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Abstract
Acquired social disinhibition refers to a debilitating behavioural syndrome commonly reported after a severe traumatic brain injury (TBI) and is characterised by inappropriate social behaviour, often described as immaturity and insensitivity towards others. These behaviours can have enduring effects on the social capability of the individual and their relationships with others. However, research into socially disinhibited behaviour after TBI has been thwarted by a lack of consensus in the literature on definition and measurement. Further, although strong evidence exists of an association between orbitofrontal damage following TBI and social disinhibition, there exists no conclusive evidence on what cognitive mechanisms might be responsible for this disinhibited behaviour. A better understanding of what mechanisms underlie this syndrome will enable the development of targeted rehabilitation to improve the social functioning, and thus the wellbeing, of individuals with acquired social disinhibition after TBI.
Study 1 of this thesis aimed to validate a new observational measure of socially disinhibited behaviour for use in a population of individuals with TBI. Participants were 22 adults with severe TBI and 21 healthy control participants. Participants were rated by two independent judges on the appropriateness of their social behaviour in a structured interview with an experimenter. Further, the disinhibition domain of the Neuropsychiatric Inventory (NPI-D) and the interpersonal relationships subscale of the Sydney Psychosocial Reintegration Scale (SPRS-IR) were completed by someone close to the individual with TBI. Results demonstrated good inter-rater absolute agreement for the social disinhibition ratings. Participants with TBI were rated as significantly more disinhibited than control participants. Further, these ratings were positively correlated with the frequency of disinhibited behaviour and with the level of distress caused by these behaviours as reported by a close other on the NPI-D. Thus, Study 1 demonstrated good inter-rater reliability and construct validity of the new objective observational measure, evidencing the usefulness of this measure for detecting social disinhibition after TBI. However, the social disinhibition ratings were not related to informant-reported change in employment or in interpersonal relationships on the SPRS. As such, social disinhibition observed in the laboratory did not predict social and vocational outcome as reported by close others.
Study 2 aimed to determine whether smell impairment could predict social disinhibition after TBI, since it has been suggested in the literature that smell impairment can act as an indicator of orbitofrontal damage following TBI. The Brief Smell Identification Test (BSIT) and the observational measure of social disinhibition developed in Study 1 was completed by 23 individuals with severe TBI and 15 controls matched for age and years of education. Further, the disinhibition domain of the Neuropsychiatric Inventory (NPI-D) and the interpersonal relationships subscale of the Sydney Psychosocial Reintegration Scale (SPRS-IR) were completed by a close other of the individual with TBI. Results showed that BSIT scores predicted informant-reported change in interpersonal relationships on the SPRS-IR but did not predict disinhibition, whether reported by an informant or observed in the laboratory. While these results do support previous claims that smell impairment has prognostic significance following TBI, no evidence was found for a relationship between smell impairment and social disinhibition specifically. It was concluded that smell impairment may indicate frontal damage broadly, but not orbitofrontal damage specifically.
Study 3 aimed to determine whether emotion perception deficits play a role in social disinhibition following TBI. Further, this study aimed to extend upon previous inconclusive literature by improving measurement of emotion perception. This study was the first to assess the relationship between emotion perception and social disinhibition specifically, rather than social competence more broadly. An emotion labelling task and an emotion intensity rating task, as well as the observational measure of social disinhibition, were completed by 23 individuals with severe TBI. The interpersonal relationships subscale of the Sydney Psychosocial Reintegration Scale (SPRS-IR) was completed by a close other. Fifteen control participants provided norms against which to assess performance on the emotion perception tasks. Results showed that while participants with TBI were impaired in terms of accuracy scores on both emotion perceptions tasks, intensity ratings did not differ between groups. This suggested that people with TBI are not actually impaired at detecting intensity of emotion but are less likely to perceive the target emotion as the dominant emotion. Further, emotion perception was not related to disinhibition or change in interpersonal relationships. It was concluded that emotion perception impairment measured by standardised tasks does not appear to be an important factor in interpersonal outcomes broadly, or in disinhibited behaviour specifically.
Finally, Study 4 aimed to determine whether reversal learning impairments might play a role in social disinhibition after TBI. Reversal learning impairment refers to the inability to flexibly adjust behaviour when reinforcement contingencies in the environment change. Further, the study aimed to determine whether feedback-related negativity (FRN), reflecting reward prediction error signals, were associated with social disinhibition. The number of reversal errors on a social and a non-social reversal learning task and the FRN associated with these errors were examined for 21 participants with TBI and 21 control participants matched for age. Participants with TBI were also divided into low and high disinhibition groups based on ratings on the observational measure of social disinhibition. Results showed that participants with TBI made more reversal errors than control participants. Further, participants with TBI high on social disinhibition made more social reversal errors than did those low on social disinhibition. Finally, although participants with TBI did produce smaller FRN’s than control participants, FRN amplitude was not related to disinhibition. These results suggest that impairment in the ability to update behaviour when social reinforcement contingencies change plays a role in social disinhibition after TBI. Further, the social reversal learning task used in this study may be a useful neuropsychological tool for detecting susceptibility to acquired social disinhibition following TBI. Finally, that the FRN amplitude was not associated with social disinhibition suggests that reward prediction error signals are not critical for behavioural adaptation in the social domain.
This empirical investigation adds significantly to the literature by providing a novel objective measure of social disinhibition and an improved understanding of the mechanisms which underlie socially disinhibited behaviour after TBI. Specifically, the findings of this thesis suggest that it is not the inability to perceive social cues, but rather the inability to flexibly change behaviour based on those cues, that underlies social disinhibition.