, pp. 141–162 Langdon, R., Coltheart, M., The Cognitive Neuropsychology of Delusions, Mind & Language, Vol. 15, No.1, Feb 2000, pp.184-218 Maher, B. A., Delusional Thinking and Perceptual Disorder, Journal of individual psychology, Vol.30 (1), 1974, pp.98-113 Maher, B.A., Anomalous experience in everyday life: Its significance for psychopathology, The Monist, 82, 1999, pp. 547–70 McKay, R., Langdon, R., Coltheart, M., “Sleights of Mind”: Delusions, defences, and self-deception, Cognitive Neuropsychiatrym 10 (4), 2005, pp.305-326 McKay, R., Langdon, R., Coltheart,
M., Models of Misbelief: Integrating Motivational and Deficit Theories of Delusion, Consciousness and Cognition, 16, 2007, pp.932-941 Ortolotti, L., Delusion, The Stanford Encyclopedia of Philosophy, Edward N. Zalta (ed.), Fall 2010 Edition, URL = http://plato.stanford.edu/archives/fall2010/entries/delusion/ Radden, J., On Delusion, London, Routledge , 2011
Stone, T., Young, A. W., Delusions and Brain Injury: The Philosophy and Psychology of Belief, Mind & Language, Vol. 12, Nos. 3/4, 1997, pp. 327-364
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