How neuropsychological and attributional processes are involved in the evolution
Delusional beliefs are a common positive symptom of schizophrenia, among other disorders. Neuropsychological and attributional processes are involved significantly in the evolution and maintenance of delusional beliefs and subsequent studies will enhance this view. The argument is which of these views better explains the prevalence of delusions and their evolution and specifically which aspect allows the preservation of these beliefs. Delusional beliefs have been defined as a false perception (Frith 1987). The term belief has obtained additional meanings implied by the ideas that beliefs cause behaviour and they are attributes of people.
In her book, Boyle (1996) suggests that there are several characteristics, which are necessary for the perception to be endorsed as a delusional belief. The foremost idea is falsity, the presence of which determines the delusional status of the belief in question. The belief must also be held with absolute conviction that is incorrigible, it is often preoccupying, it is usually absurd and it is not culturally shared. Delusional distress can fluctuate over time and can be reduced by specific cognitive behaviour interventions.
Delusions are therefore now conceptualised as dimensional entities rather than categorical ones, lying at the extreme end of a belief continuum. According to one view, Maher (1974), delusions arise when a patient applies normal logic to an abnormal experience or perception. An example transpires that a man who is hearing voices may deduce that the BBC have invented a machine to broadcast these voices and are experimenting on him using this machine. There seems though to be an apparent ease with which irrational beliefs can be provoked in ordinary people during abnormal experimental conditions.
This explanation is only upheld if the patient has a prominent symptom, which they are trying to rationalise. However, it works less well in cases where there is no perceptual abnormality that needs to be explained. This theory also predicts that if normal people are subjected to abnormal experiences, then they too would develop delusions. However, this logic is un-testable as it is not ethically viable. This theory could also be disproved if it could be demonstrated that patients with delusions have abnormal logic.
If we continue with the theme of abnormal logic, it then transpires that if the perceptions are normal, the subject must be misinterpreting the incoming information to result in delusions. The fundamental idea suggests that some information is ignored, whereas the rest is over emphasised (Frith 1992). It is difficult to see how an adequate account of the development of individual belief systems can be offered without reference to their content, people will presumably construct explanations or infer meanings about events which are of concern to themselves.
These hypothesis surrounding events are maintained often in the face of very conflicting information in normal people. Brennan and Hemsley (1984) suggested the term illusionary correlation for this idea that subjects sometimes perceive relationships between unrelated stimuli. It was suggested that paranoid delusions were perhaps a very exaggerated form of this natural human tendency. Illusionary correlations were found between words paired at random in paranoid patients, especially when the words were of a persecutory content. This evidence indicates that the idea of delusional thinking might just be an extreme form of natural thinking.
The question arises as to the origin of these delusions. Brennan and Helmsley suggests that rather than a failure of reasoning of deluded patients, they suggest that reasoning fails only in relation to the understanding of human interactions. The maintenance of these delusional beliefs could be a result of the schizophrenic who has an impairment of social knowledge and his friends allow this line of thinking to continue, however, this is only speculation on my part. Periodically, patients with delusions report that the thoughts in their heads are not their own thoughts, e. g. he man from the BBC is inserting them.
This implies that the patients have some way of labelling their own thoughts and the abnormal thoughts and making a deduction over which are their own and which are foreign. It is not an irrational supposition then to suggest that alien thoughts are the result of a flawed labelling system. Frith (1992) proposes that this idea is the backbone of all delusions, and many more positive symptoms of schizophrenia. He also suggests that is not only monitoring of action that is impaired in schizophrenia but also the monitoring of intentions to act.
Frith suggests there is a two step process in the utilisation of central monitoring. Firstly the individual must be able to distinguish between events caused by their own actions and events caused by other people, therefore the relationship between actions and external events are monitored. Secondly the individual must be able to discriminate between activities caused by willed actions, such as their own goals and plans and stimulus driven actions, such as actions in response to external events. The awareness of the cause of our actions is resultant from the monitoring of such events.
Frith (1992) advocates that different areas of the brain are associated with willed action and stimulus driven action and the distinction of these delusions could be made on which brain system is active. Frith proposes no concrete evidence for this piece of information and could merely be speculation on his part. However, it account effectively for the evolution of delusional beliefs. Evidence put forward by Frith supports that central monitoring systems are faulty in schizophrenia (Frith and Done, 1989; Malenka 1982; cited in Frith 1992).
In both these experiments, subjects were asked to follow a target on a computer screen with a joystick and their ability to correct errors in the absence of visual feedback. The patients were unable to correct their errors in the absence of visual feedback. This supports the theory as the patients were unable to monitor their own intentions and couldn’t make rapid error corrections. Other studies also cited in Frith 1992 (Cohen 1991; Mlakar 1990) also support the idea using very similar procedures to obtain the result.
This could be a point in this analysis; obviously the studies were predisposed to reaching similar conclusions if the procedure was the same. However, it still remains that the results confirm and impairment in self-monitoring. This lack of self-monitoring would have the consequence of a lack of awareness in intended actions and thus could underlie the evolution of delusions. The ability to infer mental states of others in order to predict and explain behaviour has been conceptualised as the possession of a theory of mind.
Persecutory delusions reflect false beliefs about the intentions and behaviour of others and these could arise from theory of mind deficits. Frith (1992) proposed that theory of mind deficits underpin the origins of delusions of persecution, delusions of reference, delusions of misidentification. There has been much research into this area using different methods of assessment to establish the attributional processes involved in the evolution and maintenance of delusional beliefs.
A study by Corcoran and Frith (1996) demonstrated that deluded patients frequently had difficulties in theory of mind tests, such as the ability to infer the reasoning behind the sentence ‘its hot in here’ – which should have been taken to mean ‘open the window’. However, this study was flawed by the failure to match the patient and comparison groups for IQ, and as this was a theory of mind test, should not have been overlooked. A quantity of research to support this theory has been put forward but the majority has been confounded by measures such as current IQ and memory, as the information processing load for ill patients was to great.
However, it is still possible to draw tenable conclusions from the data, there still remains a degree of poor performance by schizophrenic subgroups which are too large to dismiss as memory and IQ problems alone. Only two studies have provided indisputable support for a theory of mind hypothesis in subjects with persecutory delusions (Frith 1995, Frith 1996, cited in Blackwood) and even these lean to the angle of psychomotor poverty. Paranoid patients have demonstrated a consistent reasoning bias in one particular area, that of jumping to conclusions in tests of probabilistic reasoning.
Bayesian models specify whether a subject’s confidence in a current belief should increase or decrease according to the value of new evidence received, (Hemsley & Garrety 1986). This study used Bayes’ decision-making theorem as a theoretical basis for examining reasoning biases in deluded subjects. It argues that Bayesian theory provides a normative model of the way in which evidence relevant to normal beliefs may be evaluated making it possible to classify delusional beliefs in terms of deviations from optimal Bayesian inference.
The hypothesis that patients with delusions are more prone than normal individuals to draw firm conclusions based on ambiguous evidence was examined in a series of studies using affectively neutral material. The subjects were asked to make inferences from which jars a bead had been drawn, where jar A contained predominantly white beads and jar B, predominantly black. The subjects were relatively overconfident in their decisions, which were, on the whole based on significantly fewer beads than the control subjects.
However, again the study’s limitations are grounded in the idea that delusional severity is not measured, nor is symptom specificity examined. This study merely suggests preliminary evidence that there are data gathering biases in delusional states suggesting that they may be implicated in delusion formation rather than simply maintenance of existing false beliefs. A study by Freeman (1999) examined a role for a neglected factor, anxiety in the maintenance of delusional beliefs.
It was hypothesised that the processes responsible for chronic worry, as detailed by A Wells’ 1994 metacognitive model (Cited in Freeman 1999), contribute to delusional distress. Questionnaire measures of anxiety, chronic worry and of meta- worry and related processes were administered to 15 individuals with persecutory delusions and 14 with generalised anxiety disorder (GAD). It was found that many of the individuals with persecutory delusions had high levels of general worry, and the factors implicated in the metacognitive model of anxiety were also present in this group.
The results indicated that delusional distress is not simply related to content but is associated with whether the individual experiences meta-worry concerning the control of delusion relevant worries, that is, whether they worry about not being able to control thoughts about the belief. This evidence suggests no origin for the evolution of these beliefs and must only be considered as an explanation for the maintenance of already present delusions. Attributional theory provides a framework for understanding the causal explanations that individuals give for their own behaviour and the behaviour of others.
Normal people consistently demonstrate a self-serving attributional bias in explaining the causes of events. Internal attribution of positive events would take the form of taking credit for success, this is self-enhancing bias, whereas, in opposition the external attribution of negative events would be the denial of responsibility for failure. This self-protective bias may serve to enhance self-esteem. Blackwood’s (2001) work in this area used questionnaires to ask participants to surmise the likely causes of hypothetical positive and negative events.
It exposed that patients with persecutory delusions show an exaggeration of this self-serving attributional bias. It gives the impression that these patients excessively attribute hypothetical positive events to internal causes and hypothetical negative events to external causes. Deluded patients with non-persecutory delusions do not differ from normal subjects in their attributional style suggesting that attributional bias in paranoid subjects shapes delusional content rather than form.
The study also makes the suggestion that paranoid patients are additionally abnormal in that negative self-referent events are attributed to functioning evil on the part of the other person that would be seen as external personal attribution rather than to chance, for example. Blackwood suggests that this exaggerated attributional bias functions to preserve self-esteem by limiting conscious awareness of negative aspects of the self, stored in the semantic memory.
The creation of these inconsistencies would lead to a loss of self-esteem. This attributional bias ensues at the expense of contributing to the paranoid patients negative perceptions on the intentions of others. This study is valuable if we are looking for the mechanisms under which delusions evolve as the “persecutory delusion as defence hypothesis” (emphasis in original) predicts that persecutory delusions will be associated with firstly normal levels of overt self-esteem and secondly low levels of covert self-esteem.
The study however was flawed with limitations such as its cross sectional nature, a failure to measure the dimensional severity of delusional beliefs, and a failure to examine symptom specificity. There seems to be evidence for externalising personal attributional bias for negative events for subjects with delusions. However the support for the persecutory delusion as defence hypothesis is less well supported. Longitudinal studies of the relationship between the attributional bias and delusional ideation are required to infer if the relationship is at all causal or merely secondary.
A Neuropsychiatric perspective on the causes of delusions might suggest the correlation between regional cerebral blood flow and delusions (Neufield 1996). A positron emission topography (PET) study of a group of patients with chronic schizophrenia demonstrated significant positive correlations between the reality distortion dimension and regional cerebral blood flow in left frontal (lateral prefrontal cortex), ventral striatal and temporal areas. These results were obtained as a result of a study on matched groups and have highlighted the importance of the medial, temporal and ventral striatal limbic areas.
Research has also highlighted another area of the brain, which is involved in the evolution of delusions. Neufield and Gardner (1996) investigated inferior lobe functioning which has been shown to be a factor in schizophrenic patients, yet studies are limited on the symptoms of delusions as a separate entity. The Wisconsin Card Sorting Test was administered to paranoid, non-paranoid, undifferentiated and disorganised schizophrenics and also to non-patient controls.
The outcome of the experiment showed that the performance of paranoid patients was significantly inferior to the controls on each of the two frontal measures. Perseverative errors on the WSCT are known to covary with symptoms displayed by frontal lobe patients. Another clue about the brain systems underlying the positive symptoms such as delusional beliefs comes from the beneficial effects of dopamine blocking drugs. The action of these drugs gives an indication to the maintenance of delusional beliefs.
Treatment with these drugs can markedly reduce the severity of positive symptoms but has little or no effect on negative symptoms. Dopamine is involved with the creation of willed action. It has been suggested by Frith (1987) that a reduction of domaminergic activity, as happens in Parkinson’s disease, or after treatment with antipsychotics should reduce the ability of the subject to generate willed actions. In other words, dopamine-blocking drugs should if anything, intensify negative symptoms.
Positive symptoms on the other hand occur because patients act without being aware of any intention to act, as suggested earlier. The patients have abnormal experiences because of the discrepancy between what they are doing and their awareness of what they intended to do. This analysis is based on the effects of a medical drug, which could give us a false idea surrounding the neuropsychological processes, which underlie the formation of delusions, as the brain is a very misunderstood entity.
In conclusion, it is only correct to summarise that delusions are still a complex symptom and the processes that lead to their formation are numerous in suggestion. However, some evidence is more concrete than others, which is merely circumstantial. The evolution and maintenance of delusional beliefs can be concluded to be a result of numerous events neuropsychological and attributional, yet more research world clarify the reasoning.