Exploring neuropsychological underpinnings of poor communication after traumatic brain injury: The role of apathy, disinhibition and social cognition.

BACKGROUND: Dysarthria, aphasia and executive processes have been examined for their role in producing impaired communicative competence post traumatic brain injury (TBI). Less understood is the role of emotional dysregulation, that is, apathy and disinhibition, and social cognition, that is, reading and interpreting social cues. METHODS & PROCEDURES: In this study, we examined 49 adults with moderate to severe TBI and 18 neurologically healthy adults. We hypothesised that apathy and disinhibition would predict communication outcomes as would social cognition. We also predicted that apathy and disinhibition would influence social cognition. Communication outcomes were measured by the La Trobe Communication Questionnaire (LCQ) and the Social Skills Questionnaire-TBI (SSQ-TBI). Apathy and disinhibition were measured by the Frontal Systems Behavior Scale (FrSBe). We measured four aspects of social cognition: emotion perception and theory of mind using The Awareness of Social Inference Test (TASIT) and the Complex Audio-Visual Evaluation of Affect Test (CAVEAT), empathy using the Questionnaire of Cognitive and Affective Empathy (QCAE) and the Balanced Emotional Empathy Scale (BEES), and alexithymia using the Toronto Alexithymia Scale (TAS-20) and the Bermond-Vorst Alexithymia Questionnaire. OUTCOMES & RESULTS: Consistent with predictions, the LCQ and SSQ-TBI were associated with disinhibition and the LCQ was also associated with apathy. The LCQ was associated with the full range of social cognition constructs although the SSQ-TBI was not. Finally, apathy and disinhibition predicted a number of social cognition measures. CONCLUSIONS AND IMPLICATIONS: These results are discussed in relation to understanding the nature of communication disorders following TBI and how they are measured, as well as the interrelation between emotion dysregulation and social cognition. WHAT THIS STUDY ADDS: What is already known on this subject The role of emotional dysregulation and social cognition in producing impaired communicative competence post traumatic brain injury (TBI) is not well understood. Although most adults with severe TBI have minimal or possibly no language impairment, they often struggle with functional communication in everyday situations. Many have been reported to be overtalkative, insensitive, childish and self-centred, displaying an inappropriate level of self-disclosure and making tangential and irrelevant comments. Conversely, some speakers with TBI have been noted to have impoverished communication, producing little language either spontaneously or in response to the speaker's questions and prompts. What this paper adds to existing knowledge We found that both apathy and disinhibition were strongly associated with the Latrobe Communication Questionnaire both empirically and conceptually, despite the LCQ being developed from a different, pragmatic orientation. Disinhibition was also associated with the Social Skills Questionnaire for TBI. We also found that poor social cognition scores predicted communication difficulties. Finally, we found that behavioural dysregulation itself, i.e., both apathy and disinhibition, predicted poor social cognition. What are the potential or actual clinical implications of this work? Our findings highlight the central role that apathy and disinhibition play in both communication and social cognition. These insights point to the importance of remediation to target behavioural and autonomic dysregulation as a means to improve everyday social function.

The complex audio visual emotion assessment task (CAVEAT): development of a shorter version for clinical use.

PURPOSE: The Complex Audio Visual Emotion Assessment Task (CAVEAT) is a measure of emotion recognition using dynamic, naturalistic videos to assess recognition of 22 different emotional states (11 positive, 11 negative). It has established construct validity and demonstrated sensitivity to emotion perception impairments in those with moderate-severe traumatic brain injury (TBI). Despite this, its lengthy administration has limited its use in clinical practice and rehabilitation. The current paper aimed to develop shortened versions of the CAVEAT and examine their psychometric properties. METHODS: The CAVEAT-S A and CAVEAT-S B (22 items each) and the CAVEAT-S AB (44 items) were developed using the original data. Comparability, reliability, construct and predictive validity were examined in the original sample (Study 1: 32 people with TBI and 32 demographically matched control participants) and a replication sample (Study 2: 18 adults with TBI and 21 demographically matched controls). RESULTS: All short forms produced comparable accuracy ratings to the full measure, as well as discriminating between people with or without a TBI. Shortened forms all correlated with other measures of emotion perception and social cognition and also predicted psychosocial outcomes in terms of self-reported interpersonal relationships. Internal reliability of the short forms was low relative to the longer forms, especially for the two very short measures. CONCLUSIONS: The new shortened forms of the CAVEAT are promising tools that are sensitive and valid for assessing emotion perception in people with TBI for clinical purposes. Their application in other clinical disorders is yet to be examined.Implications for rehabilitationEmotion perception deficits are present in many clinical populations and an important target for rehabilitation.CAVEAT Short provides ecologically valid emotional stimuli. Such stimuli are important for assessing real world function and to set rehabilitation targets.By having parallel versions of CAVEAT, there is the opportunity to test pre and post intervention while minimising practice effects.Alternatively, one version of CAVEAT-S can be used for assessment, while the other is used for training purposes during remediation.

Learning from the minds of others: A review of social cognition treatments and their relevance to traumatic brain injury.

Social cognition is widely regarded as an essential skill with which to understand the social world. Despite this, the role that social cognition plays in outcome, and whether deficits are remediable after traumatic brain injury (TBI), are not yet well known. The current review examines the construct of social cognition and presents a conceptual biopsychosocial model with which to understand the social cognitive process. This is related to the literature on social cognitive deficits in TBI and we discuss relevant treatment developments to date within this population. We then review social cognition treatment programmes researched in other clinical populations in order to advise and inform approaches for those living with TBI. Whilst treatments have focused on emotion perception skills in the TBI literature, programmes developed for other clinical populations have had broader targets, focusing on Theory of Mind skills and/or modifying interpretational cognitive biases. Moreover, they have largely proven to be efficacious. Programmes that are contextualised, collaborative, and experiential seem optimal in enabling generalisation relevant to individuals' everyday social lives. We argue that there is therefore scope to improve the evidence-based social cognitive treatment options available for those with TBI, taking into account specific adaptations necessary for this population.

Have we forgotten about forgetting? A critical review of 'accelerated long-term forgetting' in temporal lobe epilepsy.

Forgetting has been researched for over a century. This literature highlighted how forgetting rates can vary dependent on factors in the design and method. Recent interest in forgetting revived with evidence suggesting that seizures experienced almost immediately after matched learning could accelerate forgetting. This was followed by a growth in forgetting studies in patients with temporal lobe epilepsy (TLE), including a subset of those with transient epileptic amnesia (TEA). These patients have been described as expressing concerns about memory, yet often perform within 'normal' ranges on standard neuropsychological memory assessments. It was argued that such patients were experiencing a phenomenon termed 'accelerated long-term forgetting': apparently normal learning and initial retention with abnormal forgetting over days to weeks after learning. In this review, we critically evaluate aspects of this definition, namely whether learning and initial retention is, in fact, 'normal' at first, and further what this means in relation to 'when' abnormal forgetting starts. We propose a shift in the understanding of accelerated forgetting in TLE from an emphasis on late-onset forgetting to greater focus on early-onset, progressively greater forgetting. We argue that most evidence from studies to date could be conceptualized within the latter framework, with differences in forgetting patterns reflective of a continuum of severity and/or sensitivity.

Forgetting in temporal lobe epilepsy: When does it become accelerated?

The notion of 'accelerated long-term forgetting' has often been attributed to disrupted 'late' memory consolidation. Nevertheless, methodological issues in the literature have left this theory unproven, leading some to suggest such findings may be reflective of subtle acquisition or early retention deficits. This study attempts to address such issues, and also to explore which pathophysiological variables are associated with forgetting rates. Eighteen participants with temporal lobe epilepsy (TLE) and eighteen matched controls completed background neuropsychological measurement of immediate and short-delay memory that showed comparable performance, both on verbal and visual tests. Using two novel experimental tasks to measure long-term forgetting, cued recall of verbal and visuospatial material was tested 30 sec, 10 min, one day, and one week after learning. Forgetting of verbal material was found to be progressively faster during the course of a week in the TLE group. For visuospatial memory, participants in the TLE group exhibited faster early forgetting in the first 10 min after learning, as indicated by planned comparisons, with comparable forgetting rates thereafter. Our findings provide evidence for two patterns of disruption to 'early' memory consolidation in this population, occurring either at the initial delay only or continuing progressively through time. Differences in how soon after learning accelerated forgetting was detectable were related to factors associated with greater severity of epilepsy, such as presence of medial temporal lobe sclerosis (MTS) on magnetic resonance imaging (MRI) and use of multiple anti-epileptic agents.

Psychological therapy for psychogenic amnesia: Successful treatment in a single case study.

Psychogenic amnesia is widely understood to be a memory impairment of psychological origin that occurs as a response to severe stress. However, there is a paucity of evidence regarding the effectiveness of psychological therapy approaches in the treatment of this disorder. The current article describes a single case, "Ben", who was treated with formulation-driven psychological therapy using techniques drawn from cognitive behavioural therapy (CBT) and acceptance and commitment therapy (ACT) for psychogenic amnesia. Before treatment, Ben exhibited isolated retrograde and anterograde memory impairments. He received 12 therapy sessions that targeted experiential avoidance followed by two review sessions, six weeks and five months later. Ben's retrograde and anterograde memory impairments improved following therapy to return to within the "average" to "superior" ranges, which were maintained at follow-up. Further experimental single case study designs and larger group studies are required to advance the understanding of the effectiveness and efficacy of psychological therapy for psychogenic amnesia.

Visual representation of eye gaze is coded by a nonopponent multichannel system.

To date, there is no functional account of the visual perception of gaze in humans. Previous work has demonstrated that left gaze and right gaze are represented by separate mechanisms. However, these data are consistent with either a multichannel system comprising separate channels for distinct gaze directions (e.g., left, direct, and right) or an opponent-coding system in which all gaze directions are coded by just 2 pools of cells, one coding left gaze and the other right, with direct gaze represented as a neutral point reflecting equal activation of both left and right pools. In 2 experiments, the authors used adaptation procedures to investigate which of these models provides the optimal account. Both experiments supported multichannel coding. Previous research has shown that facial identity is coded by an opponent-coding system; hence, these results also demonstrate that gaze is coded by a different representational system to facial identity.