Delusions

What is a delusion? Include all key characteristics.

A delusion is a false belief that is maintained in the face of convincing evidence to the contrary. It is a prominent feature of psychoses such as schizophrenia. Psychotic individuals typically have delusions about only a single topic, known as monothematic delusions.

What distinguishes monothematic delusions from other types of delusions?

Monothematic delusions focus on only a single topic, whereas other delusions may involve multiple topics or themes.

Define Capgras delusion and provide its key characteristic.

Capgras delusion is the belief that a close relative or spouse has been replaced by an identical-looking impostor.

What is mirrored-self misidentification?

Mirrored-self misidentification is the belief that one's reflection in the mirror is some other person (not oneself).

Define Cotard delusion.

Cotard delusion is the belief that one is dead or does not exist.

What is reduplicative paramnesia?

Reduplicative paramnesia is the belief that a place has been duplicated.

Define somatoparaphrenia.

Somatoparaphrenia is the belief that a limb or an entire side of one's body belongs to someone else.

What are the three main approaches to understanding delusions mentioned in the material?

The three approaches are: (1) Psychodynamic approach, (2) Neurochemical approach, and (3) Cognitive neuropsychological approach.

Explain the psychodynamic interpretation of Capgras delusion.

The psychodynamic interpretation suggests that Capgras delusion resolves conflicting feelings of love and hate. It becomes acceptable to hate the double (impostor) rather than the actual loved one.

What are the key principles of the cognitive neuropsychological approach to delusions?

The cognitive neuropsychological approach: (1) treats belief formation and evaluation as cognitive processes, (2) considers how these processes could be disrupted, (3) relates disruptions to neural mechanisms and dysfunctions, and (4) is applied primarily to monothematic delusions.

According to the two-factor theory by Coltheart and colleagues, what causes monothematic delusions?

Monothematic delusions result from two co-occurring cognitive deficits: one deficit that suggests the belief, and a second deficit that prevents it from being rejected as absurd.

What is Deficit A in the two-factor theory? What question does it answer?

Deficit A is the deficit that suggests the belief. It answers the question: "Where did the delusion come from?" or "What suggested the false belief?"

What is Deficit B in the two-factor theory? What question does it answer?

Deficit B is the deficit in belief evaluation. It answers the question: "Why did the patient not reject the belief?"

Why are TWO deficits necessary to explain delusions according to this theory?

Two deficits are necessary because: (1) Deficit A alone creates a situation that could be explained by the belief but doesn't guarantee the delusion will form, and (2) many people with only Deficit A do not develop the delusion. Deficit B is needed to explain why the false belief persists despite strong contradictory evidence.

Describe the case of Mr. A (Silva et al., 1995). What were his specific beliefs?

Mr. A believed that his sister, mother, and grandmother had been replaced by physical doubles; the original family members had been kidnapped by the mafia; and the doubles were mafia members with plans to kill him.

What dangerous behaviors did Mr. A exhibit as a result of his Capgras delusion?

Mr. A held a gun on his grandmother, threatened to burn down the house to kill the doubles, and turned on the gas during the night to kill the imposters.

What is the hypothesized Deficit A in Capgras delusion?

Deficit A is a deficit affecting emotional responses to faces. Specifically, familiar faces fail to evoke the normal affective response, even though the face is recognized and knowledge about the person is activated.

How does the affective response deficit explain the CONTENT of Capgras delusion?

The absence of the accustomed emotional response when seeing a familiar person suggests the possibility: "Maybe this is not really my mother/wife/husband/child." This explains why the delusion specifically involves imposters.

Why is the affective response deficit alone NOT sufficient to explain Capgras delusion?

Two reasons: (1) Many people with the affective response deficit do not develop the delusion, and (2) the delusion persists in the face of strong evidence to the contrary, suggesting another factor is needed.

What is Deficit B in Capgras delusion? What brain region is implicated?

Deficit B is impaired belief evaluation—an impairment in rationally evaluating grounds for belief. It is hypothesized to be caused by right frontal damage.

Explain the complete two-factor interpretation of Capgras delusion.

The failure of faces to evoke affective response (Deficit A) suggests the possibility that family members are imposters. If this is the only deficit, belief evaluation processes would reject the possibility. But if there is also a deficit in belief evaluation (Deficit B), the false belief may be accepted and maintained despite contradictory evidence.

Describe the normal face processing mechanism and where it goes wrong in Capgras patients.

Normally, a familiar face activates the stored face representation and knowledge about the person, AND triggers the usual emotional response. In Capgras patients, the face activates recognition and knowledge, but the usual emotional response does not occur.

What evidence supports the idea that familiar faces fail to elicit affective responses in some Capgras patients?

Evidence has been reported (though the specific studies aren't detailed in this material) showing that some Capgras patients show absent or reduced affective/emotional responses to familiar faces.

Describe patient FE's demographic information and delusion.

FE was a 78-year-old man who owned several successful businesses before retiring. He believed his reflection in the mirror was another person who followed him around. He was diagnosed with early-stage dementia.

How did FE's delusion evolve over time?

Eventually, FE also had difficulty recognizing his wife's reflection and incorporated it into his delusion, stating: "I have met the stranger's wife, seen her. I don't think she talks either."

Did reasoning and evidence shake FE's belief? What does this tell us?

No. His family's attempts to reason with him did not shake the belief, although he could state their arguments. This demonstrates the persistence of the delusion despite contrary evidence.

List ALL of FE's face processing test results.

Face matching (Benton test): Severely impaired; Simpler matching test: Severely impaired; Male/female face classification: Mildly impaired; Famous face identification: 1/40 correct—severely impaired; Distinguishing famous and unfamiliar faces: Severely impaired (classified 9/10 famous faces as familiar AND 9/10 stranger faces as familiar); Recognizing immediate family members: Successful, but some difficulty with other relatives.

What does FE's severe face matching impairment specifically suggest about his deficit?

It suggests a perceptual processing deficit: FE is impaired in generating a structural description from a visual face stimulus. This is a low-level face processing problem.

What is Deficit A in FE's case according to the two-factor interpretation?

Deficit A is a face perception deficit. When FE looks in the mirror, the person he sees doesn't look exactly like himself, suggesting the possibility: "It's someone else who looks quite a bit like me." His poor face recognition may have resulted in uncertainty about the identity of the face in the mirror.

What is Deficit B in FE's case? What evidence supports it?

Deficit B is a belief evaluation deficit. However, no specific evidence for this deficit was presented, except that MRI and neuropsychological testing indicated right-hemisphere dysfunction.

Describe patient TH's demographic information and neurological findings.

TH was a 77-year-old man who worked as a farm laborer, truck driver, maintenance worker, and evangelical missionary. He had mirrored-self misidentification delusion. MRI showed diffuse cerebral atrophy and a small cortical infarct in the posterior right frontal lobe.

How did TH's face processing abilities compare to FE's?

Unlike FE, TH showed normal or nearly normal performance on face perception and recognition tasks. This means his Deficit A must be different from FE's.

What is Deficit A in TH's case according to Breen et al.?

Deficit A is impaired understanding of how mirrors work (mirror agnosia). Due to his neurodegenerative disease, TH thinks that a mirror is like a window that shows a scene behind the mirror, rather than a reflection of the scene in front of the mirror.

How does TH's mirror agnosia lead to his delusion according to the two-factor theory?

TH's misunderstanding of mirrors suggests the belief: "The person I see in the mirror looks like me, but is someone else" (because he thinks he's looking through a window at someone behind it, not at his own reflection).

Describe the mirror understanding test conducted with TH and his responses.

TH sat facing a mirror. Objects (such as an apple) were held up behind his left or right shoulder. He was asked to identify the object and then reach for it. The correct response would be to reach back over his shoulder. Instead, TH reached toward the mirror on each occasion, scratching on the mirror surface or attempting to reach into or behind the mirror. This occurred repeatedly over 20 trials.

In the post-test discussion, what did TH say when asked where his reflection was?

TH said: "It's behind me. It would have to be. When you look in a mirror, you can see the reflection of everything in front of the mirror... My reflection would be on something behind me, behind my back. I've never seen my reflection and the other person together."

What does TH's statement "I could take it if I could get up and walk around this glass" reveal about his understanding?

It reveals that TH treats the mirror as a physical barrier (like glass or a window) that he could walk around to reach what he sees "behind" it, rather than understanding it as a reflective surface.

What is Deficit B in TH's case?

Deficit B is a belief evaluation deficit (same as in other cases), though specific evidence for this particular deficit in TH is limited.

Compare and contrast the Deficit A in FE versus TH's mirrored-self misidentification.

FE: Face perception deficit—impaired in generating structural descriptions from visual face stimuli, so faces don't look quite right. TH: Mirror agnosia—misunderstands how mirrors work, treating them like windows rather than reflective surfaces. Both deficits lead to the same delusion but through different cognitive mechanisms.

Why is it significant that both FE and TH have the same delusion but different Deficit A patterns?

It demonstrates that the same delusional content can arise from different underlying cognitive deficits. This supports the idea that delusions are the result of a cognitive attempt to explain abnormal experiences, rather than having a single unified cause.

What aspects of the cognitive neuropsychological approach to delusions are considered promising?

The cognitive neuropsychological approach is promising, at least for monothematic delusions, because it provides a systematic framework for understanding how cognitive deficits lead to specific delusional beliefs.

Why does the two-factor theory seem plausible according to the material?

The theory seems plausible because: (1) a cognitive deficit creates a situation that could be explained by the belief, and (2) a belief evaluation deficit prevents proper evaluation and rejection of the belief in light of available evidence. This explains both the origin and persistence of delusions.

What are the two main challenges or limitations of the two-factor theory?

The two challenges are: (1) The theory is somewhat vague, especially regarding deficits in belief evaluation, and (2) Evidence for the belief evaluation deficit in individual cases is typically weak or absent.

Why is the lack of specific evidence for Deficit B (belief evaluation deficit) problematic for the two-factor theory?

It's problematic because the theory requires two deficits to explain delusions, but if researchers cannot consistently demonstrate or measure the second deficit in individual patients, it weakens the empirical support for the theory and makes it difficult to test or falsify.

How would you apply the two-factor theory to explain why most people with prosopagnosia (face blindness) do NOT develop Capgras delusion?

People with prosopagnosia may have a face processing deficit (potential Deficit A), but they likely have intact belief evaluation systems (no Deficit B). Therefore, even though faces may seem unfamiliar or strange, their belief evaluation processes lead them to the more rational explanation (face recognition problem) rather than accepting the impostor hypothesis.

According to the material, which approaches to delusions are considered "traditional" as opposed to the cognitive neuropsychological approach?

The traditional approaches are psychodynamic and neurochemical approaches.

What makes the cognitive neuropsychological approach different from traditional approaches?

The cognitive neuropsychological approach specifically treats belief formation and evaluation as cognitive processes that can be studied systematically, considers how these processes could be disrupted, and relates them to specific neural mechanisms and dysfunctions—rather than focusing on unconscious conflicts (psychodynamic) or chemical imbalances (neurochemical).

Why is the two-factor theory applied primarily to monothematic delusions rather than all delusions?

The material states that the cognitive neuropsychological approach is applied primarily to monothematic delusions, suggesting these are more amenable to this type of analysis because they involve a specific, circumscribed false belief that can be traced to identifiable cognitive deficits, unlike more complex polythematic delusions.

For Capgras delusion, explain why family members' attempts to provide evidence against the delusion typically fail.

The attempts fail because of Deficit B—the impaired belief evaluation system. Even when presented with strong contradictory evidence, the patient cannot properly evaluate and reject the false belief due to the belief evaluation deficit (hypothesized to involve right frontal damage).

What is the relationship between right frontal lobe damage and delusions according to the material?

Right frontal damage is hypothesized to cause Deficit B (impaired belief evaluation) in the two-factor theory. TH had a small cortical infarct in the posterior right frontal lobe, and right-hemisphere dysfunction was noted in FE's case, supporting this hypothesis.