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Pathogenesis of Delusions
DELUSIONAL DISORDERS
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PATHOGENESIS OF DELUSIONS Theo C. Manschreck, MD
Delusions are the cardinal symptoms of psychopathology. Despite their importance in a wide range of psychiatric disorders, understanding of delusions is markedly limited. Virtually every facet of the subject of delusions remains uncharted according to the standards of scientific methodology. Even phenomenology, certainly biologic underpinnings but also the role of culture and the psychology of delusions are subjects sorely in need of research elaboration. Pathogenesis is a critical dimension in the study of delusion. Specifically, pathogenesis refers to the mechanisms underlying the formation and maintenance of delusional thinking. This article summarizes what has been proposed to account for the pathogenesis of delusions, identifies the gaps in our knowledge, and suggests strategies for closing these gaps. PHENOMENOLOGY
Phenomenology of delusions is a useful starting point for discussion of the pathogenesis. Phenomenology constitutes one foundation of our understanding of delusions. Unfortunately, phenomenologic advances have come slowly and have been accompanied by considerable controversy. In the European tradition, phenomenology refers to the description of the nature of the inner life of the patient. Clearly this focus has relevance to understanding the nature of delusions in that the clinical judgment that the patient has a delusion derives largely from subjective report by the patient. 54 Much of the European literature in the early part of the twentieth century was devoted to the phenomenologic method and emphasized the value of clinical dialogue with the patient to ascertain a clear understanding of delusional experience. Two major contributions to From the Department of Psychiatry and Human Behavior, Brown University School of Medicine, Providence, Rhode Island
THE PSYCHIATRIC CLINICS OF NORTH AMERICA VOLUME 18 • NUMBER 2 • JUNE 1995
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this effort are worth mentioning. The first was from Karl Jaspers, the psychopathologist and philosopher who formulated the definition of delusion widely used today. 26 Jaspers' criteria for delusions were as follows: 1. Subjective certainty 2. Incorrigibility 3. Realistic impossibility (later: falsity of content as some delusions are possible). Jaspers was tentative about the strictness of his criteria, preferring to view them as approximations to a definition; for example, impossibility of a belief was modified to falsity of the belief as some delusions are indeed possible (as in delusional disorder). Falsity of a belief depends on the availability of empirical evidence; and in the case of religious delusions, such evidence may not be available. In practice, the judgment that a belief is delusional often rests as much on the behavior of the patient who expresses the belief as on its falsity (which may be difficult to demonstrate) and the unwillingness to give in to counter argument (see section on clinical assessment). The second contribution dealt with the distinction between primary and secondary delusions. 26 • 48 A primary delusion arises from no other identifiable source; its detection has diagnostic significance in that such delusions are believed to be characteristic of schizophrenia. Kurt Schneider's concept48 of delusional perception and current descriptions of what are called mood incongruent delusions likely would be classified as primary delusions. Secondary delusions, on the other hand, arise on the basis of altered mood, personality, or other features and possess less diagnostic significance. Mood congruent delusions, as in mania or psychotic depression, would be examples of secondary delusions. Mood or affect influences on the delusion formation were proposed by Bleuler4 as well as Jaspers and Schneider; the latter viewed affect as a distinguishing feature in the recognition of primary and secondary delusions. The distinction between primary and secondary delusions derived in part from attempts to explain the differences between delusions that arose in disorders that had an organic basis, in contrast to disorders in which "functional" causes were considered likely. In practice, the distinction between primary and secondary delusions has been criticized as impractical and lacking validity because of (1) the difficulty in defining and reliably identifying or eliciting primary versus secondary delusions and (2) the vagueness and theoretic nature of the functional disorder concept. Nevertheless, phenomenologic investigation has produced important insights about the main descriptive features of delusions. These are Theme Understandability Degree of certainty Systematization Complexity Relevance to patient's life Plausibility
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CLINICAL ASSESSMENT
In clinical encounters, delusions usually are easy to detect. Certain behavioral features (hypersensitivity, irritability, guardedness, evasiveness, litigious behavior, secretiveness, self-righteousness, obstinance, fear, humorlessness, preoccupation with details, and hostility) may suggest their presence or solidify the impression that the patient's beliefs are delusional. Associated psychopathologic symptomatology, such as hallucinations, disturbed form of thought, and mood disorder, also may provide clues that delusions are part of the clinical picture (and assist in their diagnosis). 36• 39 The clinical challenge is more obvious in subtle cases wherein the suspected delusional thinking may be difficult to detect or to diagnose as delusional. Fundamentally, the clinician must make a judgment, based on assessment of the behavior and the reported private mental experience of the patient, that delusional belief(s) are present. Attempts to dissuade the patient with counter evidence and argument may be useful to determine whether the patient's feelings can be influenced with evidence usually sufficient to alter the belief of a normal person. (Recent reports 6 • 7 indicate that reality testing may be a useful treatment for delusions.) The judgment often relies on determining whether a threshold indicating psychopathologic disturbance has been passed, as reflected in the extremeness and the inappropriateness of the patient's behavior, as opposed to the simple truth or falsity of the belief. Indeed, not infrequently, the patient may not reveal the belief at all; it must be inferred from the behavior that a delusion is likely. The most sensible guideline, applicable to all suspected cases of delusional thinking, is to gather as comprehensive a picture as possible concerning the condition of the patient (especially regarding evidence for psychopathologic symptoms). Such information should reduce much of the uncertainty present in the evaluation of delusions. Until there is an objective laboratory test for delusional thinking, it will be necessary to apply clinical judgment in all cases to varying degrees. In view of this limitation and the potential significance of being wrong, the clinician should apply his or her judgment humbly. 36 In short, phenomenology and clinical assessment constitute somewhat weak methods for detecting and describing delusions, procedures necessary for establishing and testing proposals about delusion formation.
PATHOGENESIS
Establishing a scientific understanding of the pathogenesis of delusions presents a number of problems. As indicated previously, there are fundamental issues that have to do with the very definition of delusion as well as critical limitations related to its application in clinical practice. These limitations obviously pose a considerable challenge to the
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opment of a general theory of delusion formation. Nevertheless, there have been many attempts to do so,2 and these are outlined in subsequent sections. Before we review those theories, however, it would be useful to identify what is required to be explained in a theory of delusion formation. Unfortunately, most theories fail to specify this information in advance, and this has led to theoretical formulations that have limited relevance to the breadth of issues associated with pathogenesis. Also, general theories, however promising or appealing, have been of limited value to psychiatry and often have failed to provide an adequate level of conceptual precision to propose testable hypotheses for advancement of knowledge. On the other hand, this area might benefit from what might be described as mid-range theorizing; that is, identifying a selected domain of investigation and developing models and hypotheses based on empirical data so that further conceptual and theoretical refinement could occur. 38 The study of specific psychopathologic symptoms, such as delusions and hallucinations, are good candidates for such activity as Costello 10 and Persons46 have argued so persuasively. In addition to requirements for an adequate theory of delusion formation, other issues need to be taken into account. For example, one of the key and critical problems facing the field of psychopathology is the problem of heterogeneity. Heterogeneity refers to the likelihood that many of the psychopathologic syndromes arise from different and possibly numerous causes. Hence, we need to be able to relate any theory of delusion formation to the possibility that multiple causes could lead to similar manifestations and delusion formation. Related to this issue, of course, is the role of personality in the formation of delusions. We know that personality has an effect on the nature of delusion. The extent and nature of that effect remain largely unexplored areas, in part because empirical research has been limited. 2 What then are the features that need to be specified in order to have an adequate theory of delusions? An adequate hypothesis for delusion formation must deal with certain important facts: 1. Delusions occur in a number of medical and psychiatric disor-
ders.14, 36, 37, 39, 50 2. Not all individuals with these disorders will develop delusion. 59 3. The content of delusions boils down to a relatively short list of specific types, despite the variety of disorders and diseases associated with their occurrence. 33· 37 4. Delusions can respond to treatment of the underlying condition that led to their formation. 37· 59 5. Delusions can persist and become systematized. 26 6. Delusions often accompany perceptual changes such as impaired sensory input or hallucinatory experiences. 8· 9· 23 7. Delusions may be highly encapsulated features in individuals and functioning may not be compromised in terms of social, intellectual, or affective responsiveness. 37· 47
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In addition, any adequate hypothesis of delusion formation also must respond to two questions. First, why is it that the patient has a delusion? This particular question refers to the form of psychopathology. Second, why does the patient have this particular delusion? This question concerns the content of a psychopathologic experience. Winters and Neale61 organized many of the theories of delusion formation in terms of two general categories of origin: motivation and defect. This proposal is useful for many problems associated with understanding delusions but not for all, as at least one key approach is not addressed. Hence, it is convenient to address the issues of pathogenesis by thinking about three broad categories of hypotheses: 1. A pattern of deviant motivation such that an otherwise intact cognitive system is distorted in the service of motivation (psychodynamic mechanism, social attribution). 2. A fundamental cognitive defect that impairs the patient's capacity to draw valid conclusions from evidence (disorder of reasoning). 3. The cognitive processes of the deluded patient are fundamentally intact, but the delusion arises from normal cognitive activities directed at explaining abnormal experiences (psychobiologic mechanism, anomalous experience hypothesis). These hypotheses need not be mutually exclusive. It is quite possible that delusional beliefs arise as the outcome of different processes and sequences involving one or more of these mechanisms. Attempts to identify the mechanism of pathogenesis in delusion formation have been numerous. The following discussion is presented in a chronologic framework. The first major proposal about delusion formation explored the psychodynamic mechanism.
PSYCHODYNAMIC MECHANISM
Sigmund Freud19 published "Psychoanalytic Notes Upon an Autobiographical Account of a Case of Paranoia (Dementia Paranoides)" in 1911. Freud's interpretation of this case became the foundation of the psychodynamic theory of paranoia and ultimately the source of the major theoretical stance regarding delusions in the psychodynamic theory. This foundation was based on Freud's reading of personal accounts written by the presiding judge of the Dresden Appeals Court, Daniel Paul Schreber, who had suffered two episodes of psychiatric illness in 1884 to 1885 and again in 1893. The second of these episodes led to two prolonged hospitalizations from which the patient obtained discharge in 1902 on the basis of a legal action, although he remained delusional. Freud asserted that Schreber's 190349 account of his experiences, entitled Memoirs of My Nervous Illness, offered a legitimate basis for theory. He argued that paranoiacs cannot be compelled to overcome their internal resistance, and as in any case, they say only what they choose to say.
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Therefore, the written case report could take the place of personal acquaintance with the patient. Freud proposed that Schreber's case illustrated a mechanism of general applicability to delusion formation involving denial, contradiction, and projection of repressed homosexual impulses that break out from the unconscious. The forms of delusion in paranoia, he argued, could be represented as contradictions of a basic proposition: I (a man) love him (a man). The Freudian formulation of delusions then involved a combination of (motivation elements) unconscious mechanisms and forms of logical transformation (reasoning elements) of these mechanisms into new propositions. The result of these unconscious logical syntheses was different forms of delusions, for example: 1. The delusion of persecution. In this delusion the contradiction, "I do not love him; I hate him."; the hate being unacceptable at the conscious level was transformed and becomes, "He hates (elaborated to: persecutes) me." Patients can then rationalize their angry feelings by consciously hating those persons whom they perceive to hate them. 2. The delusion of love (erotomania), "I do not love him. I love her." This proposition is transformed through projection to, "She loves me, so I love her." 3. Delusional jealousy. To protect against unwarranted, threatening impulses, the patient transforms the proposition in this way, "I do not love him; she (a wife, lover) loves him." Hence, jealous delusions represent the transformed attractions of the delusion for the lover. 4. Delusions of grandiosity (megalomania) . Here the contradiction is, "I do not love him-I love myself."
The essence of the psychodynamic theory is that delusions represent attempts to manage the arousal of unconscious homosexuality. The dynamics of unconscious homosexuality are similar for female as well as for male patients according to the classical theory. Many theorists have added to these views particularly from the standpoint of understanding personality factors. For example, some of the vulnerability to delusion formation may be related to deficiently developed trust, narcissistic dynamics, or exaggerated traits such as hypersensitivity. Contributors such as Vaillant56 have suggested that the development of defense mechanisms offers a means for understanding the complex manifestations of delusional thinking and its relationship to personality. Freud's proposal did not deal with the distinction between the form and content of delusions. 37 Although he proposed an inferential process to account for the particular delusion, he did not clearly address why a delusion is formed rather than another symptom such as an hallucination. Obviously, the verification of these hypothesized mechanisms rests on finding evidence that delusions are associated with indications of
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homosexual tendency. The theory has been perpetuated in part because an absence of homosexual feelings can never be proved. The few experimental attempts to test the hypothesis have been inconclusive or equivocal.35 In addition, although homosexual tendencies have been found among some delusional patients, the variety of conditions with delusions argues against a common mechanism of unconscious sexuality. Indeed, the persons who persecute delusional patients are not always known by them. Furthermore, the persistence of such delusions is not explicitly accounted for in this formulation. Nevertheless, the overall approach has had immense influence and has provided important concepts such as projection and awareness that development is relevant to the content of delusional thinking. A systematic empirical investigation would be valuable to furthering understanding of this proposal.
DISORDERED REASONING
The DSM-IV defines delusion as thus: A false belief based on incorrect inference about external reality that is firmly sustained despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary. The belief is not one ordinarily accepted by other members of the person's culture or subculture (eg, it is not an article of religious faith). When a false belief involves a value judgment, it is regarded as a delusion only when the judgment is so extreme as to defy credibility. Delusional conviction occurs on a continuum and can sometimes be inferred from an individual's behavior. It is often difficult to distinguish between a delusion and an overvalued idea (in which case the individual has an unreasonable belief or idea but does not hold it as firmly as is the case with a delusion). (p 765)1
Because the standard definition for the delusion rests largely on the operation of an inferential process that has gone awry, it is not surprising that a number of attempts have been made to establish that disordered reasoning is related to delusion formation, and that such disorders can be observed empirically in patients who are delusional. 30 There are different forms of disordered reasoning proposed as the source of delusions. These include disturbances in the processes governing formal deductive reasoning as exemplified in syllogisms; and disturbances in using observations to assign probabilities or predictions to future events, often referred to as Bayesian reasoning. Another hypothesis about disordered reasoning29 concerns the issue of attribution and the suggestion that there is a disorder in the social reasoning of patients that characteristically translates into making judgments or interpretations about situations that belie the patient's social and environmental circumstances and the concerns that the patient has about those. Rather than clearly being based on disturbances associated with perceptual change or the circumstances themselves, this form of reasoning then is influenced by a
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patient's tendencies to assign meaning in a biased manner. It represents a combined form of motivational and reasoning difficulties. Earlier formulations 2 , 5 emphasized various aspects of this view as well.
Formal Reasoning
In 1944, von Domarus58 postulated that delusions in schizophrenia arise from faulty logical reasoning. The defect apparently consists of the assumption of the identity of two subjects on the grounds of identical predicates (eg, Jesus was a healer; I am a healer; therefore, I am Jesus.) Von Domarus's hypothesis was quite popular during the 1950s, but empirical investigations failed to find evidence in favor of a specific kind of logical error made by schizophrenic patients. 44 , 60 Spitzer53 pointed out that the apparent logical content of delusional statements can be interpreted retrospectively and may be due to one of several kinds of formal logical error in addition to the principle of identity, which was proposed by Von Domarus. Further, the hypothesis based on the Von Domarus principle is not itself falsifiable, and hence, has limitations in scientific application. It is of interest to note that De Bonis et al1 5 found low reliability of psychiatric judgments about deficiencies in logical reasoning in a schizophrenic patient among some 32 psychiatrists. Further, a logician performed a detailed analysis of the most deviant verbal productions of this patient and concluded that the statements were in fact logical. In addition, attempts to identify logical difficulties among patients with schizophrenia have been frustrated by observations that the same kinds of logical problems that patients have occur as often among individuals who are deemed normal.35 Therefore, the available evidence suggests that the formation of delusions is not due to some defect of formal reasoning that is absent in nondeluded persons but present in the deluded.
Bayesian Reasoning
Contemporary models of human reasoning actually do not use the principles of syllogistic inference as an appropriate description of how human beings actually develop beliefs, make choices, and draw conclusions. Instead, emphasis is often placed on a separate model-the model of Bayesian processes. 22 According to the Bayesian model, individuals approach events or propositions and then assign, either implicitly or explicitly, probabilities about their reality. Hypothetically, these probabilities range from 0% to 100%, although the extreme values are unusual. Effective Bayesian reasoning is thus based on the correct assessment of the probabilities involved in empirical evidence. Displaying of evidence requires recognition of base rates for the occurrence of classes of events and due allowance for the impact of small sample effects. It also requires
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that the individual allow for biases that might be present in the collection of the evidence that is presented for consideration. Certain contemporary statistical methods provide a good example for the conscious, systematic use of this approach in human beings. Bayesian procedures imply that there is a sequence of steps that goes into forming assignments of probability. These are l. The identification and selection of observations and other evidence that are relevant to the validity of the belief; 2. The assessment of the evidence obtained with respect to the belief and to other possibly competing beliefs; 3. The compilation of data available from all sources and assessment of its effect on the belief; and 4. The selection of appropriate action. Hemsley and Garety21 • 22 suggested that delusions result from defects in the ability to weigh evidence along Bayesian lines. The problem is that the defect of the deluded patient is the acceptance of conclusions at levels of probability too low for acceptance by normal persons, A recent test of this hypothesis has been reported by Huq, Garety, and Hemsley.24 Deluded schizophrenic patients and controls were presented with a task in which the investigator indicated that colored beads would be drawn from one of two jars, One jar contained pink and green beads in a ratio of approximately 85:15, whereas the other jar contained beads of the same colors with the ratio reversed. The task was explained, and the jars were concealed, One jar was selected, and the subject was presented with beads drawn from that particular jar one at a time with the return of the bead to the jar after each drawing. Each of the subjects was then asked to draw a bead and after each successive drawing to estimate which jar was the source; this was the major response recorded, How sure the subject was about each estimate was also recorded, Errors of decision were recorded. Few decision errors were made by any group, and there were no significant differences between groups on the measures. Interestingly, the deluded patients made as many correct decisions as did other subjects; however, deluded patients arrived at their correct decisions after significantly fewer draws than the other subjects did and did so with greater estimates of confidence in their decisions. The authors stated, "It may be argued that the deluded sample reached a decision at an objectively 'rational' point . , . the two control groups being somewhat overcautious."24 This finding clearly fails to support the proposition that deluded patients are poorer at Bayesian reasoning than normal subjects, Based on these observations it seems reasonable to conclude that a reasoning defect in deluded patients has not yet been demonstrated. Social Attribution Explanations (Search for a Special Bias in Reasoning)
Social attribution refers to the processes that individuals use to explain their own behavior and that of others through the assignment
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of motives and characteristic traits to the persons involved. The social attribution hypothesis regarding formation of delusions has been formulated by a number of individuals, but the underlying model came from Kelley. 31 The central concern of the model is the apparently universal fundamental attribution error-the tendency to ascribe another person's behavior to characteristics of the person concerned regardless of the circumstances that are present at the time. In 1989, Kaney and Bentall3 , 29 suggested in a series of studies that the development of delusional beliefs might be understood in terms of the social attribution processes. Specifically, the delusions of persecution may be associated with a particular style of social attribution. These investigators 29 required subjects to respond to a questionnaire in which they made attributions to hypothetical situations. By and large, patients with delusions did not differ from the depressed controls but differed from each other on one or two of the various comparisons made. In brief, no clear demonstration of support for this hypothesis could be found.
PSYCHOBIOLOGIC MECHANISM
The French neurologist de Clerambault, in 1942, put forth the view 16 that chronic delusions resulted from abnormal neurologic events. These events included infections, lesions, intoxications, and other forms of damage that produced automatisms, which in turn puzzled or distressed the patient initially and eventually demanded some form of explanation. The explanation, then, took the form of delusions. Automatisms include hallucinations, parade of memories, feelings of familiarity, false recognition, arrest of thought, disturbances of attention, bizarre tactile sensations, and kinesthetic sensations. The view that delusions represent an explanation of hallucinations is an old, somewhat vague concept in psychiatry. Southard, for example, had performed pioneering studies showing on the basis of autopsy material that there was a striking correspondence between explanations for symptoms that were incorporated into delusions and the specific diseases from which patients suffered. 51, 52 In 1974, Maher32 proposed a hypothesis that conceptualizes delusions as explanations for anomalous experiences that arise in the environment, the peripheral nervous system, or the central nervous system. A significant feature of the theory33 was the proposal that cognitive processes in general were intact in such individuals and that what constitutes the basis for delusions is the anomalous experience that demands explanation. A central tenet of Maher's view is that the processes whereby delusional beliefs are formed are similar to thosethat operate in the formation of normal beliefs and even in scientific hypotheses.33, 34 Central to the proposal is the assumption that components of the normal operation of belief formation arise in a sequence that has a neural substrate that may be activated by sensory input (as in hallucinatory effects of drugs) or by the effects of brain damage
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(as in head injury). The activation of any part of the sequence demands an explanation and may thus give rise to delusions. The sequence, activated by disturbances in sensory experience, emotional incongruity, and central nervous system abnormalities, has the following stages: 1. Anomalous experience,
2. 3. 4. 5. 6. 7.
Feelings of significance, Testing for the reality of the experience, Developing tentative hypotheses to explain the experience, Additional observation, Exploring insight, and Confirmation of the insight by selective observation.
The argument is that the patient is delusional because he or she actually experiences anomalies that demand explanation. Particulars of the delusion, that is, its content, are drawn from the past or current circumstances, experience, and personal and cultural background of the patient. The anomalies are sources for explanatory material available to the patient. The explanation answers questions such as, what is happening? Why is it happening? Why do other people deny that it is happening? Why is it happening only to me? Who's responsible for its happening? The delusional explanation offers a relief from the sense of puzzlement that accompanies odd or unusual experiences of anomalous nature, and this relief works against the abandoning of the explanation; that is, it reinforces the delusional belief and helps to establish its fixedness. Thus, once the explanation has been established, new data that are not consistent with the explanation are disturbing and either become ignored or reinterpreted to fit the explanation. Maher34• 35 has elaborated his views to suggest that the content of the delusional explanation is likely to come from the individual experience and preoccupations of the individual. Thus, the patient whose basic problem is the experience that his or her thoughts are not his or her own is most likely to conclude that someone is controlling them and will then turn to aspects of his or her present or past life to explain why this might be. For a patient, for example, who has been guilty of some act of which he or she is ashamed may reach the conclusion that he or she is being punished for this act by the distressing experience of having his or her thoughts taken over. The sequence may easily mislead clinicians into concluding that the recollection of the guilty act has given rise to the delusional state, thereby confusing effect with cause. What is the evidence to support the model? One source of evidence is the lack of success of attempts to find fundamental defects in the cognitive processes of delusional patients. And from evidence about the processes of belief formation, normal subjects are indistinguishable from those supposed to be characteristic of delusional patients. Indeed, delusions are found in persons of every level of intelligence and education, further supporting the view that disruption or defect in cognitive processes is not the basis of the problem. On the other hand, positive
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evidence comes from the prevalence of delusions in a wide range of medical and psychiatric disorders in which deluded individuals have no prior history of cognitive impairment. Secondly, there is evidence that delusions can be induced in normal subjects under conditions in which they have anomalous experiences; third, the presence of delusions in cases of undiagnosed sensory defect, the frequent coexistence of delusions and their possible development from psychotic symptoms such as hallucinations, thought insertion, thought withdrawal, and passivity phenomena that become elaborated fully in the delusion. Empirical studies, in summation, have reported that anomalies of experiences are correlated with the presence of delusions in many different ways. 35
Other Sources of Anomalous Experience and Delusion Formation
Delusions have been explained in terms of disturbed experiences of time at least since the 1930s when Binswanger and Minkowski proposed that schizophrenic patients suffered from disordered experiences of space and time, leading possibly to feeling imprisoned or controlled. In 1975, Melges and Freeman43 proposed a cybernetic model for the formation of delusions based on the assumption of a temporal disturbance of formal thought as a primary cause of the delusions. A disintegration of the temporal sequence of thought is experienced by the patient as a loss of control, which in several stages, leads to the formation of delusions. The concept that an attentional deficit is related to delusion formation also has been popular. The attentional deficit may alter the content of consciousness, heighten awareness, or sharpen focus on particular details of the environment.2°, 41 The relationship between altered attention and the formation of delusions per se has not been well developed, probably because the deficit view has been applied generally to a wide range of psychopathologic symptoms, especially in schizophrenia, and not simply to delusions. A recent exception is the proposal of Vinogradov and colleagues57 who have created a model linking attentional features and delusional thinking that is based on alterations in associational mechanisms, as a contemporary formulation reminiscent of Eugen Bleuler's views4 about affect and delusion. In 1934, Pavlov45 proposed a theory that related delusions of reference and control to perceptual disturbances that he viewed to be the consequences of pathologic absence of activity in cells of the sensory cortex. Pathologic arousal in other cells causes irrelevant ideas to intrude into consciousness. According to Pavlov, the delusion consists of nothing but reflections about such irrelevant ideas. His formulation had little impact and has not been subjected to empirical testing.
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On the other hand, it has been known that delusions may develop in patients with sensory deficits. For example, Kraepelin commented on the connection between hearing deficits and delusions. Empirical studies generally have shown increased frequency of delusions among patients with hearing deficits 23 as well as an increase of hearing deficits in paranoid schizophrenic patients.30 Visual disturbances also have been found more frequently in paranoid patients. 9 Cooper and Porter8 demonstrated a much higher incidence of visual and auditory perceptual disturbances in paranoid patients compared with patients with mood disorders. In 1981, Zimbardo and colleagues62 were able to show that hypnotically induced hearing loss in normal subjects led to higher scores on the paranoia scale of the MMPI. Despite these observations, there is controversy about the connection of paranoid behavior and auditory perceptual disturbances,28 so that a final model has yet to be developed. Nevertheless, these reports suggest important testable relationships.
Neu ropsychological Theories
A variety of neuropsychological theories have been proposed to account for delusions. Perhaps one of the most famous of these was the proposal of James Hughlings Jackson25 who suggested that features of insanity including delusions could be understood as the result of the interaction between two processes: disruption and loss of the function associated with the failure in areas of the brain that are damaged by disease, on the one hand, and the resulting disinhibition of behaviors in those areas left undamaged. The latter of these factors produces the experience of delusions, a new symptom. Other factors, personality and experience, influence the character of these new symptoms (which we now call positive symptoms). In addition to the theories that have dealt with disordered reasoning, changes in perceptual experience, and the psychodynamic mechanism underlying delusions, there have been more focused attempts in recent years to identify a neurologic basis for delusional thinking. 17• 18• 40 The problem with this approach is that, like other approaches, the assessment of the correlation between delusions and particular anatomic loci depends fundamentally on the reliability and the validity of the distinctions and features associated with delusion itself. In other words, if we cannot identify delusions accurately and reliably, then attempts to make connections between their occurrence and specific lesions in the brain are likely to fail. In the past it has been noted that delusions occur with considerable frequency in nonpsychiatric conditions. This proposal has been amply documented by Manschreck and Petri39 as well as by others.11· 14• 27 This suggests that there is much to account for in trying to explain delusions arising in varied conditions. In recent years there have been more thorough and comprehensive attempts to evaluate the psychopathology associated with specific neurologic disorders.4° Cummings has been a leading contributor in this area
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and has summarized a current view of the relationship between delusions and specific neurologic disease in a series of publications.11-13 He points out that psychosis is not an uncommon occurrence in the course of neurologic disease. In fact, a wide variety of conditions can induce psychosis but particularly those that affect the limbic system and, especially within the limbic system, the temporal lobe and caudate nuclei. Disturbances in these structures are most likely to be associated with the formation of delusions. 42• 50• 55 There appears, in addition, to be an increased frequency of psychosis in conditions that are associated with bilateral involvement of brain structures. At the neurotransmitter level, it is recognized that dopaminergic excess or reduced cholinergic activity also may predispose to psychosis. Left-sided epileptic foci are associated with Schneiderian first rank symptoms, suggesting a lateralization influence in the formation of delusional experience. 40 Indeed, other factors are relevant as well including age at onset, gender, and the type of pathology that in concert or singly can influence the experience of psychosis. On the other hand, it appears that psychosis is independent of the severity of intellectual deficits that occur in patients with neurologic disease. It is also clear that delusions do not correlate with abnormalities in any specific neurologic domain such as language, memory, visuospatial skills, abstraction abilities, and the like, again suggesting that cognitive defect is not the source of delusions. Integrity of intellectual function appears rather to determine the complexity of delusional beliefs. In other words, the more intellectually capable the individual, the greater the complexity of the delusions when they occur in neurologic disease. Cummings 12 proposes a hypothesis to explain delusional formation. He argues that the hypothesis needs to take a number of items into account including the variety of psychopathologic conditions seen in neurologic disease, the variety of delusions in particular; and that if there is to be a common model, it must arise from regularities that we identify in the nature of neurologic lesions. Specifically, Cummings 12 suggests that limbic dysfunction, the common locus, leads to misinterpretation of the environment, and this is accompanied by an inappropriate perception of threat. This, in turn, leads to paranoid belief formation. Patient- and disease-related factors also influence the content, complexity, and timing of the formation of delusions. The appealing nature of this hypothesis derives from its midrange attempt to connect what is known to what we need to explain, its cautious approach to claiming generalizability, and its reliance on a range of observations to generate testable hypotheses about a possible common mechanism. It stands ready to be tested. It complements the anomalous experience proposal in many ways.
SUMMARY AND CONCLUSIONS
This overview of attempts to shed light on the pathogenesis of delusions provides a sense of promise, because we are grappling with
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the right problems, and reasons for both optimism and skepticism. Optimism is justified because some of the approaches have yielded empirical support and can be tested profitably in research. Skepticism is warranted because we remain unclear about precisely what delusions are; and we have as yet no means of identifying them with a laboratory test. Hence, we must rely on the problematic nature of clinical observation of the inner experiences of patients to make progress. The different mechanisms proposed still require considerable testing, but scrutiny of current results suggests that anomalous experience as a stimulus for delusion formation has been better documented than proposals invoking disordered reasoning or motivational deviances. Nevertheless, no view is as yet established, and each may have some relevance to solving the delusion puzzle. References l. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disor-
ders, ed 4. Washington, American Psychiatric Press, 1994 2. Arthur AZ: Theories and explanations of delusions: A review. Am J Psychiatry 121:105- 115, 1964 3. Bentall RP, Kaney S: Content-specific information processing and persecutory and persecutory delusions: An investigation using the emotional Stroop test. Br J Med Psycho! 62:355-364, 1989 4. Bleuler E: Dementia Praecox or the Group of Schizophrenias. New York, International Universities Press, 1950 5. Cameron N: The paranoid pseudo-community revisited. Am J Social 65:52-56, 1959 6. Chadwick PDJ, Lowe CF: Measurement and modification of delusional beliefs. Consult Clin Psych o! 58:225-232, 1990 7. Chadwick PDJ, Lowe CF, Horne PJ, et al: Modifying delusions: The role or empirical testing. Behav Ther 25:35-49, 1994 8. Cooper AE, Porter R: Visual acuity and ocular pathology in the paranoid and affective psychoses of later life. J Psychosom Res 20:107-114, 1976 9. Cooper AE, Curry AR: The pathology of deafness in the paranoid and affective psychoses of later life. J Psychosom Res 20:97-105, 1976 10. Costello CG: Research on symptoms versus research on syndromes: Arguments in favor of allocating more research time to the study of symptoms. Br J Psychiatry 160:304-308, 1992 11. Cummings JL: Organic delusions: Phenomenology, anatomical correlation, and review. Br J Psychiatry 146:184-197, 1985 12. Cummings JL: Psychosis in neurologic disease: Neurobiology and pathogenesis. Neuropsychiatry, Neuropsychology and Behavioral Neurology 5:144-150, 1992 13. Cummings JL, Miller B, Hill MA, et al: Neuropsychiatric aspects of multi-infarct dementia and dementia of the Alzheimer's type. Arch Neural 44:389- 393, 1987 14. Davison K, Bagley CR: Schizophrenia-like psychoses associated with organic disorders of the central nervous system: A review of the literature. Br J Psychiatry 4:113-184, 1969 15. De Bonis M, Epelbaum C, Feline A, et al: Pensee formelle, operations logico-discursives et schizophrenie: etude experimentale d'un cas clinique. Revue Canadienne-de psychiatie 35:64-70, 1990 16. de Clerambault GG: Les Psychoses Passionelles. In Oeuvre Psychiatrique. Paris, Presses Universitaires, 1942 17. de Leon J, Antelo RE, Simpson G: Delusion of parasitosis or chronic tactile hallucinosis: Hypothesis about their brain physiopathology. Comp Psychiatry 33:25-33, 1992 18. Ellis HD, Young AW: Accounting for delusional misidentification. Br J Psychiatry 157:239-248, 1990
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19. Freud S: Psychoanalytic notes upon an autobiographical account of a case of paranoia (dementia paranoides). In Collected Papers 3. London, Hogarth Press, 1950 (originally published, 1911) 20. Frith CD: Consciousness, information processing, and schizophrenia. Br J Psychiatry 134:225-235, 1979 21. Garety PA, Hemsley DR: Characteristics of delusional experiences, Arch Psychiatry Neurol Sci 236:294-298, 1987 22. Hemsley DR, Garety PA: The formation and maintenance of delusions: A Bayesian analysis. Br J Psychiatry 149:51-56, 1986 23. Houston F, Royse AB: Relationship between deafness and psychotic illness. Journal of Mental Science 100:990-993, 1954 24. Huq SF, Garety PA, Hemsley DR: Probabilistic judgments in deluded and non-deluded subjects. Q J Exp Psycho! 40:801-812, 1988 25. Jackson JH: Selected Writings by JH Jackson: I and II [J Taylor, ed.]. New York, Basic Books, 1958 26. Jaspers K: General Psychopathology [Hamilton M & Hoenig J, trans.]. Manchester, University of Manchester Press, 1963 (originally published, 1913) 27. Johnstone EC, Cooling NJ, Frith CD, et al: Phenomenology of organic and functional psychoses and the overlap between them. Br J Psychiatry 153:770-776, 1988 28. Jones EM, White AJ: Mental health and acquired hearing impairment: A review. Br J Audio! 24:3-9, 1990 29. Kaney S, Bentall RP: Persecutory delusions and attributional style. Br J Med Psycho! 62:191-198, 1989 30. Kay DWK, Roth M: Environmental and hereditary factors in the schizophrenias of old age. Journal of Mental Science 107:649-686, 1961 31. Kelley HI: Attribution theory in social psychology. In Levine D (ed): Nebraska Symposium on Motivation, vol 15. Lincoln, University of Nebraska Press, 1967 32. Maher BA: Delusional thinking and perceptual disorder. Journal of Individual Psychology 30:98- 113, 1974 33. Maher BA: Delusions as the product of normal cognitions. In Oltmanns TF, Maher BA (eds): Delusional Beliefs. New York, Wiley-Interscience, 1988 34. Maher BA: Delusions: Contemporary etiologic hypotheses. Psychiatr Ann 22:260- 268, 1992 35. Maher BA, Spitzer M: Delusions. In Adams HE, Sutker PB (eds): Comprehensive Handbook of Psychopathology, ed 2. New York, Plenum Publishing, 1992 36. Manschreck TC: The assessment of paranoid features. Comp Psychiatry 20:370-377, 1979 37. Manschreck TC: Delusional disorder and shared psychotic disorder. In Kaplan HI, Sadock BJ (eds): Comprehensive Textbook of Psychiatry VI. Baltimore, Williams and Wilkins, 1995, in press 38. Manschreck TC, Kleinman AM: Psychiatry's identity crisis: A critical national remedy. Gen Hosp Psychiatry 1:166-179, 1979 39. Manschreck TC, Petri M: The paranoid syndrome. Lancet 2:251-253, 1978 40. McAllister TW: Neuropsychiatric aspects of delusions. Psychiatr Ann 22:232-240, 1992 41 . McGhie A: The Pathology of Attention. London, Penguin Books, 1970 42. McKenna PJ, Kane JM, Parrish K: Psychotic syndromes in epilepsy. Am J Psychiatry 142:895-904, 1985 43. Melges FT, Freeman AM: Persecutory delusions: A cybernetic model. Am J Psychiatry 132:1038-1044, 1975 44. Nims JP: Logical Reasoning in Schizophrenia: The von Domarus Principle. Los Angeles, University of Southern California, unpublished doctoral dissertation, 1959 45. Pavlov IP: An attempt at a psychological interpretation of obsessional neurosis and paranoia. J Ment Sci 80:187-197, 1934 46. Persons JB: The advantages of studying psychological phenomena rather than psychiatric diagnoses. American Psychologist 41:1252-1260, 1986 47. Roth M: Delusional (paranoid) disorders. In Gabbard GO (ed): Treatment of Psychiatric Disorders. Washington, American Psychiatric Association Press, 1989, pp 1609-1652 48. Schneider K: Clinical Psychopathology. New York, Grune and Stratton, 1959
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49. Schreber D: Memoirs of My Nervous Illness. R Bentley, Cambridge, MA, 1955 (originally published, 1903) 50. Slater E, Beard RW: The schizophrenia-like psychoses of epilepsy I: Psychiatric aspects. Br J Psychiatry 109:95-150, 1963 51. Southard EE: On descriptive analysis of manifest delusions from the subject's point of view. J Abnorm Psycho! 11:189-202, 1916 52. Southard EE: On the application of grammatical categories to the analysis of delusions. Philosophical Review 25:424--455, 1916 53. Spitzer M: On the logic of thought disorder. In Klein P (ed): Praktische Logik: Traditionen und Tendenzen. Gottingen, Vandenhoeck und Ruprecht, 1989 54. Spitzer M: The phenomenology of delusions. Psychiar Ann 22:252-259, 1992 55. Trimble MR: Interictal psychoses of epilepsy. Adv Neurol 55:143-152, 1991 56. Vaillant GE: Theoretical hierarchy of adaptive ego mechanisms. Arch Gen Psychiatry 4:107-118, 1971 57. Vinogradov S, King RJ, Huberman BA: An associationist model of the paranoid process: Application of phase transitions in spreading activation networks. Psychiatry 55:79-94, 1992 58. Von Domarus E: The specific law of logic in schizophrenia. In Kasanin JS (ed): Language and Thought in Schizophrenia. Berkeley, University of California Press, 1944 59. Webb W: Paranoid conditions seen in psychiatric medicine. Psychiatr Med 8:37-48, 1990 60. Williams EB: Deductive reasoning in schizophrenia. J Abnorm Social Psycho! 69:4761, 1964 61. Winters KC, Neale JM: Delusions and delusional thinking in psychotics: A review of the literature. Clin Psycho! Rev 3:227- 253, 1983 62. Zimbardo PG, Anderson SM, Kabat LG: Induced hearing deficit generates experimental paranoia. Science 212:1529-1531, 1981
Address reprint requests to Theo C. Manschreck, MD Brown University School of Medicine Corrigan Mental Health Center 49 Hillside street Fall River, MA 02720
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PATHOGENESIS OF DELUSIONS Theo C. Manschreck, MD
Delusions are the cardinal symptoms of psychopathology. Despite their importance in a wide range of psychiatric disorders, understanding of delusions is markedly limited. Virtually every facet of the subject of delusions remains uncharted according to the standards of scientific methodology. Even phenomenology, certainly biologic underpinnings but also the role of culture and the psychology of delusions are subjects sorely in need of research elaboration. Pathogenesis is a critical dimension in the study of delusion. Specifically, pathogenesis refers to the mechanisms underlying the formation and maintenance of delusional thinking. This article summarizes what has been proposed to account for the pathogenesis of delusions, identifies the gaps in our knowledge, and suggests strategies for closing these gaps. PHENOMENOLOGY
Phenomenology of delusions is a useful starting point for discussion of the pathogenesis. Phenomenology constitutes one foundation of our understanding of delusions. Unfortunately, phenomenologic advances have come slowly and have been accompanied by considerable controversy. In the European tradition, phenomenology refers to the description of the nature of the inner life of the patient. Clearly this focus has relevance to understanding the nature of delusions in that the clinical judgment that the patient has a delusion derives largely from subjective report by the patient. 54 Much of the European literature in the early part of the twentieth century was devoted to the phenomenologic method and emphasized the value of clinical dialogue with the patient to ascertain a clear understanding of delusional experience. Two major contributions to From the Department of Psychiatry and Human Behavior, Brown University School of Medicine, Providence, Rhode Island
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this effort are worth mentioning. The first was from Karl Jaspers, the psychopathologist and philosopher who formulated the definition of delusion widely used today. 26 Jaspers' criteria for delusions were as follows: 1. Subjective certainty 2. Incorrigibility 3. Realistic impossibility (later: falsity of content as some delusions are possible). Jaspers was tentative about the strictness of his criteria, preferring to view them as approximations to a definition; for example, impossibility of a belief was modified to falsity of the belief as some delusions are indeed possible (as in delusional disorder). Falsity of a belief depends on the availability of empirical evidence; and in the case of religious delusions, such evidence may not be available. In practice, the judgment that a belief is delusional often rests as much on the behavior of the patient who expresses the belief as on its falsity (which may be difficult to demonstrate) and the unwillingness to give in to counter argument (see section on clinical assessment). The second contribution dealt with the distinction between primary and secondary delusions. 26 • 48 A primary delusion arises from no other identifiable source; its detection has diagnostic significance in that such delusions are believed to be characteristic of schizophrenia. Kurt Schneider's concept48 of delusional perception and current descriptions of what are called mood incongruent delusions likely would be classified as primary delusions. Secondary delusions, on the other hand, arise on the basis of altered mood, personality, or other features and possess less diagnostic significance. Mood congruent delusions, as in mania or psychotic depression, would be examples of secondary delusions. Mood or affect influences on the delusion formation were proposed by Bleuler4 as well as Jaspers and Schneider; the latter viewed affect as a distinguishing feature in the recognition of primary and secondary delusions. The distinction between primary and secondary delusions derived in part from attempts to explain the differences between delusions that arose in disorders that had an organic basis, in contrast to disorders in which "functional" causes were considered likely. In practice, the distinction between primary and secondary delusions has been criticized as impractical and lacking validity because of (1) the difficulty in defining and reliably identifying or eliciting primary versus secondary delusions and (2) the vagueness and theoretic nature of the functional disorder concept. Nevertheless, phenomenologic investigation has produced important insights about the main descriptive features of delusions. These are Theme Understandability Degree of certainty Systematization Complexity Relevance to patient's life Plausibility
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CLINICAL ASSESSMENT
In clinical encounters, delusions usually are easy to detect. Certain behavioral features (hypersensitivity, irritability, guardedness, evasiveness, litigious behavior, secretiveness, self-righteousness, obstinance, fear, humorlessness, preoccupation with details, and hostility) may suggest their presence or solidify the impression that the patient's beliefs are delusional. Associated psychopathologic symptomatology, such as hallucinations, disturbed form of thought, and mood disorder, also may provide clues that delusions are part of the clinical picture (and assist in their diagnosis). 36• 39 The clinical challenge is more obvious in subtle cases wherein the suspected delusional thinking may be difficult to detect or to diagnose as delusional. Fundamentally, the clinician must make a judgment, based on assessment of the behavior and the reported private mental experience of the patient, that delusional belief(s) are present. Attempts to dissuade the patient with counter evidence and argument may be useful to determine whether the patient's feelings can be influenced with evidence usually sufficient to alter the belief of a normal person. (Recent reports 6 • 7 indicate that reality testing may be a useful treatment for delusions.) The judgment often relies on determining whether a threshold indicating psychopathologic disturbance has been passed, as reflected in the extremeness and the inappropriateness of the patient's behavior, as opposed to the simple truth or falsity of the belief. Indeed, not infrequently, the patient may not reveal the belief at all; it must be inferred from the behavior that a delusion is likely. The most sensible guideline, applicable to all suspected cases of delusional thinking, is to gather as comprehensive a picture as possible concerning the condition of the patient (especially regarding evidence for psychopathologic symptoms). Such information should reduce much of the uncertainty present in the evaluation of delusions. Until there is an objective laboratory test for delusional thinking, it will be necessary to apply clinical judgment in all cases to varying degrees. In view of this limitation and the potential significance of being wrong, the clinician should apply his or her judgment humbly. 36 In short, phenomenology and clinical assessment constitute somewhat weak methods for detecting and describing delusions, procedures necessary for establishing and testing proposals about delusion formation.
PATHOGENESIS
Establishing a scientific understanding of the pathogenesis of delusions presents a number of problems. As indicated previously, there are fundamental issues that have to do with the very definition of delusion as well as critical limitations related to its application in clinical practice. These limitations obviously pose a considerable challenge to the
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opment of a general theory of delusion formation. Nevertheless, there have been many attempts to do so,2 and these are outlined in subsequent sections. Before we review those theories, however, it would be useful to identify what is required to be explained in a theory of delusion formation. Unfortunately, most theories fail to specify this information in advance, and this has led to theoretical formulations that have limited relevance to the breadth of issues associated with pathogenesis. Also, general theories, however promising or appealing, have been of limited value to psychiatry and often have failed to provide an adequate level of conceptual precision to propose testable hypotheses for advancement of knowledge. On the other hand, this area might benefit from what might be described as mid-range theorizing; that is, identifying a selected domain of investigation and developing models and hypotheses based on empirical data so that further conceptual and theoretical refinement could occur. 38 The study of specific psychopathologic symptoms, such as delusions and hallucinations, are good candidates for such activity as Costello 10 and Persons46 have argued so persuasively. In addition to requirements for an adequate theory of delusion formation, other issues need to be taken into account. For example, one of the key and critical problems facing the field of psychopathology is the problem of heterogeneity. Heterogeneity refers to the likelihood that many of the psychopathologic syndromes arise from different and possibly numerous causes. Hence, we need to be able to relate any theory of delusion formation to the possibility that multiple causes could lead to similar manifestations and delusion formation. Related to this issue, of course, is the role of personality in the formation of delusions. We know that personality has an effect on the nature of delusion. The extent and nature of that effect remain largely unexplored areas, in part because empirical research has been limited. 2 What then are the features that need to be specified in order to have an adequate theory of delusions? An adequate hypothesis for delusion formation must deal with certain important facts: 1. Delusions occur in a number of medical and psychiatric disor-
ders.14, 36, 37, 39, 50 2. Not all individuals with these disorders will develop delusion. 59 3. The content of delusions boils down to a relatively short list of specific types, despite the variety of disorders and diseases associated with their occurrence. 33· 37 4. Delusions can respond to treatment of the underlying condition that led to their formation. 37· 59 5. Delusions can persist and become systematized. 26 6. Delusions often accompany perceptual changes such as impaired sensory input or hallucinatory experiences. 8· 9· 23 7. Delusions may be highly encapsulated features in individuals and functioning may not be compromised in terms of social, intellectual, or affective responsiveness. 37· 47
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In addition, any adequate hypothesis of delusion formation also must respond to two questions. First, why is it that the patient has a delusion? This particular question refers to the form of psychopathology. Second, why does the patient have this particular delusion? This question concerns the content of a psychopathologic experience. Winters and Neale61 organized many of the theories of delusion formation in terms of two general categories of origin: motivation and defect. This proposal is useful for many problems associated with understanding delusions but not for all, as at least one key approach is not addressed. Hence, it is convenient to address the issues of pathogenesis by thinking about three broad categories of hypotheses: 1. A pattern of deviant motivation such that an otherwise intact cognitive system is distorted in the service of motivation (psychodynamic mechanism, social attribution). 2. A fundamental cognitive defect that impairs the patient's capacity to draw valid conclusions from evidence (disorder of reasoning). 3. The cognitive processes of the deluded patient are fundamentally intact, but the delusion arises from normal cognitive activities directed at explaining abnormal experiences (psychobiologic mechanism, anomalous experience hypothesis). These hypotheses need not be mutually exclusive. It is quite possible that delusional beliefs arise as the outcome of different processes and sequences involving one or more of these mechanisms. Attempts to identify the mechanism of pathogenesis in delusion formation have been numerous. The following discussion is presented in a chronologic framework. The first major proposal about delusion formation explored the psychodynamic mechanism.
PSYCHODYNAMIC MECHANISM
Sigmund Freud19 published "Psychoanalytic Notes Upon an Autobiographical Account of a Case of Paranoia (Dementia Paranoides)" in 1911. Freud's interpretation of this case became the foundation of the psychodynamic theory of paranoia and ultimately the source of the major theoretical stance regarding delusions in the psychodynamic theory. This foundation was based on Freud's reading of personal accounts written by the presiding judge of the Dresden Appeals Court, Daniel Paul Schreber, who had suffered two episodes of psychiatric illness in 1884 to 1885 and again in 1893. The second of these episodes led to two prolonged hospitalizations from which the patient obtained discharge in 1902 on the basis of a legal action, although he remained delusional. Freud asserted that Schreber's 190349 account of his experiences, entitled Memoirs of My Nervous Illness, offered a legitimate basis for theory. He argued that paranoiacs cannot be compelled to overcome their internal resistance, and as in any case, they say only what they choose to say.
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Therefore, the written case report could take the place of personal acquaintance with the patient. Freud proposed that Schreber's case illustrated a mechanism of general applicability to delusion formation involving denial, contradiction, and projection of repressed homosexual impulses that break out from the unconscious. The forms of delusion in paranoia, he argued, could be represented as contradictions of a basic proposition: I (a man) love him (a man). The Freudian formulation of delusions then involved a combination of (motivation elements) unconscious mechanisms and forms of logical transformation (reasoning elements) of these mechanisms into new propositions. The result of these unconscious logical syntheses was different forms of delusions, for example: 1. The delusion of persecution. In this delusion the contradiction, "I do not love him; I hate him."; the hate being unacceptable at the conscious level was transformed and becomes, "He hates (elaborated to: persecutes) me." Patients can then rationalize their angry feelings by consciously hating those persons whom they perceive to hate them. 2. The delusion of love (erotomania), "I do not love him. I love her." This proposition is transformed through projection to, "She loves me, so I love her." 3. Delusional jealousy. To protect against unwarranted, threatening impulses, the patient transforms the proposition in this way, "I do not love him; she (a wife, lover) loves him." Hence, jealous delusions represent the transformed attractions of the delusion for the lover. 4. Delusions of grandiosity (megalomania) . Here the contradiction is, "I do not love him-I love myself."
The essence of the psychodynamic theory is that delusions represent attempts to manage the arousal of unconscious homosexuality. The dynamics of unconscious homosexuality are similar for female as well as for male patients according to the classical theory. Many theorists have added to these views particularly from the standpoint of understanding personality factors. For example, some of the vulnerability to delusion formation may be related to deficiently developed trust, narcissistic dynamics, or exaggerated traits such as hypersensitivity. Contributors such as Vaillant56 have suggested that the development of defense mechanisms offers a means for understanding the complex manifestations of delusional thinking and its relationship to personality. Freud's proposal did not deal with the distinction between the form and content of delusions. 37 Although he proposed an inferential process to account for the particular delusion, he did not clearly address why a delusion is formed rather than another symptom such as an hallucination. Obviously, the verification of these hypothesized mechanisms rests on finding evidence that delusions are associated with indications of
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homosexual tendency. The theory has been perpetuated in part because an absence of homosexual feelings can never be proved. The few experimental attempts to test the hypothesis have been inconclusive or equivocal.35 In addition, although homosexual tendencies have been found among some delusional patients, the variety of conditions with delusions argues against a common mechanism of unconscious sexuality. Indeed, the persons who persecute delusional patients are not always known by them. Furthermore, the persistence of such delusions is not explicitly accounted for in this formulation. Nevertheless, the overall approach has had immense influence and has provided important concepts such as projection and awareness that development is relevant to the content of delusional thinking. A systematic empirical investigation would be valuable to furthering understanding of this proposal.
DISORDERED REASONING
The DSM-IV defines delusion as thus: A false belief based on incorrect inference about external reality that is firmly sustained despite what almost everyone else believes and despite what constitutes incontrovertible and obvious proof or evidence to the contrary. The belief is not one ordinarily accepted by other members of the person's culture or subculture (eg, it is not an article of religious faith). When a false belief involves a value judgment, it is regarded as a delusion only when the judgment is so extreme as to defy credibility. Delusional conviction occurs on a continuum and can sometimes be inferred from an individual's behavior. It is often difficult to distinguish between a delusion and an overvalued idea (in which case the individual has an unreasonable belief or idea but does not hold it as firmly as is the case with a delusion). (p 765)1
Because the standard definition for the delusion rests largely on the operation of an inferential process that has gone awry, it is not surprising that a number of attempts have been made to establish that disordered reasoning is related to delusion formation, and that such disorders can be observed empirically in patients who are delusional. 30 There are different forms of disordered reasoning proposed as the source of delusions. These include disturbances in the processes governing formal deductive reasoning as exemplified in syllogisms; and disturbances in using observations to assign probabilities or predictions to future events, often referred to as Bayesian reasoning. Another hypothesis about disordered reasoning29 concerns the issue of attribution and the suggestion that there is a disorder in the social reasoning of patients that characteristically translates into making judgments or interpretations about situations that belie the patient's social and environmental circumstances and the concerns that the patient has about those. Rather than clearly being based on disturbances associated with perceptual change or the circumstances themselves, this form of reasoning then is influenced by a
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patient's tendencies to assign meaning in a biased manner. It represents a combined form of motivational and reasoning difficulties. Earlier formulations 2 , 5 emphasized various aspects of this view as well.
Formal Reasoning
In 1944, von Domarus58 postulated that delusions in schizophrenia arise from faulty logical reasoning. The defect apparently consists of the assumption of the identity of two subjects on the grounds of identical predicates (eg, Jesus was a healer; I am a healer; therefore, I am Jesus.) Von Domarus's hypothesis was quite popular during the 1950s, but empirical investigations failed to find evidence in favor of a specific kind of logical error made by schizophrenic patients. 44 , 60 Spitzer53 pointed out that the apparent logical content of delusional statements can be interpreted retrospectively and may be due to one of several kinds of formal logical error in addition to the principle of identity, which was proposed by Von Domarus. Further, the hypothesis based on the Von Domarus principle is not itself falsifiable, and hence, has limitations in scientific application. It is of interest to note that De Bonis et al1 5 found low reliability of psychiatric judgments about deficiencies in logical reasoning in a schizophrenic patient among some 32 psychiatrists. Further, a logician performed a detailed analysis of the most deviant verbal productions of this patient and concluded that the statements were in fact logical. In addition, attempts to identify logical difficulties among patients with schizophrenia have been frustrated by observations that the same kinds of logical problems that patients have occur as often among individuals who are deemed normal.35 Therefore, the available evidence suggests that the formation of delusions is not due to some defect of formal reasoning that is absent in nondeluded persons but present in the deluded.
Bayesian Reasoning
Contemporary models of human reasoning actually do not use the principles of syllogistic inference as an appropriate description of how human beings actually develop beliefs, make choices, and draw conclusions. Instead, emphasis is often placed on a separate model-the model of Bayesian processes. 22 According to the Bayesian model, individuals approach events or propositions and then assign, either implicitly or explicitly, probabilities about their reality. Hypothetically, these probabilities range from 0% to 100%, although the extreme values are unusual. Effective Bayesian reasoning is thus based on the correct assessment of the probabilities involved in empirical evidence. Displaying of evidence requires recognition of base rates for the occurrence of classes of events and due allowance for the impact of small sample effects. It also requires
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that the individual allow for biases that might be present in the collection of the evidence that is presented for consideration. Certain contemporary statistical methods provide a good example for the conscious, systematic use of this approach in human beings. Bayesian procedures imply that there is a sequence of steps that goes into forming assignments of probability. These are l. The identification and selection of observations and other evidence that are relevant to the validity of the belief; 2. The assessment of the evidence obtained with respect to the belief and to other possibly competing beliefs; 3. The compilation of data available from all sources and assessment of its effect on the belief; and 4. The selection of appropriate action. Hemsley and Garety21 • 22 suggested that delusions result from defects in the ability to weigh evidence along Bayesian lines. The problem is that the defect of the deluded patient is the acceptance of conclusions at levels of probability too low for acceptance by normal persons, A recent test of this hypothesis has been reported by Huq, Garety, and Hemsley.24 Deluded schizophrenic patients and controls were presented with a task in which the investigator indicated that colored beads would be drawn from one of two jars, One jar contained pink and green beads in a ratio of approximately 85:15, whereas the other jar contained beads of the same colors with the ratio reversed. The task was explained, and the jars were concealed, One jar was selected, and the subject was presented with beads drawn from that particular jar one at a time with the return of the bead to the jar after each drawing. Each of the subjects was then asked to draw a bead and after each successive drawing to estimate which jar was the source; this was the major response recorded, How sure the subject was about each estimate was also recorded, Errors of decision were recorded. Few decision errors were made by any group, and there were no significant differences between groups on the measures. Interestingly, the deluded patients made as many correct decisions as did other subjects; however, deluded patients arrived at their correct decisions after significantly fewer draws than the other subjects did and did so with greater estimates of confidence in their decisions. The authors stated, "It may be argued that the deluded sample reached a decision at an objectively 'rational' point . , . the two control groups being somewhat overcautious."24 This finding clearly fails to support the proposition that deluded patients are poorer at Bayesian reasoning than normal subjects, Based on these observations it seems reasonable to conclude that a reasoning defect in deluded patients has not yet been demonstrated. Social Attribution Explanations (Search for a Special Bias in Reasoning)
Social attribution refers to the processes that individuals use to explain their own behavior and that of others through the assignment
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of motives and characteristic traits to the persons involved. The social attribution hypothesis regarding formation of delusions has been formulated by a number of individuals, but the underlying model came from Kelley. 31 The central concern of the model is the apparently universal fundamental attribution error-the tendency to ascribe another person's behavior to characteristics of the person concerned regardless of the circumstances that are present at the time. In 1989, Kaney and Bentall3 , 29 suggested in a series of studies that the development of delusional beliefs might be understood in terms of the social attribution processes. Specifically, the delusions of persecution may be associated with a particular style of social attribution. These investigators 29 required subjects to respond to a questionnaire in which they made attributions to hypothetical situations. By and large, patients with delusions did not differ from the depressed controls but differed from each other on one or two of the various comparisons made. In brief, no clear demonstration of support for this hypothesis could be found.
PSYCHOBIOLOGIC MECHANISM
The French neurologist de Clerambault, in 1942, put forth the view 16 that chronic delusions resulted from abnormal neurologic events. These events included infections, lesions, intoxications, and other forms of damage that produced automatisms, which in turn puzzled or distressed the patient initially and eventually demanded some form of explanation. The explanation, then, took the form of delusions. Automatisms include hallucinations, parade of memories, feelings of familiarity, false recognition, arrest of thought, disturbances of attention, bizarre tactile sensations, and kinesthetic sensations. The view that delusions represent an explanation of hallucinations is an old, somewhat vague concept in psychiatry. Southard, for example, had performed pioneering studies showing on the basis of autopsy material that there was a striking correspondence between explanations for symptoms that were incorporated into delusions and the specific diseases from which patients suffered. 51, 52 In 1974, Maher32 proposed a hypothesis that conceptualizes delusions as explanations for anomalous experiences that arise in the environment, the peripheral nervous system, or the central nervous system. A significant feature of the theory33 was the proposal that cognitive processes in general were intact in such individuals and that what constitutes the basis for delusions is the anomalous experience that demands explanation. A central tenet of Maher's view is that the processes whereby delusional beliefs are formed are similar to thosethat operate in the formation of normal beliefs and even in scientific hypotheses.33, 34 Central to the proposal is the assumption that components of the normal operation of belief formation arise in a sequence that has a neural substrate that may be activated by sensory input (as in hallucinatory effects of drugs) or by the effects of brain damage
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(as in head injury). The activation of any part of the sequence demands an explanation and may thus give rise to delusions. The sequence, activated by disturbances in sensory experience, emotional incongruity, and central nervous system abnormalities, has the following stages: 1. Anomalous experience,
2. 3. 4. 5. 6. 7.
Feelings of significance, Testing for the reality of the experience, Developing tentative hypotheses to explain the experience, Additional observation, Exploring insight, and Confirmation of the insight by selective observation.
The argument is that the patient is delusional because he or she actually experiences anomalies that demand explanation. Particulars of the delusion, that is, its content, are drawn from the past or current circumstances, experience, and personal and cultural background of the patient. The anomalies are sources for explanatory material available to the patient. The explanation answers questions such as, what is happening? Why is it happening? Why do other people deny that it is happening? Why is it happening only to me? Who's responsible for its happening? The delusional explanation offers a relief from the sense of puzzlement that accompanies odd or unusual experiences of anomalous nature, and this relief works against the abandoning of the explanation; that is, it reinforces the delusional belief and helps to establish its fixedness. Thus, once the explanation has been established, new data that are not consistent with the explanation are disturbing and either become ignored or reinterpreted to fit the explanation. Maher34• 35 has elaborated his views to suggest that the content of the delusional explanation is likely to come from the individual experience and preoccupations of the individual. Thus, the patient whose basic problem is the experience that his or her thoughts are not his or her own is most likely to conclude that someone is controlling them and will then turn to aspects of his or her present or past life to explain why this might be. For a patient, for example, who has been guilty of some act of which he or she is ashamed may reach the conclusion that he or she is being punished for this act by the distressing experience of having his or her thoughts taken over. The sequence may easily mislead clinicians into concluding that the recollection of the guilty act has given rise to the delusional state, thereby confusing effect with cause. What is the evidence to support the model? One source of evidence is the lack of success of attempts to find fundamental defects in the cognitive processes of delusional patients. And from evidence about the processes of belief formation, normal subjects are indistinguishable from those supposed to be characteristic of delusional patients. Indeed, delusions are found in persons of every level of intelligence and education, further supporting the view that disruption or defect in cognitive processes is not the basis of the problem. On the other hand, positive
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evidence comes from the prevalence of delusions in a wide range of medical and psychiatric disorders in which deluded individuals have no prior history of cognitive impairment. Secondly, there is evidence that delusions can be induced in normal subjects under conditions in which they have anomalous experiences; third, the presence of delusions in cases of undiagnosed sensory defect, the frequent coexistence of delusions and their possible development from psychotic symptoms such as hallucinations, thought insertion, thought withdrawal, and passivity phenomena that become elaborated fully in the delusion. Empirical studies, in summation, have reported that anomalies of experiences are correlated with the presence of delusions in many different ways. 35
Other Sources of Anomalous Experience and Delusion Formation
Delusions have been explained in terms of disturbed experiences of time at least since the 1930s when Binswanger and Minkowski proposed that schizophrenic patients suffered from disordered experiences of space and time, leading possibly to feeling imprisoned or controlled. In 1975, Melges and Freeman43 proposed a cybernetic model for the formation of delusions based on the assumption of a temporal disturbance of formal thought as a primary cause of the delusions. A disintegration of the temporal sequence of thought is experienced by the patient as a loss of control, which in several stages, leads to the formation of delusions. The concept that an attentional deficit is related to delusion formation also has been popular. The attentional deficit may alter the content of consciousness, heighten awareness, or sharpen focus on particular details of the environment.2°, 41 The relationship between altered attention and the formation of delusions per se has not been well developed, probably because the deficit view has been applied generally to a wide range of psychopathologic symptoms, especially in schizophrenia, and not simply to delusions. A recent exception is the proposal of Vinogradov and colleagues57 who have created a model linking attentional features and delusional thinking that is based on alterations in associational mechanisms, as a contemporary formulation reminiscent of Eugen Bleuler's views4 about affect and delusion. In 1934, Pavlov45 proposed a theory that related delusions of reference and control to perceptual disturbances that he viewed to be the consequences of pathologic absence of activity in cells of the sensory cortex. Pathologic arousal in other cells causes irrelevant ideas to intrude into consciousness. According to Pavlov, the delusion consists of nothing but reflections about such irrelevant ideas. His formulation had little impact and has not been subjected to empirical testing.
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On the other hand, it has been known that delusions may develop in patients with sensory deficits. For example, Kraepelin commented on the connection between hearing deficits and delusions. Empirical studies generally have shown increased frequency of delusions among patients with hearing deficits 23 as well as an increase of hearing deficits in paranoid schizophrenic patients.30 Visual disturbances also have been found more frequently in paranoid patients. 9 Cooper and Porter8 demonstrated a much higher incidence of visual and auditory perceptual disturbances in paranoid patients compared with patients with mood disorders. In 1981, Zimbardo and colleagues62 were able to show that hypnotically induced hearing loss in normal subjects led to higher scores on the paranoia scale of the MMPI. Despite these observations, there is controversy about the connection of paranoid behavior and auditory perceptual disturbances,28 so that a final model has yet to be developed. Nevertheless, these reports suggest important testable relationships.
Neu ropsychological Theories
A variety of neuropsychological theories have been proposed to account for delusions. Perhaps one of the most famous of these was the proposal of James Hughlings Jackson25 who suggested that features of insanity including delusions could be understood as the result of the interaction between two processes: disruption and loss of the function associated with the failure in areas of the brain that are damaged by disease, on the one hand, and the resulting disinhibition of behaviors in those areas left undamaged. The latter of these factors produces the experience of delusions, a new symptom. Other factors, personality and experience, influence the character of these new symptoms (which we now call positive symptoms). In addition to the theories that have dealt with disordered reasoning, changes in perceptual experience, and the psychodynamic mechanism underlying delusions, there have been more focused attempts in recent years to identify a neurologic basis for delusional thinking. 17• 18• 40 The problem with this approach is that, like other approaches, the assessment of the correlation between delusions and particular anatomic loci depends fundamentally on the reliability and the validity of the distinctions and features associated with delusion itself. In other words, if we cannot identify delusions accurately and reliably, then attempts to make connections between their occurrence and specific lesions in the brain are likely to fail. In the past it has been noted that delusions occur with considerable frequency in nonpsychiatric conditions. This proposal has been amply documented by Manschreck and Petri39 as well as by others.11· 14• 27 This suggests that there is much to account for in trying to explain delusions arising in varied conditions. In recent years there have been more thorough and comprehensive attempts to evaluate the psychopathology associated with specific neurologic disorders.4° Cummings has been a leading contributor in this area
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and has summarized a current view of the relationship between delusions and specific neurologic disease in a series of publications.11-13 He points out that psychosis is not an uncommon occurrence in the course of neurologic disease. In fact, a wide variety of conditions can induce psychosis but particularly those that affect the limbic system and, especially within the limbic system, the temporal lobe and caudate nuclei. Disturbances in these structures are most likely to be associated with the formation of delusions. 42• 50• 55 There appears, in addition, to be an increased frequency of psychosis in conditions that are associated with bilateral involvement of brain structures. At the neurotransmitter level, it is recognized that dopaminergic excess or reduced cholinergic activity also may predispose to psychosis. Left-sided epileptic foci are associated with Schneiderian first rank symptoms, suggesting a lateralization influence in the formation of delusional experience. 40 Indeed, other factors are relevant as well including age at onset, gender, and the type of pathology that in concert or singly can influence the experience of psychosis. On the other hand, it appears that psychosis is independent of the severity of intellectual deficits that occur in patients with neurologic disease. It is also clear that delusions do not correlate with abnormalities in any specific neurologic domain such as language, memory, visuospatial skills, abstraction abilities, and the like, again suggesting that cognitive defect is not the source of delusions. Integrity of intellectual function appears rather to determine the complexity of delusional beliefs. In other words, the more intellectually capable the individual, the greater the complexity of the delusions when they occur in neurologic disease. Cummings 12 proposes a hypothesis to explain delusional formation. He argues that the hypothesis needs to take a number of items into account including the variety of psychopathologic conditions seen in neurologic disease, the variety of delusions in particular; and that if there is to be a common model, it must arise from regularities that we identify in the nature of neurologic lesions. Specifically, Cummings 12 suggests that limbic dysfunction, the common locus, leads to misinterpretation of the environment, and this is accompanied by an inappropriate perception of threat. This, in turn, leads to paranoid belief formation. Patient- and disease-related factors also influence the content, complexity, and timing of the formation of delusions. The appealing nature of this hypothesis derives from its midrange attempt to connect what is known to what we need to explain, its cautious approach to claiming generalizability, and its reliance on a range of observations to generate testable hypotheses about a possible common mechanism. It stands ready to be tested. It complements the anomalous experience proposal in many ways.
SUMMARY AND CONCLUSIONS
This overview of attempts to shed light on the pathogenesis of delusions provides a sense of promise, because we are grappling with
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the right problems, and reasons for both optimism and skepticism. Optimism is justified because some of the approaches have yielded empirical support and can be tested profitably in research. Skepticism is warranted because we remain unclear about precisely what delusions are; and we have as yet no means of identifying them with a laboratory test. Hence, we must rely on the problematic nature of clinical observation of the inner experiences of patients to make progress. The different mechanisms proposed still require considerable testing, but scrutiny of current results suggests that anomalous experience as a stimulus for delusion formation has been better documented than proposals invoking disordered reasoning or motivational deviances. Nevertheless, no view is as yet established, and each may have some relevance to solving the delusion puzzle. References l. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disor-
ders, ed 4. Washington, American Psychiatric Press, 1994 2. Arthur AZ: Theories and explanations of delusions: A review. Am J Psychiatry 121:105- 115, 1964 3. Bentall RP, Kaney S: Content-specific information processing and persecutory and persecutory delusions: An investigation using the emotional Stroop test. Br J Med Psycho! 62:355-364, 1989 4. Bleuler E: Dementia Praecox or the Group of Schizophrenias. New York, International Universities Press, 1950 5. Cameron N: The paranoid pseudo-community revisited. Am J Social 65:52-56, 1959 6. Chadwick PDJ, Lowe CF: Measurement and modification of delusional beliefs. Consult Clin Psych o! 58:225-232, 1990 7. Chadwick PDJ, Lowe CF, Horne PJ, et al: Modifying delusions: The role or empirical testing. Behav Ther 25:35-49, 1994 8. Cooper AE, Porter R: Visual acuity and ocular pathology in the paranoid and affective psychoses of later life. J Psychosom Res 20:107-114, 1976 9. Cooper AE, Curry AR: The pathology of deafness in the paranoid and affective psychoses of later life. J Psychosom Res 20:97-105, 1976 10. Costello CG: Research on symptoms versus research on syndromes: Arguments in favor of allocating more research time to the study of symptoms. Br J Psychiatry 160:304-308, 1992 11. Cummings JL: Organic delusions: Phenomenology, anatomical correlation, and review. Br J Psychiatry 146:184-197, 1985 12. Cummings JL: Psychosis in neurologic disease: Neurobiology and pathogenesis. Neuropsychiatry, Neuropsychology and Behavioral Neurology 5:144-150, 1992 13. Cummings JL, Miller B, Hill MA, et al: Neuropsychiatric aspects of multi-infarct dementia and dementia of the Alzheimer's type. Arch Neural 44:389- 393, 1987 14. Davison K, Bagley CR: Schizophrenia-like psychoses associated with organic disorders of the central nervous system: A review of the literature. Br J Psychiatry 4:113-184, 1969 15. De Bonis M, Epelbaum C, Feline A, et al: Pensee formelle, operations logico-discursives et schizophrenie: etude experimentale d'un cas clinique. Revue Canadienne-de psychiatie 35:64-70, 1990 16. de Clerambault GG: Les Psychoses Passionelles. In Oeuvre Psychiatrique. Paris, Presses Universitaires, 1942 17. de Leon J, Antelo RE, Simpson G: Delusion of parasitosis or chronic tactile hallucinosis: Hypothesis about their brain physiopathology. Comp Psychiatry 33:25-33, 1992 18. Ellis HD, Young AW: Accounting for delusional misidentification. Br J Psychiatry 157:239-248, 1990
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Address reprint requests to Theo C. Manschreck, MD Brown University School of Medicine Corrigan Mental Health Center 49 Hillside street Fall River, MA 02720