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December 10, 2017 - March 14, 2018
have already criticized this account for being far too subjective – the understandability of delusions seems to depend, to some extent, on the effort made to understand them.
(The philosopher of science Sir Karl Popper argued that data that refute a hypothesis are nearly always more informative than data that appear to support it.43 This is because negative evidence can be decisive whereas positive evidence may support several alternative hypotheses. Popper therefore suggested that scientists should vigorously seek evidence that disconfirms their pet theories in the hope that there will be no such evidence. Ordinary people, however, usually seek evidence that favours their ideas, a phenomenon known to psychologists as the confirmation bias.44 Interestingly, some
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Mirowsky and Ross were able to show that, in their sample, persecutory beliefs, beliefs about external control, and mistrust were connected to socio-economic status and educational attainment in roughly the manner they had expected.
No matter how bizarre the ideas expressed by patients, it is usually possible to identify events in their lives that have contributed to their content. Of course, this observation does not imply that delusions are rational. (Very few people really are victims of government plots.) The nugget of truth is usually distorted in some way, and the challenge to psychologists is to discover how this happens.
The evidence we have considered so far concerns the impact of perceptual deficits on delusional thinking. An interesting but nearly overlooked possibility is that delusions might arise as a consequence of perceptual skills that are over-developed.
Despite the limited evidence for Maher’s theory, it is possible that perceptual and especially attentional processes play a role in maintaining delusional ideas, once they have been formed.
Frith and Corcoran’s ideas sparked off a series of studies by other researchers. Unfortunately, although these generally found that ToM skills are impaired in currently ill psychotic patients, the evidence that this kind of deficit is specifically associated with paranoid symptoms proved to be unclear.
This self-serving bias was markedly exaggerated in our paranoid patients, who appeared to be experts at blaming themselves for positive events and at avoiding blame for negative events.
This explanation would be consistent with a neglected theory of schizophrenia proposed by American psychologist Kurt Salzinger, who argued that many of the cognitive deficits experienced by patients are a consequence of their tendency to respond to the most immediate stimuli in their environment.
According to Popper, a single piece of disconfirmatory evidence can be enough to bring a theory to its knees, whereas confirmatory evidence may be equally consistent with rival theories.
Typically, the strategy we adopt when testing a hypothesis depends on the nature of the hypothesis. When some kind of choice is believed to have resulted in a good outcome (for example, when we believe that a cake is particularly nice because we used honey instead of sugar), it is sensible to test the hypothesis by looking for confirmatory evidence (for example, by baking another cake with honey but changing some of the other ingredients). This is because the result of the test is likely to be a further positive outcome (another nice cake). However, if the outcome is negative (for example, if
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It is possible that the ability of deluded patients to evaluate their hypotheses may be limited, not only by their inability to weigh evidence appropriately, but also by their avoidance of disconfirmatory information.
First, given that paranoid ideas involve worries about relationships with other people, they surely must have something to do with social cognition. Second, most people who have thought seriously about delusions in general have assumed that they arise from attempts to explain unusual or troubling experiences. This assumption seems to lie behind nearly every study that we considered in the last chapter.
In this case, a stumbling block seems to be the concept of self-esteem, which, as we saw in Chapter 10, fails to capture adequately the psychological processes involved in self-representation and can be measured in many different ways. Clearly, we need to turn to methods of assessing the self that more accurately reflect its dynamic nature.
our paranoid patients showed very little discrepancy between their self-actual and self-ideal concepts but very marked discrepancies between their self-actual concepts and their beliefs about how their parents saw them.
These implicit judgements echo relatively enduring stored knowledge and beliefs about the self, rather than what we consider to be our virtues and deficits at the present moment in time.
As perfectionistic self-standards presumably make individuals vulnerable to negative self-evaluations, these findings are consistent with the hypothesis that paranoid patients are strongly motivated to avoid threats to the self.
This picture is, of course, consistent with the idea of the attribution – self-representation cycle, which we arrived at a few chapters back (see Figure 10.6, p. 260). Remember that, according to this idea, attributions and self-representations are coupled in a cyclical relationship. Current beliefs about the self influence attributions, but attributions have the power to bring about changes in beliefs about the self (a psychological chicken-or-egg phenomenon).
However, the effects of external attributions depended on the precise nature of the attributions. External-situational attributions (the essence of good excuse-making, as in ‘I’m sorry I’m late but the traffic was dreadful’) led to few changes in discrepancies between beliefs about the self and ideals (‘I’m still the sort of person I’d like to be’) and very few discrepancies between beliefs about the self and beliefs about the opinions of other people (‘and other people still think I’m wonderful’). However, external-personal attributions (‘I’m sorry I’m late but the police deliberately set all
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Paranoid patients can therefore be accommodated within the model of the attribution–self-representation cycle if we assume that, like depressed patients, their stored knowledge about the self is very negative but, unlike depressed patients, they have somehow learnt to avoid making internal attributions for negative events, and instead tend to make external-personal attributions.
Against this argument it can be said that some phenomena just are unpredictable (the weather is a familiar example), and establishing when this is the case is an important kind of scientific achievement. (This is one of the main goals of the mathematical science of non-linear systems theory, more popularly known as chaos theory.)
First, hyper-vigilance to threat-related information might lead the paranoid person to notice person-relevant information more than ordinary people. Second, paranoid patients may suffer from some kind of cognitive disability that prevents them from noticing situational information.
More intriguingly, they seem to be more proficient than ordinary people at identifying negative emotional expressions on the faces of others.
appear to be specifically connected to paranoia. Nonetheless, I would now like to suggest that ToM deficits, even though they may not be specific in this way, might indirectly influence paranoid thinking by limiting the ability of patients to make situational attributions.
to use your ToM skills. If you are unable to do this, and especially if you are anxious to avoid blaming yourself, you may well attribute your friend’s behaviour to some kind of simple disposition or
In an attempt to test this prediction, Peter Kinderman, Robin Dunbar and I administered a ToM measure and also a measure of attributional style to a large group of students.28 As we had predicted, students who performed relatively poorly on our ToM task made more paranoid-style external-personal attributions than students who performed well, a finding that has since been replicated.29 Obviously, this study was limited by our use of students, rather than of people who were actually suffering from psychiatric symptoms. The necessary studies of the relationship between ToM skills and attributions
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We saw in Chapter 7 that emotional states cannot be identified by brute introspection, because they do not come with appropriate labels attached to them. Similarly, there is no reason to believe that perceptual states have the labels ‘real’ or ‘imaginary’ printed on them. We
Drawing this evidence together, it seems that vulnerable individuals are most likely to speak in an incoherent way when they are emotionally aroused, and they are most likely to be emotionally aroused when talking about personal issues.
some kinds of speech disorder (over-inclusive or vague references, ambiguous word meanings and confused references) increase when patients are asked to speak about emotionally negative topics, whereas others (missing referents and structural unclarities) are unaffected.
This concept of a functional relationship should not be confused with the idea that certain types of processes have a function for the individual.
in Chapters 12 and 13, we considered evidence that theory-of-mind deficits (the inability to understand the beliefs, thoughts and intentions of other people) may contribute to paranoid ideas. In Chapter 15 we saw that these kinds of deficits also appear to play a role in disordered communication. These relationships are portrayed together in Figure 16.3. Note that, according to this amalgamated model, we should expect paranoid delusions and disordered speech occasionally to occur together (because they are both influenced by theory-of-mind deficits). However, we should not expect this to
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One complication is that complaints sometimes cause each other.
Psychiatric complaints are connected by a rich network of functional relationships, which may be causal, or reflect shared causal pathways. Co-occurrence of complaints depends on the strength and number of these functional relationships. The more functional relationships connecting two complaints, and the stronger they are, the more likely it is that they will occur together.
A state is said to be some characteristic of the individual (a type of cognitive organization or a facet of personality) that is present during episodes of illness. A trait, on the other hand, is a more enduring characteristic that seems to precede the onset of complaints, and which is often thought to be aetiologically important.
Clearly, mental health professionals cannot afford to be complacent about their therapeutic impact on their patients. Indeed, it seems likely that there are high EE psychiatrists, high EE nurses and (although I do not like to admit it) high EE clinical psychologists who would probably be better employed doing something different.
Robert Finlay-Jones found that events associated with loss (broadly defined to include not only the loss of a person but also the loss of a role, goal or cherished idea) were especially likely to lead to depression, whereas events associated with long-term threat were more likely to lead to anxiety.
Brown’s colleague Tirril Harris has suggested that the events most likely to lead to psychotic and especially paranoid symptoms can be characterized as intrusive, because they involve unwanted experiences being forced on the patient (examples include threats, burglaries and police investigations).62 This suggestion has been partially supported by research conducted by other investi-gators.63 In the case of mania, as we saw in Chapter 11, it
the central argument of this book is that the problems involved in explaining ‘schizophrenia’ and ‘bipolar disorder’ will disappear once we have adequately explained the complaints that lead to these diagnoses.
According to Mojtabai and Rieder, twin and family studies show that a diagnosis of schizophrenia is more heritable than any of the symptoms that contribute to the diagnosis.
These findings show that thought disorder results from an interaction between genes and the environment.
When only a small proportion of individuals carrying crucial alleles develop a trait, the alleles are said to have low penetrance. In fact, the penetrance of an allele can be expressed as a simple percentage describing the proportion of carriers who are affected. Alleles also vary in their expressivity, which refers to the extent to which genetic traits, when present, vary in magnitude. The
It has been estimated that about 30,000 genes play a role in determining the structure of the human body, a number that is remarkably invariant across mammalian species that differ dramatically in the complexity of their nervous systems. By contrast, it has been estimated that the adult human brain contains about 100 trillion synapses, and that more than a quarter of a million of these are formed every second during the very early stages of development.
We would need to know the difference that the aberrant allele makes to that process, the role of the relevant proteins in brain development, the final consequences of any developmental abnormalities for the structure and function of different brain systems in adulthood, the cognitive processes that are supported by those brain systems and, last but not least, the role of those processes in patients’ complaints.
Third – and this is perhaps the most important conclusion – it seems likely that any genetic contribution to psychosis is caused by many genes of minor effect. Despite the limitations of existing methods, if just one or two genes played a major role, they would almost certainly have been identified by now. For this reason, it seems much more likely that many genes each make a small contribution towards vulnerability to symptoms.
The more complaints people have, the more psychosis genes they are likely to have inherited, and the more likely it will be that some of those genes will be shared by close relatives. Because of the role that other factors play in each complaint, an affected person’s close relatives may not experience the same complaint. However, if they have a sufficient number of psychosis genes, enough may be expressed as complaints to enable them to meet the criteria for a global diagnosis. As a consequence, the diagnosis will appear to be more heritable than each of the complaints.
of 10 or as late as the age of 70 or afterwards. In fact, despite the over-representation of adolescents among people experiencing their first episode of psychosis, it seems likely that the number of non-adolescents experiencing psychotic symptoms for the first time exceeds the number of adolescents.
Psychopathologists have studied three different kinds of non-optimal relationships between children and their families. The first involves some kind of disruption of the emotional bond that is usually formed between parent and infant at the beginning of the infant’s life. This kind of bond, known as an attachment relationship, has been the subject of intense investigation by psychoanalysts, psychologists and animal behaviourists. The second kind concerns the emotional climate that develops in families as the child grows older, and is reflected in the concepts of expressed emotion and affective
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recent studies of insecurely attached human children have revealed that they are handicapped by subtle social-cognitive deficits that may not be obvious to the casual observer.
Peter Fonagy and his colleagues at University College London12 and by Elizabeth Meins at Durham University13 have shown that children between 4 and 6 years of age who are insecurely attached perform less well than securely attached children on tests designed to measure their ability to understand the mental states of other people (‘theory-of-mind’ skills).
parents’ emotional ambivalence towards their children increases the risk that they will grow up to suffer from positive
