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Title: Role of the autonomic nervous system in emotional experience and social communication of distress
Author: Harrison, Neil Andrew
ISNI:       0000 0004 2676 4666
Awarding Body: UCL (University College London)
Current Institution: University College London (University of London)
Date of Award: 2009
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Influential theories of emotion propose that afferent bodily information is central to the experience of emotional feeling states. Neuroanatomical studies suggest a phylogenetically unique afferent neural system in primates that conveys information regarding motivationally salient aspects of the physiological condition of the viscera and other bodily organs and supports a representation of homeostatic afferent activity engendering sensations including nausea, pain and muscular aches. This thesis focuses on brain-body interactions in neural signalling of sickness and communication of emotional distress. I begin by presenting investigations into the role of visceral afferents travelling with the autonomic nerves in the central communication of bodily inflammation and the mechanisms underlying cognitive, emotional and motivational components of sickness. Using a model of inflammation (Typhoid vaccination) and functional magnetic resonance imaging (fMRl) I show that peripheral inflammation activates the hierarchy of brain regions encoding a representation of bodily state consistent with an autonomic afferent mechanism, wherein differential insula, subgenual cingulate and substantia nigra activity predict fatigue, mood change and psychomotor retardation respectively. I then investigate the role of organ specific autonomic signals in the differential responses to bloody (mutilation) and core-ingestive forms of disgust. I present fMRl, heart rate and electrogastrogram data which suggest organ-specificity in bodily responses to different forms of disgust related to these distinct peripheral channels. Finally I present data investigating the role of autonomic signals in the communication of distress and demonstrate that pupillary signals selectively modulate perception of another’s sadness. Using fMRl and pupillometry I show that another’s pupillary signals in the context of sadness modulate activity within the observer’s brain in face processing regions. Further in sadness observed pupil size leads to a contagious mirroring of the observer’s own pupil size via a mechanism that recruits brainstem pupillary control (Edinger Westphal) nuclei.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available