Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.807956
Title: Cognition in first-episode psychosis : characterisation, reserve and relationship to functioning
Author: Watson, Andrew James
ISNI:       0000 0004 9353 1432
Awarding Body: UCL (University College London)
Current Institution: University College London (University of London)
Date of Award: 2020
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Abstract:
Schizophrenia is marked by deficits in cognition and social functioning that present early in the course of illness. A relationship between neurocognitive impairment (e.g. memory and processing speed), and social functioning is reported in the literature, with poorer neurocognition associated with worse social outcomes. There is emerging evidence for the existence of neurocognitive subtypes with different cognitive trajectories, hypothesised to reflect separate etiological processes and risk factors for clinical and social outcomes. Despite neurocognition being considered one of the best predictors of social outcomes, there is still a large amount of variance in outcomes left unexplained. In addition to neurocognitive deficits, processes required for successful social interactions, collectively known as ‘social cognition’ i.e. theory of mind, attribution bias, social perception and emotion perception, have been shown to be impaired in those with established schizophrenia. There is some evidence that social cognition mediates the relationship between neurocognition and functional outcomes. Studying individuals with a first-episode psychosis (FEP) allows the examination of the fundamental features of schizophrenia, without the confounding effects of prolonged medication, hospitalisation and social isolation. Using two clinical-trial FEP groups, the studies presented in this thesis examined: the existence and magnitude of global and domain-specific neuro- and social cognitive impairment; the existence of neurocognitive-trajectory based subtypes and their brain volumetric and inflammatory profiles; the relationship between neurocognition and social functioning; and whether social cognition mediates the relationship between neurocognition and social functioning. Three IQ-trajectory based subtypes that were stable over time and distinguished by biological underpinnings were found. Social cognition deficits were present early in the course of illness and significantly overlapped with neurocognitive impairments, but it could not be concluded that social cognition mediates the relationship between neurocognition and social functioning. The results of the studies enabled recommendations for remedial strategies to improve social functioning and quality of life of individuals early in the course of illness.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.807956  DOI: Not available
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