Emotion regulation after acquired brain injury

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  • Christian Salas

    Research areas

  • PhD, School of Psychology

Abstract

Emotion dysregulation is a common phenomenon after brain injury, often compromising socioemotional adjustment and participation. Nevertheless, there has been little research exploring the mechanisms by which brain damage impacts emotion regulation [ER]. In contrast, outside the field of neuropsychology, the study of ER has matured during the last decade, generating a robust body of evidence on the strategies that people use to modulate their feelings. The main goal of this thesis is to bring together, for the first time, these two fields of knowledge. Chapter two presents three articles touching key conceptual issues, such as the description of self-regulation and self-other regulation problems after brain injury, the relationship between neuropsychological profiles of impairment and ER strategies deficits, and the impact of concrete behaviour on emotional experience. Chapter three explore the problem of emotion elicitation and emotional reactivity. In two articles, the efficacy of internal and external forms of elicitation is explored on a student sample [n = 40], as well as compared between people with right hemisphere [RH] damage and matched healthy controls [RH: n = 10, HC: n = 15]. The main finding of both studies is that internal elicitation procedures generate higher levels of subjective reported emotion across populations of different age. In addition, patients with RH damage present similar levels of emotional reactivity compared to controls. Chapter four explores how specific ER strategies are compromised by focal brain injury. In the first study, people with RH frontal lesions [n = 10] were compared to healthy control [n = 15] on a response modulation task. It was found that RH patients were impaired voluntarily manipulating emotional facial expressions, and that a subgroup of RH patients was unable to inhibit emotional displays. The second study explored the impact of unilateral lesions in the capacity to reappraise [RH: n = 8, LH: n = 8, HC: n = 14]. Individuals with RH and LH lesions were equally slow, compared to controls, generating reappraisals. However, when time was not considered, both groups were equally productive. Finally, Chapter five uses a single case study methodology to explore the mechanism by which ER, and particularly reappraisal, is disrupted after left prefrontal lesions. Here, two articles offer important insight into how concreteness and executive impairment are associated to emotion dysregulation, and the mechanisms by which such dysregulation can be externally compensated.

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Original languageEnglish
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Award date14 Jun 2013