AbstractThe present PhD project investigated the role of psychophysiological stress-function and adversity exposure in auditory verbal hallucinations and the clinical status of voice-hearers. Psychosis is associated with several alterations in biological stress systems, including the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal (HPA) axis, as well as subjective stress levels and -reactivity. Exposure to childhood trauma has been particularly linked to the emergence of auditory verbal hallucinations in psychosis, as well as a dysregulation of stress-psychophysiology. However, it remains unclear whether changes in stress-function and -reactivity are related to auditory hallucinations specifically, or only to psychosis more generally. Further, auditory verbal hallucinations occur in both clinical and non-clinical populations. Voices in healthy and clinical voice-hearers share many characteristics, including phenomenological (such as loudness) and neurophysiological correlates of auditory verbal hallucinations. However, healthy voice-hearers do not experience distress in response to their voices, and their voices contain less negative content. It remains unknown whether psychophysiological stress-function may also discriminate clinical and non-clinical voice-hearers, and whether dysregulated stress-function is associated with the experience of hearing voices, and/or need for care. Evidence suggests there is increased childhood trauma exposure in healthy voice-hearers, at similar rates to clinical voice-hearers. However, adolescence/adulthood adversity remains largely unexplored in healthy voice-hearers, as does exposure to other risk factors including socioeconomic adversity and substance use. A more recent version of the diathesis-stress model, the three hit model, has highlighted the role of adversity after childhood in shaping pathological trajectories, which may partially explain the difference in distress and need for care in clinical and healthy voice-hearers. Lastly, it is not known whether, and to what degree, voice content contributes to psychophysiological dysregulation in clinical voice-hearers. To address these issues, the present project investigated three key research questions:
1. Does adolescent/adulthood adversity exposure differ between healthy voice-hearers and clinical voice-hearers, and is the differential adversity exposure associated with increased stress-sensitivity?
2. Does the content of voices exacerbate stress-reactivity?
3. Does psychophysiological stress-function in clinical voice-hearers differ from those of healthy voice-hearers and healthy controls without voices?
Three individual studies are reported to assess these research questions:
1. A cross-sectional study of clinical and healthy voice-hearers was carried out to assess the role of familial risk and adversity exposure in childhood, and adolescence/adulthood in the context of the three hit model. Further, the association of adversity exposure with perceived stress was examined.
2. A cross-sectional design with a healthy non-voice hearing sample was carried out using simulated auditory hallucinations with negative and neutral content to assess their impact on psychophysiological stress-reactivity during psychosocial stress exposure. The potential buffering effects of mindful appraisals of voices on psychophysiological stress-reactivity were also assessed.
3. A cross-sectional study of clinical and healthy voice-hearers, as well as a healthy control group with no voices, was carried out comparing the three groups on diurnal HPA and ANS activity, HPA response to pharmacologically induced negative feedback, and HPA and ANS responses, as well as subjective reactivity, to a psychophysiological stress paradigm.
The cross-sectional study on adversity exposure showed that, unexpectedly, victimisation and discrimination experiences were similar in clinical and healthy voice-hearers in both childhood and adolescence/adulthood. However, the two groups differed on familial psychosis risk, adolescence/adulthood socioeconomic status, and substance use, with the clinical group reporting greater rates of adversity exposure. These variables were further predictive of perceived stress, after controlling for group. The analogue voice study demonstrated that negative voices exacerbated subjective, but not physiological, stress-reactivity, compared to neutral voices and ambient sounds. Having a mindful stance towards the voices during the task was associated with lessened stress-reactivity. Finally, as predicted, clinical voice-hearers showed several indices of aberrant psychophysiological stress-function of the HPA axis, compared to both healthy voice-hearers and controls without voices, although not always in the predicted direction. Contrary to our predictions, there were no differences between groups on parameters of the ANS. However, there was some evidence to suggest stress-function in healthy voice-hearers also diverges from non-voice-hearing controls on some HPA parameters, including reduced cortisol levels during stress exposure, slower speed of cortisol recovery from the stressor, and lower HPA negative feedback capacity.
The present thesis found evidence to suggest that specific types of adversity exposure and stress-function are related to the need for care of clinical voice-hearers and may be involved in pathological outcomes of voice-hearing. Differential adversity exposure, and its relationship to stress-sensitivity may therefore partially relate to psychopathological trajectories in voice-hearing. The negative content of voices may further contribute to the maintenance of need for care through exacerbated stress-reactivity. Finally, dysregulated psychophysiological stress-function is present in clinical voice-hearers, and partially discriminates them from healthy voice-hearers. Overall, the present findings identified specific potential psychophysiological markers of risk and resilience in auditory verbal hallucinations and need for care. This thesis provides an initial stepping stone for future research developments to explore precise causal and mechanistic relationships of adversity exposure, psychophysiological stress-function and need for care in voice-hearing.
|Date of Award||2017|
|Supervisor||Emmanuelle Peters (Supervisor) & Paul Chadwick (Supervisor)|