Auditory Verbal Hallucinations, phenomenology and neurocognitive mechanisms

Background Auditory verbal hallucinations (AVH) can be a symptom in several psychiatric and neurological disorders, but are also prevalent in the general population. These non-psychotic individuals are not disturbed by their sub-clinical symptoms and function well both socially and occupationally. The question remains whether AVH in patients with a psychotic disorder are comparable to those in non-psychotic individuals. With this aim, the studies presented in the first part of this thesis investigated the phenomenology of AVH. The second part focussed on neurocognitive mechanisms that are related to AVH in these groups. Methods The non-psychotic individuals and the voices they hear were described with the help of several questionnaires in the first two studies. With respect to neurocognitive mechanisms in the second part of this thesis, the third study explored the relationship of AVH in non-psychotic individuals with cognitive functioning using several cognitive tests. Finally, healthy controls, non-psychotic individuals with AVH and psychotic patients with AVH were compared on the presence of cognitive biases in the fifth study, on semantic top-down processing in the sixth study and on the presence of reported childhood trauma in the last study. Results These studies showed phenomenological differences between AVH in non-psychotic individuals and psychotic patients with respect to age at onset, emotional valence, frequency and control, while some characteristics were similar. Furthermore, AVH were found to be related to poorer but not impaired inhibition and working memory within the verbal domain, increased semantic top-down functioning and the absence of most cognitive biases in non-psychotic individuals with AVH. In psychotic patients with AVH however, no relation with semantic top-down processing was found and several cognitive biases were present. Finally, both AVH groups experienced significantly more childhood trauma than healthy controls. Conclusion The differences in cognitive processes that were found in these studies suggest that underlying mechanisms of AVH in non-psychotic individuals and psychotic patients are not completely similar and in fact differ on rather fundamental aspects. This can be explained by making a distinction between biological and cognitive factors in the generation in AVH. The biological basis for AVH (genetic predisposition and factors influencing brain development, for example childhood trauma) is dominant in psychotic patients and thereby limiting their functioning in many ways. As such, little room may be left for (intact) cognitive processes to play a part in the generation of AVH. In the non-psychotic individuals, this biological influence is weaker. Their psychotic symptoms are less severe and their cognitive alterations are not of clinical significance. This gives these intact cognitive processes, such as semantic top-down processing, more opportunity to exert their influence and thereby possibly shaping the phenomenology or experience of AVH. Furthermore, relative intact cognitive functioning instead of cognitive impairment may even have served as a protective factor in the non-psychotic individuals, and prevented them to progress further along the continuum to the help-seeking minority with the clinical phenotype