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.

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.

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 seconds, 10 minutes, 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 minutes 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 on MRI and use of multiple anti-epileptic agents.

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.