http://schizophreniabulletin.oxfordjournals.org/content/39/2/278/suppl/DC1
Supplementary Text Boxes for on line publication of The Phenomenology and Neurobiology of Delusion Formation During Psychosis Onset: Jaspers, Truman Symptoms, and Aberrant Salience
S1. Incomplete perceptual processing, need for closure and jumping to conclusions
One of the “most well-established cognitive anomalies” associated with delusions is the jumping to conclusions (JTC) reasoning bias, whereby individuals with delusions consider less evidence and are more hasty in their decision making than controls.[1] JTC is associated with the intensity of delusional ideation, and has been found in individuals with at risk mental state.[2] Garety and colleagues report that the association between JTC and intensity of delusional ideation is mediated by belief inflexibility defined as the absence of “the metacognitive capacity of reflecting on one’s own beliefs, changing them in the light of reflection and evidence, and generating and considering alternatives.”[3] This is of particular interest because cognitive behavioral interventions which target JTC in conjunction with belief inflexibility have lead to improvements in delusional conviction between pre- and post-intervention measures.[4] Moreover, delusion-prone individuals score higher than healthy controls on a need for closure scale.[5] These various findings overlap with the phenomenological approach to delusions. The construct “cognitive inflexiblity” has resemblance to the loss of the ability to shift or transcend the current momentary perspective (as proposed by Binswanger, Blankenburg and Conrad). As depicted in table 1, this loss is related to the “shrinking” of temporal perspective to the present moment and which, as we indicate, is consilient with the aberrant salience model. Conrad’s approach to delusions also anticipates the later findings of the relationship between delusion-proneness and need for closure. Conrad[6] believed that the compromised perceptual processing in early schizophrenia was modeled by the experimental procedure of “microgenesis” (for reviews, see[7],[8]). The experimental method, “microgenesis” interrupts or diminishes the percept by means of tatiscopic presentation (often too briefly to be consciously experienced), reduced illumination of the field, diminishing the size of the stimulus, or presentation in peripheral vision. These impoverished conditions lead to a loosening of the object’s perceptual binding (gelockerten Reizbindung). Conrad’s microgenesis model indicates that the perceptual experiences leading to delusions provide reduced information progression from diffuse, feeling toned qualities to an ever more articulated, or finalized Gestalt in predetermined phases of longer and more detailed presentation. In the progression to an ever more articulated, or finalized Gestalt, the healthy subject is ultimately able to ‘‘detach emotionally’’ and experiences a sense of completeness or closure, recognizing suddenly, with relief and surprise, the actual Gestalt. The delusional patient, on the other hand, remains attached to earlier, arrested phases of meaning unable to detach
from the incomplete perceptual meaning or the pre-Gestalt (Vorgestalt). In their 1957 review, Flavell and Draguns suggest that schizophrenia is a “condition which early cognitive formations intrude into consciousness and get expressed as though they were completed thoughts.” [9](p. 197) In this way, Conrad’s microgenetic model anticipates the later JTC findings.
S2. The individual interpretation of the delusional experience
The individual’s interpretation of the experience, including the delusional themes[10],[11],[12]
derived from this experience, is likely to reflect the patient’s own prior beliefs and historical experience.[13] In this sense it is not surprising then, that primary delusions are nevertheless often personal, rooted in long-held beliefs, and that their content varies by culture, influenced by socio-cultural factors.[14] This of course does not make the delusions more understandable in Jaspers’ method.
S3. Phenomenology of Delusion-formation after Jaspers
We have suggested that Jaspers phenomenological approach to delusions is consilient with later neurobiological models of aberrant salience, dopamine dysregulation and prediction error.[15] It is important to add that other phenomenologically-oriented psychiatrists further developed Jaspers’ observations in a manner relevant to the later neurobiological models. Matussek,[16],[17],[18] Conrad,6,7 Binswanger10,11 and Blankenburg12,[19] pointed to a loss of context as fundamental to delusional-formation both in the original perceptual experience and its memory. For Matussek, the perceptual-Gestalt is part of, and thus organized in terms of the total organization between self and world (see also[20]). He proposes that the delusional symbolic-meaning is not first derived from thought but experienced directly in the percept. This results from a “loosening of the natural connectedness” between perceptual-objects in the background perceptual-field. As indicated in Supplementary Text Box 1, Conrad6 describes this process as a loosening of the object’s perceptual binding (gelockerten Reizbindung) in which the patient is unable to see another point-of-view (i.e., “transcend/shift” the current perspective; see Table 1). Harmless or accidental occurrences in the environment are nevertheless experienced as obtrusively salient and perception becomes tunnel-like as in the Truman sign patients. While Matussek and Conrad focused on the delusion’s perceptual origins,[21] Binswanger and Blankenburg focused on its memory. Binswanger 10,11 observed that it is not only the perception which, due to its abnormal salience, is loosened from its background-context in the original delusional experience but also how it is remembered. The delusional theme becomes independent from its original scene (Urszene) and “monotonously” spreads to more and more situations in the patient’s life.
S4. Working self, episodic memory and autobiographical knowledge
The phenomenological view conforms with more recent cognitive-neurobiological research that indicates that the working self, which organizes the psychological present in terms of current goals, event or episodic memory, and autobiographical self knowledge constrain one another. Coherent self-experience plays a key role in integrating episodic memories into the more enduring self-knowledge: “When the connection between episodic memories and the self becomes disrupted, as occurs following several different types of brain damage… and in certain forms of psychopathological illness, then coherence breaks down and ungrounded delusional versions of the self, divorced from reality, emerge.”[22](p496) Notably, autobiographical memory impairments in established schizophrenia are associated with an altered sense of self.[23] The relationship between phenomenology of delusions, memory and self and specifically its contribution to more recent clinical neurobiological research is its own topic and will be examined in a subsequent contribution.
S5. “Original phenomenon” of delusions and its impact on subsequent research
At the time of writing their monograph, Huber and Gross write: “Jaspers’ description of primary delusion as an ‘original phenomenon’ (Urphaenomenon) is a fundamental question for psychopathology and has been over the past 60 years the central concern of innumerable studies concerning delusion.”[24] (our translation)
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