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The effects of transcranial direct current stimulation (tDCS) for improving attention and working memory have been generally mixed and small, potentially due to variability between studies with montages, stimulus parameters and outcome measures. The tDCS montage is an important parameter which determines the degree and intensity of stimulation in targeted brain regions. This study aimed to examine the effects of using three different montages for modulating attention and working memory performance: Bi-frontal, Broad-frontal and Broad-parietal. Ninety-three healthy adults participated in a counterbalanced cross-over study. Participants received both active and sham tDCS with either the Bi-frontal, Broad-frontal or Broad-parietal montage during performance of both a 1- and 2-back task. TDCS montage moderated 2-back working memory reaction time performance, though not accuracy, with faster reaction times observed for active compared to sham tDCS with the Broad-frontal montage only (F (1,90) = 5.26, p = .024, η2 = 0.06). TDCS montage did not significantly moderate performance on the 1-back task. The cognitive effects of tDCS varied according to montage, task, and outcome measure. TDCS administered with the cathode placed extracephalically in a Broad-frontal montage may be beneficial for improving working memory.

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BACKGROUND: In this study, we asked whether differences in striatal activity during a reinforcement learning (RL) task with gain and loss domains could be one of the earliest functional imaging features associated with carrying the Huntington's disease (HD) gene. Based on previous work, we hypothesized that HD gene carriers would show either neural or behavioral asymmetry between gain and loss learning. METHODS: We recruited 35 HD gene carriers, expected to demonstrate onset of motor symptoms in an average of 26 years, and 35 well-matched gene-negative control subjects. Participants were placed in a functional magnetic resonance imaging scanner, where they completed an RL task in which they were required to learn to choose between abstract stimuli with the aim of gaining rewards and avoiding losses. Task behavior was modeled using an RL model, and variables from this model were used to probe functional magnetic resonance imaging data. RESULTS: In comparison with well-matched control subjects, gene carriers more than 25 years from motor onset showed exaggerated striatal responses to gain-predicting stimuli compared with loss-predicting stimuli (p = .002) in our RL task. Using computational analysis, we also found group differences in striatal representation of stimulus value (p = .0004). We found no group differences in behavior, cognitive scores, or caudate volumes. CONCLUSIONS: Behaviorally, gene carriers 9 years from predicted onset have been shown to learn better from gains than from losses. Our data suggest that a window exists in which HD-related functional neural changes are detectable long before associated behavioral change and 25 years before predicted motor onset. These represent the earliest functional imaging differences between HD gene carriers and control subjects.

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BACKGROUND: Pathological processes in Huntington's disease (HD) begin many years prior to symptom onset. Recently we demonstrated that in a premanifest cohort approximately 24 years from predicted disease onset, despite intact function, there was evidence of subtle neurodegeneration. Here, we use novel imaging techniques to determine whether macro- and micro-structural changes can be detected across the whole-brain in the same cohort. METHODS: 62 premanifest HD (PreHD) and 61 controls from the HD Young Adult Study (HD-YAS) were included. Grey and white matter volume, diffusion weighted imaging (DWI) measures of white matter microstructure, multiparametric maps (MPM) estimating myelin and iron content from magnetization transfer (MT), proton density (PD), longitudinal relaxation (R1) and effective transverse relaxation (R2*), and myelin g-ratio were examined. Group differences between PreHD and controls were assessed; associations between all imaging metrics and disease burden and CSF neurofilament light (NfL) were also performed. Volumetric and MPM results were corrected at a cluster-wise value of familywise error (FWE) 0.05. Diffusion and g-ratio results were corrected via threshold-free cluster enhancement at FWE 0.05. FINDINGS: We showed significantly increased R1 and R2*, suggestive of increased iron, in the putamen, globus pallidum and external capsule of PreHD participants. There was also a significant association between lower cortical R2*, suggestive of reduced myelin or iron, and higher CSF NfL in the frontal lobe and the parieto-occipital cortices. No other results were significant at corrected levels. INTERPRETATION: Increased iron in subcortical structures and the surrounding white matter is a feature of very early PreHD. Furthermore, increases in CSF NfL were linked to microstructural changes in the posterior parietal-occipital cortex, a region previously shown to undergo some of the earliest cortical changes in HD. These findings suggest that disease related process are occurring in both subcortical and cortical regions more than 20 years from predicted disease onset.

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BACKGROUND: Disease-modifying treatments are in development for Huntington's disease; crucial to their success is to identify a timepoint in a patient's life when there is a measurable biomarker of early neurodegeneration while clinical function is still intact. We aimed to identify this timepoint in a novel cohort of young adult premanifest Huntington's disease gene carriers (preHD) far from predicted clinical symptom onset. METHODS: We did the Huntington's disease Young Adult Study (HD-YAS) in the UK. We recruited young adults with preHD and controls matched for age, education, and sex to ensure each group had at least 60 participants with imaging data, accounting for scan fails. Controls either had a family history of Huntington's disease but a negative genetic test, or no known family history of Huntington's disease. All participants underwent detailed neuropsychiatric and cognitive assessments, including tests from the Cambridge Neuropsychological Test Automated Battery and a battery assessing emotion, motivation, impulsivity and social cognition (EMOTICOM). Imaging (done for all participants without contraindications) included volumetric MRI, diffusion imaging, and multiparametric mapping. Biofluid markers of neuronal health were examined using blood and CSF collection. We did a cross-sectional analysis using general least-squares linear models to assess group differences and associations with age and CAG length, relating to predicted years to clinical onset. Results were corrected for multiple comparisons using the false discovery rate (FDR), with FDR <0·05 deemed a significant result. FINDINGS: Data were obtained between Aug 2, 2017, and April 25, 2019. We recruited 64 young adults with preHD and 67 controls. Mean ages of participants were 29·0 years (SD 5·6) and 29·1 years (5·7) in the preHD and control groups, respectively. We noted no significant evidence of cognitive or psychiatric impairment in preHD participants 23·6 years (SD 5·8) from predicted onset (FDR 0·22-0·87 for cognitive measures, 0·31-0·91 for neuropsychiatric measures). The preHD cohort had slightly smaller putamen volumes (FDR=0·03), but this did not appear to be closely related to predicted years to onset (FDR=0·54). There were no group differences in other brain imaging measures (FDR >0·16). CSF neurofilament light protein (NfL), plasma NfL, and CSF YKL-40 were elevated in this far-from-onset preHD cohort compared with controls (FDR<0·0001, =0·01, and =0·03, respectively). CSF NfL elevations were more likely in individuals closer to expected clinical onset (FDR <0·0001). INTERPRETATION: We report normal brain function yet a rise in sensitive measures of neurodegeneration in a preHD cohort approximately 24 years from predicted clinical onset. CSF NfL appears to be a more sensitive measure than plasma NfL to monitor disease progression. This preHD cohort is one of the earliest yet studied, and our findings could be used to inform decisions about when to initiate a potential future intervention to delay or prevent further neurodegeneration while function is intact. FUNDING: Wellcome Trust, CHDI Foundation.

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OBJECTIVE: The aim of this study was to use various measures of emotion recognition, such as sensitivity to emotional intensity, accuracy-based emotion labeling, and the ability to differentiate among emotional displays, to examine whether these abilities are associated with emotional and cognitive empathy. We also sought to determine whether these relationships differ between individuals with traumatic brain injury (TBI) and healthy adults. METHOD: TBI participants (n = 28) and healthy adults (n = 29) matched for age, biological sex, and education, were tested on an emotion intensity rating and recognition task. Self-reported emotional and cognitive empathy questionnaires, together with a neuropsychological battery, were also completed. RESULTS: Participants with TBI reported reduced emotional and cognitive empathy. TBI participants also had reduced overall accuracy in recognizing emotion, specifically for happy and sad emotions, although they had no difficulty identifying the intensity or differentiating among emotional displays. Intensity labeling and sensitivity to differentiate among emotions positively correlated with emotional empathy for healthy adults but not for TBI participants. No facet of emotion recognition correlated with cognitive empathy for healthy adults or TBI participants. CONCLUSIONS: The ability to identify the intensity and differentiate among emotions is associated with emotional empathy. Although individuals with severe TBI may be able to differentiate emotions, they may be unable to utilize this information to share and understand the emotions of others, or vice versa. These results could have implications for understanding poor interpersonal relationships and impaired social functioning following TBI. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

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Introduction: A significant proportion of people with traumatic brain injury (TBI) report low levels of empathy, yet there is a paucity of research investigating the mechanisms which underpin this. In this study, we investigated empathy after TBI through the lens of the perception-action model of empathy. Specifically, we looked at the effect of similarity of experience on self-reported empathy and skin conductance in participants with TBI and controls.Method: Thirty people with a traumatic brain injury and 30 matched healthy controls initially recounted three emotional events they had experienced in the past (one happy, one angry and one sad). Then, at a second visit, participants heard three stories which were written to be similar their own stories and three which were based on someone else's stories. We recorded skin conductance while participants listened and then collected self-reported levels of empathy for protagonists in the stories.Results: We found that self-reported empathy, but not skin conductance levels, was greater for similar compared to dissimilar stories. Further, participants with TBI were able to empathise with others despite having markedly reduced autonomic arousal and overall impairment in cognitive functioning.Conclusions: Our results suggest that the PAM has relevance with respect to explaining self-reported empathy for the experiences of others, but cannot explain the role of physiological responses associated with empathy. Further, our results suggest that intact cognitive functioning and physiological responses are not necessary for normal experiences of empathy after TBI.

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OBJECTIVE: Although the presence of empathy deficits following traumatic brain injury (TBI) is well established, there is a paucity of research investigating the underpinning mechanisms. This study investigated whether feedback from posed emotional expressions and psychophysiological responsivity, thought to play a role in emotional empathy, are impaired after TBI. METHOD: Thirty adults with TBI and 30 demographically matched healthy controls completed 2 feedback tasks while skin conductance and heart rate were recorded. In Feedback Task 1, participants assumed different emotional postures and rated how this made them feel. In Feedback Task 2, participants held a smile or frown while viewing neutral images and rated the pleasantness of each image. RESULTS: Participants with TBI did not differ from controls in their subjective ratings in response to posed emotional expressions. However, we found reduced skin conductance responses to rapid facial manipulations and some evidence of altered physiological arousal to sad emotional postures in participants with TBI. Finally, there was no relationship between emotional empathy and facial feedback or physiological responsivity. CONCLUSIONS: We failed to replicate past research that demonstrated an impairment in the feedback effect in people with TBI. These normal subjective responses, though, were in the context of reduced psychophysiological responding to the posed expressions, suggesting that another mechanism can contribute to normal feedback effects after TBI. Finally, we did not find the expected relationship between the feedback effect and emotional empathy but may have been limited by the lower than expected rates of low emotional empathy in our sample. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

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OBJECTIVE: Emotional empathy is critical to successful social interactions and is often compromised after traumatic brain injury (TBI). Using the Emostroop task, we investigated whether adults with moderate to severe TBI (N = 26) have problems with rapid conceptual processing of emotional stimuli compared with controls (N = 30). Further, we investigated whether rapid conceptual processing of emotions relates to emotion recognition and emotional empathy. METHOD: In the Emostroop task, participants categorize emotional words (e.g., joyous, furious, and woeful) into three emotion categories: happy, sad, and angry. Each word is superimposed onto an image of a face, which expresses an emotion that is congruent to the word (congruent condition), incongruent to the word (incongruent condition), or is neutral (neutral condition). Slowed responding in the incongruent condition (interference) and speeded responding in the congruent condition (facilitation) indicates rapid conceptual processing of the faces. Participants also completed an emotion perception task, an empathy questionnaire (the BEES) and neuropsychological tests measuring processing speed, working memory, and executive function. RESULTS: Contrary to our hypotheses, we found that rapid conceptual processing of emotional faces was preserved in people with TBI, despite diminished neuropsychological performance, emotion recognition, emotional empathy, and slowed responding. Further, the Emostroop effect was not correlated with self-reported emotional empathy or with emotion recognition. CONCLUSIONS: We conclude that in people with TBI, reduced empathy may be explained by processes downstream of the initial rapid conceptual processing of emotional information, such as flexibly attending and responding to this information in a goal-directed manner in complex environments. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

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OBJECTIVES: Previous research has demonstrated an association between emotion recognition and apathy in several neurological conditions involving fronto-striatal pathology, including Parkinson's disease and brain injury. In line with these findings, we aimed to determine whether apathetic participants with early Huntington's disease (HD) were more impaired on an emotion recognition task compared to non-apathetic participants and healthy controls. METHODS: We included 43 participants from the TRACK-HD study who reported apathy on the Problem Behaviours Assessment - short version (PBA-S), 67 participants who reported no apathy, and 107 controls matched for age, sex, and level of education. During their baseline TRACK-HD visit, participants completed a battery of cognitive and psychological tests including an emotion recognition task, the Hospital Depression and Anxiety Scale (HADS) and were assessed on the PBA-S. RESULTS: Compared to the non-apathetic group and the control group, the apathetic group were impaired on the recognition of happy facial expressions, after controlling for depression symptomology on the HADS and general disease progression (Unified Huntington's Disease Rating Scale total motor score). This was despite no difference between the apathetic and non-apathetic group on overall cognitive functioning assessed by a cognitive composite score. CONCLUSIONS: Impairment of the recognition of happy expressions may be part of the clinical picture of apathy in HD. While shared reliance on frontostriatal pathways may broadly explain associations between emotion recognition and apathy found across several patient groups, further work is needed to determine what relationships exist between recognition of specific emotions, distinct subtypes of apathy and underlying neuropathology. (JINS, 2019, 25, 453-461).

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BACKGROUND: Recognizing how others feel is paramount to social situations and commonly disrupted following traumatic brain injury (TBI). This study tested whether problems identifying emotion in others following TBI is related to problems expressing or feeling emotion in oneself, as theoretical models place emotion perception in the context of accurate encoding and/or shared emotional experiences. METHODS: Individuals with TBI (n = 27; 20 males) and controls (n = 28; 16 males) were tested on an emotion recognition task, and asked to adopt facial expressions and relay emotional memories according to the presentation of stimuli (word and photos). After each trial, participants were asked to self-report their feelings of happiness, anger and sadness. Judges that were blind to the presentation of stimuli assessed emotional facial expressivity. RESULTS: Emotional experience was a unique predictor of affect recognition across all emotions while facial expressivity did not contribute to any of the regression models. Furthermore, difficulties in recognizing emotion for individuals with TBI were no longer evident after cognitive ability and experience of emotion were entered into the analyses. CONCLUSIONS: Emotion perceptual difficulties following TBI may stem from an inability to experience affective states and may tie in with alexythymia in clinical conditions.

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Acquired social disinhibition refers to a debilitating behavioural syndrome commonly reported after a severe traumatic brain injury (TBI) and is characterized 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. This review provides an overview of our current understanding of the definition, measurement, prevalence, associated outcomes, neuropathology, and underlying mechanisms of social disinhibition after TBI. In addition, suggestions are made for future research to further our understanding of this syndrome with the eventual aim of rehabilitating problematic behaviours. It is concluded that an improved understanding of what causes disinhibited behaviour after TBI will be necessary for the development of effective treatment strategies aimed at the rehabilitation of underlying impairments.

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OBJECTIVE: To describe the reliability and validity of a new measure, the Social Skills Questionnaire for Traumatic Brain Injury (SSQ-TBI). METHODS: Fifty-one adults with severe TBI completed the SSQ-TBI questionnaire. Scores were compared to informant- and self-report on questionnaires addressing frontal lobe mediated behaviour, as well as performance on an objective measure of social cognition and neuropsychological tasks, in order to provide evidence of concurrent, divergent and predictive validity. RESULTS: Internal consistency was excellent at α = 0.90. Convergent validity was good, with informant ratings on the SSQ-TBI significantly correlated with Neuropsychiatric Inventory Disinhibition sub-scales (r = 0.50-63), the Current Behaviour Scale (r = 0.39-0.48) and Frontal Systems Behaviour Scale (r = 0.60-0.83). However, no relationship was seen with an objective measure of social skills or neuropsychological tasks of disinhibition. There was a significant relationship with real-world psychosocial outcomes on the Sydney Psychosocial Reintegration Scale-2 (r = -0.38--0.69) Conclusions: This study provides preliminary findings of good internal consistency and convergent and predictive validity of a social skills questionnaire adapted to be appropriate for individuals with TBI. Further assessment of psychometric properties such as test-re-test reliability and factor structure is warranted.

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OBJECTIVE: The current study aimed to determine whether 2 variables associated with orbitofrontal damage, hyposmia and emotion perception deficits, are associated with socially disinhibited behavior and psychosocial outcome after traumatic brain injury (TBI). METHODS: The Brief Smell Identification Test (BSIT), an emotion labeling task, an emotion intensity rating task, and an observational measure of social disinhibition were completed by 23 individuals with severe TBI. The disinhibition domain of the Neuropsychiatric Inventory and the interpersonal relationships subscale of the Sydney Psychosocial Reintegration Scale (SPRS-IR) were completed by a close other. Fifteen control participants provided norms against which to assess performance on the emotion intensity rating task. RESULTS: BSIT scores predicted informant-reported change in interpersonal relationships on the SPRS-IR. Hyposmia, though, was not associated with informant-reported or observed social disinhibition. An impairment in accuracy scores on both emotion perceptions tasks was found for participants with TBI, yet intensity ratings did not differ between groups. This suggests 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. Emotion perception was not related to disinhibition or change in interpersonal relationships. CONCLUSIONS: These results support previous claims that hyposmia has prognostic significance following TBI. On the other hand, emotion perception impairment measured by standardized tasks does not appear to be an important factor in interpersonal outcomes. Finally, these results suggest that standardized emotion perception tasks may underestimate the emotion perception capabilities of people with TBI. (PsycINFO Database Record

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OBJECTIVES: The current study aimed to determine whether reversal learning impairments and feedback-related negativity (FRN), reflecting reward prediction error signals generated by negative feedback during the reversal learning tasks, were associated with social disinhibition in a group of participants with traumatic brain injury (TBI). METHODS: Number of reversal errors on a social and a non-social reversal learning task and FRN 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 rated videotaped interviews. RESULTS: Participants with TBI made more reversal errors and produced smaller amplitude FRNs than controls. Furthermore, participants with TBI high on social disinhibition made more reversal errors on the social reversal learning task than did those low on social disinhibition. FRN amplitude was not related to disinhibition. CONCLUSIONS: These results suggest that impairment in the ability to update behavior when social reinforcement contingencies change plays a role in social disinhibition after TBI. Furthermore, 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 behavioral adaptation in the social domain.

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INTRODUCTION: This study aimed to validate a new observational measure of socially disinhibited behavior for use in a population of individuals with traumatic brain injury (TBI). METHOD: Participants were twenty-two adults with severe TBI (mean age = 50.45 years) and 21 healthy comparison participants (mean age = 45.29 years). Ratings of observed social disinhibition were correlated with the disinhibition domain scores of the Neuropsychiatric Inventory-Disinhibition (NPI-D) and with Sydney Psychosocial Reintegration Scale (SPRS) scores. A regression analysis was undertaken to determine whether formal measures of disinhibition could predict observed disinhibition. RESULTS: The interrater absolute agreement for the social disinhibition ratings was good, intraclass correlation coefficient (ICC) = .69. Participants with TBI were rated as significantly more disinhibited than comparison participants, t(25.05) = -2.07, p = .049. The ratings were positively correlated with the NPI frequency score (r = .45, p = .038) and distress score (r = .45, p = .035). The ratings were not related to change in employment or in interpersonal relationships on the SPRS, and formal measures of disinhibition were unable to predict observed social disinhibition. CONCLUSIONS: This study demonstrates good interrater reliability and construct validity of the observational measure. The results evidence the usefulness of this measure and the NPI-D for detecting social disinhibition after TBI.

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