| Summary: | Neurological confabulation is a prototypical form of false remembering and as such, it can provide insight into the nature of human memory. The main aims of the thesis was to empirically investigate the neuropsychological hypothesis that the content of confabulation is motivated. This was addressed by studying the neuropathological and neuropsychological profiles of 13 neurological patients with severe forms of confabulation, and by conducting three original experimental group studies and two single-case studies. Confabulating patients were compared with frontal and amnesic non-confabulating patients, as well as with neurologically healthy controls. Neuropathological findings confirmed previous indications of orbital and medial prefrontal cortex (OMPFC) damage or disconnection. Neuropsychological data showed that the presence of amnesia and executive function varied across confabulating patients. The first experimental study revealed that bilateral confabulating patients showed a positive emotional bias in their spontaneous confabulations. The second study, based on a recognition experiment, confirmed the presence of this bias, over and above the deficits of temporality and reality monitoring. The third study was based on an emotional prose recall experiment, in which the self- relevance of the material was manipulated. This revealed that the emotional biases shown by confabulating patients were self-serving, and not explicable by deficits of amnesia or executive dysfunction. These self-serving biases were common to bilateral and unilateral confabulating patients, but their confabulations showed valence differences. Two single-case studies provided further specification to these findings and showed that confabulating patients form confabulations according to the values and goals of their premorbid self-representation. In conclusion, this thesis provided experimental support for the hypothesis that the content of confabulation is motivated. This finding was conceptualised as a disinhibition of emotional memory associations, most likely caused by damage or functional disconnection of the OMPFC from adjacent limbic structures. These conclusions have wider implications about the role of the OMPFC in mediating the relation between emotion and memory.
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