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Socio-Emotional Deficits in Severe Alcohol Use Disorders
C H A P T E R
39 Socio-Emotional Deficits in Severe Alcohol Use Disorders Pierre Maurage1, Benjamin Rolland2,3 and Fabien D’Hondt4,5 1
Laboratory for Experimental Psychopathology, Psychological Science Research Institute, Universite´ catholique de Louvain, Louvain-la-Neuve, Belgium 2UCBL, CRNL, INSERM U1028, CNRS UMR5292, Universite of Lyon, Lyon, France 3UPMOPHA Department, Le Vinatier Hospital Centre, University Service of Addictology of Lyon (SUAL), Bron, France 4University of Lille, CNRS, UMR 9193, SCALab - Sciences Cognitives et Sciences Affectives, Lille, France 5CHU Lille, Clinique de Psychiatrie, CURE, Lille, France
LIST OF ABBREVIATIONS AUD ToM
alcohol use disorders theory of mind
THE IMPORTANCE OF SOCIOEMOTIONAL FACTORS IN SEVERE ALCOHOL USE DISORDERS Severe alcohol-use disorders (AUD, following DSM5 nomenclature, Hasin et al., 2013) are a widespread pathology affecting 5% 10% of adults in Western countries, and constitute the most frequent psychiatric disorder (Rehm et al., 2010). In view of their omnipresence and large-scale negative consequences, they have emerged as a central experimental and clinical research field for a wide range of scientific disciplines during the past few decades, among which are psychology and neurosciences. Neuropsychological models of AUD have mostly conceptualized this disorder as characterized by a strongly increased attraction toward the substance, combined with a progressive loss of cognitive control over consumption. This consensual view is illustrated in the currently dominant theoretical proposals, namely the dual-process models (Stacy & Wiers, 2010), stating that AUD relies on the imbalance between an over-activated limbic-automatic system (involved in the appetitive responses towards alcohol-related stimuli) and an under-activated
Neuroscience of Alcohol. DOI: https://doi.org/10.1016/B978-0-12-813125-1.00039-8
prefrontal-cognitive system (involved in cognitive evaluation and behavioral control). This theoretical framework has received strong empirical support: on the one hand, the excessive activation of the automatic system has been documented by studies showing intense craving and attentional biases toward alcohol in AUD (Field & Cox, 2008); on the other hand, AUD is obviously characterized by impaired performance in a wide range of cognitive abilities, these impairments being particularly massive for inhibition and underpinned by large-scale frontal lobe dysfunctions (Stavro, Pelletier, & Potvin, 2013). Following this view, therapeutic programs should, thus, centrally aim at reestablishing an equilibrium between these two systems, by reducing automatic attraction, and/or increasing cognitive control. While offering a reliable conceptualization of AUD leading to fruitful experimental and clinical implications, dual-process models have neglected other key processes involved in the emergence and maintenance of AUD, among which are emotional and interpersonal disorders. Indeed, patients with AUD cannot only be defined as “dysregulated machines” presenting an automatic-control imbalance. As repeatedly reported in clinical observations, AUD is also an affective and relational disease: firstly, the comorbidity between AUD and mood disorders has long been established, most patients with AUD presenting intense negative emotionality, as well as depressive and anxious symptoms (Schuckit, 2006). Secondly, AUD is associated
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with familial, professional, and social difficulties, a majority of patients with AUD presenting reduced social networking, limited social support, or even persistent social isolation. Centrally, these socio-emotional disturbances should not be considered as secondary variables in AUD treatment as empirical studies have identified social support as a major factor for abstinence (Gordon & Zrull, 1991), and as 40% of relapses are directly attributed to persistent negative effects or reduced social networking (Zywiak, Westerberg, Connors, & Maisto, 2003). Negative emotionality and disrupted interpersonal functioning are, thus, at the heart of the addictive pathology, and a more inclusive conceptualization of AUD should include socioemotional impairments. However, evidence-based studies have long neglected these factors and their experimental exploration in AUD has only emerged during the past two decades. To underline the importance of social cognition in AUD, this chapter will propose a typology-based description of the currently available data regarding socio-emotional abilities in patients with AUD, and then identify the main fundamental and therapeutic perspectives in this field to encourage an in-depth experimental exploration of these factors, as well as their implementation in clinical evaluation and remediation settings.
A TYPOLOGICAL REVIEW OF SOCIAL COGNITION IN PATIENTS WITH AUD Social cognition is the ability to use psychological and cognitive resources to efficiently detect, understand, regulate, and react to stimulations emerging from interpersonal environments and social interactions (Green, Horan, & Lee, 2015). Although recent, the psychological and neuroscience exploration of social cognition in AUD constitutes a blooming research field. To offer the clearest possible description of this literature, this chapter’s review will use a classification of social cognition subcomponents proposed in schizophrenia research (Green et al., 2008), dividing these abilities into five subcategories (Fig. 39.1): Theory of Mind (ToM), social perception, social knowledge, attributional bias, and emotional processing. While these categories present some overlap and while several tasks simultaneously assess multiple categories, data will be described following this typology. First, ToM constitutes a complex social cognition component repeatedly shown as impaired in several psychopathological states, such as schizophrenia or depression (Bora, Bartholomeusz, & Pantelis, 2016). In AUD, several paradigms have been used to explore ToM abilities, from quite large batteries (Bosco, Capozzi, Colle, Marostica, & Tirassa, 2014) to more
specific investigations using the false-beliefs task (Fig. 39.2; Maurage, de Timary, Tecco, Lechantre, & Samson, 2015) or the faux-pas task (Thoma, Winter, Juckel, & Roser, 2013). These works led to coherent results documenting reduced ToM abilities in AUD; this deficit being present for all subcomponents of ToM (first-/third-person perspective taking, first-/ second-order inferences). Moreover, beyond this generalized deficit, other studies have explored the dissociation between cognitive and affective ToM, suggesting that the affective component (i.e., others’ emotions or feelings) is more strongly impaired (Nandrino et al., 2014). Beyond these dissociations, patients with AUD, thus, present significantly reduced ToM abilities, as clearly confirmed by meta-analyses (Bora & Zorlu, 2017; Onuoha, Quintana, Lyvers, & Guastella, 2016). Additionally, a social cognition component strongly associated with ToM is empathy. The links between ToM and empathy are still being debated (Green et al., 2015), but empathy is clearly a key component to develop and maintain efficient social interactions, and this ability is impaired in AUD: a first study observed lower empathy levels in AUD (Martinotti, Di Nicola, Tedeschi, Cundari, & Janiri, 2009), while later explorations (Maurage et al., 2011) showed a dissociation between impaired affective (i.e., detecting and feeling others’ emotional states) and preserved cognitive (i.e., understanding others’ nonemotional, mental states) empathy subcomponents. Second, social perception is evaluated by tasks presenting pictures or videos of social interactions, based on which the participant has to interpret verbal and nonverbal content to understand multifaceted interpersonal relations. This subcomponent had already been partly measured in the ToM tasks (Nandrino et al., 2014), but the measure of social perception abilities in AUD has been more directly conducted in two studies: A recent one (Maurage et al., 2016) used the “Movie for Assessment of Social Cognition task” (Fig. 39.3; Dziobek et al., 2006), requiring the participant to detect and categorize the thoughts, affects, and actions of four characters, and to infer their intentions and interpersonal relations. Patients with AUD were impaired in understanding the emotions expressed by the characters, but remained able to comprehend their nonemotional thoughts or behaviors. This result thus extends, on the basis of a more direct measure of the interpersonal relationships’ perception, the proposal of a dissociation between an impaired emotional subcomponent of social cognition and a preserved cognitive one. Another study, using neuroimaging measures, went one step beyond this by exploring the cerebral correlates of social perception in AUD, but also the self-related consequences of negative social interactions (Maurage et al., 2012). This study used the
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FIGURE 39.1 Subcomponents of social cognition. Graphical presentation of the five subcomponents related to social cognition, as defined by Green et al. (2008).
cyberball paradigm (Williams & Jarvis, 2006), a balltossing game in which a situation of social rejection is created by leading two other computer-guided players to exclude the participant from the game. When confronted with rejection, patients with AUD presented an increased social perception of this ostracism (indexed by more intense ostracism feelings and insula/cingulate cortex activities). These results, thus, suggest that, regarding social perception, AUD is associated with: (1) a reduced ability to take into account others’ emotional states during tasks in which the participant is not involved; (2) conversely, an increased sensitivity to the social perception of others thoughts and behaviors when these are directed toward the participant, threatening their social integration. Third, preliminary results suggest that AUD is associated with abnormalities in social knowledge, which might constitute a core deficit provoking a cascade of negative consequences for social interactions. Specifically, patients
with AUD have a reduced ability to correctly perform a humor detection task based on written jokes involving interpersonal contexts (Uekermann, Channon, Winkel, Schlebusch, & Daum, 2007). This indexes a difficulty to use social knowledge to identify the humoristic break of social rules provoked by an incongruity in the described interactions. It has also been shown that AUD is related to a reduced detection of irony (Amenta, Noe¨l, Verbanck, & Campanella, 2013), witnessing a reduced knowledge of the social rules and roles underlying human interactions. Another social knowledge facet measured in patients with AUD is the presence of maladaptive self-beliefs related to social standards: patients with AUD present a specific tendency to over-evaluate the standards required in social interactions (Maurage et al., 2013). In other words, AUD is related to an exaggerated estimation of the requested interpersonal performance to obtain a satisfactory social outcome. This biased social knowledge, strongly correlated with interpersonal difficulties, could, thus, contribute to the emergence of a
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FIGURE 39.2 False-beliefs task. Schematic illustration of the events’ sequence in the false-beliefs task used to explore ToM in AUD. (A) Track-Task (spontaneous tracking of the other person’s perspective): (1) The woman (right) watches in which box the green object is located (while the participant cannot see it); (2) She leaves the room and the man (left) switches boxes; (3) She returns and gives a hint by placing the pink object on one of the boxes to help finding the green object. At this point, the participant has to point to the box containing the green cube; (B) Inhibit-Task (self-perspective inhibition): (1) The woman watches in which box the green object is located. The participant can also see the object‘s location; (2) The woman leaves the room and the man changes the object‘s location; (3) The woman returns and the participant has to indicate which of the two boxes the woman will open first. Note: for description’s clarity, the green cube is visible in the illustration whereas it is hidden in the box during the experiment.
FIGURE 39.3 Movie for Assessment of Social Cognition task. Illustration of an item of the Movie for Assessment of Social Cognition task used to explore social perception in AUD. The upper part describes the critical sequences of the video. The lower part gives the four possible answers proposed to the participant.
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vicious cycle: the exaggerated standards may lead to negative feelings during social interactions, which might, in turn, increase social isolation. Fourth, attributional bias is the only subcomponent of social cognition still to be explored in patients with AUD. Many studies have been conducted on attentional or cognitive biases among patients (Field & Cox, 2008), but this approach has not yet been applied to interpersonal biases. Several studies have identified attributional biases in other psychiatric states, and these results should encourage future works to explore these processes in patients with AUD by using attributional bias tasks (e.g., Combs, Penn, Wicher, & Waldheter, 2007). Fifth and finally, numerous studies have been conducted to explore emotional processing in patients with AUD. After a seminal study (Philippot et al., 1999) describing a reduced ability to identify the emotional states expressed by human faces, a large variety of experimental designs have been used (Donadon & Oso´rio, 2014) presenting various facial emotions by means of numerous procedures, most results confirming the presence of this deficit: patients with AUD need more emotional intensity to detect others’ affective states (Fig. 39.4; D’Hondt, de Timary, Bruneau, & Maurage, 2015). Importantly, this deficit appears specific for emotional states and more intense for negative emotions (Bora & Zorlu, 2017). However, it is generalized to all emotional stimulations, including voice prosody or body posture (Maurage et al., 2009). As the aptitude to decode emotional cues offered by others is crucial to efficiently understand their state-of-mind and affective feelings, it has been suggested that this global emotion decoding difficulty in patients with AUD plays a role in the reduction of interpersonal bonds and in the social isolation frequently observed
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in this population (D’Hondt, Campanella, Kornreich, Philippot, & Maurage, 2014). Moreover, the impaired capacity to identify others’ emotions in patients with AUD also extends towards the identification of one’s own emotions, as AUD is related to increased alexithymia, that is, an impaired ability to feel, identify, and express internal affective states (Stasiewicz et al., 2012).
TOWARDS A DEEPER UNDERSTANDING OF SOCIAL COGNITION IN PATIENTS WITH AUD Overall, the large majority of studies exploring social cognition in AUD have documented substantial impairments, particularly for ToM and emotional processing. In view of the key role played by these aptitudes in interpersonal relations, these impairments might contribute to the personal, professional, and societal difficulties reported in patients with AUD (Kornreich et al., 2002) and should, thus, be further considered in clinical settings beyond the classical focus on cognitive functions. In this respect, it is noteworthy that the correlation between AUD-related deficits in social cognition and standard clinical features of AUD severity—for example, DSM-5 AUD criteria (Hasin et al., 2013), “Alcohol Use Disorder Identification Test” score (Bohn, Babor, & Kranzler, 1995), or features of AUD outcomes like postdetoxification relapse rates—have hardly been explored, as only one study (Rupp, Derntl, Osthaus, Kemmler, & Fleischhacker, 2017) showed that reduced emotional processing abilities at the start of treatment is associated with higher relapse rates, thus, confirming the involvement of social cognition in clinical outcomes.
FIGURE 39.4 Emotional processing paradigm. Example of stimuli illustrating the various emotional valences and intensities used to explore emotion processing in AUD. (A) Example of a realistic face depicting four different prototypical emotional facial expressions (neutral, happy, angry, and sad); (B) Example of a morphing continuum (angry sad) for one identity. The percentage of each emotion contained in each of the 10-morph step is mentioned at the bottom of the figure (e.g., 95% 5% means that this stimulus contains 95% of anger and 5% of sadness).
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Furthermore, future studies should also couple the neuropsychological assessment of social cognition with more clinically-focused tools used to assess social functioning—for example, Measurement in Addictions for Triage and Evaluation, whose assessment is partly based on the WHO international classification of functioning (Schippers, Broekman, Buchholz, Koeter, & van den Brink, 2010). Another challenge regarding future studies is that this research field suffers from a lack of theoretical background and experimental coherence, as studies have not been integrated into a clear fundamental model. The present attempt to offer a typology of social cognition data in patients with AUD, based on the proposals emerging in other psychiatric states, has clearly shown that, while ToM and emotional processing have been largely studied (using scattered and often multidetermined paradigms), other components of social cognition have not been thoroughly measured. A first major research perspective would, thus, be to capitalize on the typology presented here to develop a coherent research program which would propose, for each identified social cognition subcomponent, an in-depth exploration based on controlled and component-specific tasks, as initiated in schizophrenia (Green et al., 2015), as well as on a strict control of AUD characteristics and comorbid psychopathological states. Recent papers (Kwako, Momenan, Litten, Koob, & Goldman, 2016) have initiated this ambitious program by proposing a neuroscience-grounded battery to explore key variables in AUD, among which are some measures of emotional and social processing. This constitutes an important first step towards a rational evaluation of social cognition in patients with AUD, despite a still quite imprecise specification of the processes to be evaluated. Beyond the needed clarification and deepening of the core socio-emotional processes at stake in patients with AUD, other crucial research questions should be addressed (Fig. 39.5), among which: 1. The interactions between socio-emotional and cognitive processes: Most studies have explored social cognition in AUD in an isolated fashion, but these abilities might strongly interact with other AUD deficits, and centrally cognitive functions. Preliminary results have indicated that social cognition in AUD is influenced by working (Uekermann et al., 2007) or autobiographical (Nandrino et al., 2014) memory, and that socioemotional difficulties might be partly caused by visuo-perceptive impairments (D’Hondt, Lepore, & Maurage, 2014), but these proposals should be confirmed using more controlled joint explorations of socio-emotional and cognitive abilities.
2. The interindividual variability of socio-emotional deficits: All presented studies have capitalized on a groupbased approach, considering patients with AUD as a homogeneous population. However, when going one step beyond this to analyze individual performances, it appeared that only 50% of patients with AUD present a genuine ToM deficit (Maurage et al., 2015). Moreover, this heterogeneity in socioemotional disorders has been specifically explored using a cluster analytic approach (Maurage, de Timary, & D’Hondt, 2017), which clearly showed that AUD is a constellation of individuals with a wide variety of socio-emotional profiles. Future studies should, thus, systematically complement the classical group approach by individual analyses specifying the interindividual variation of the deficits, as well as the differential role played by psychopathological and addictive comorbidities. 3. The causal relation between AUD and social cognition deficits, and their evolution: Previous studies have focused on recently detoxified patients with AUD. This focus did not allow determining whether socioemotional impairments are a consequence of the neurotoxicity provoked by repeated excessive alcohol use or, at least partly, a causal factor involved in AUD development. More globally, the evolution of social cognition deficits during the course of the disease (e.g., after long-term abstinence) and in its successive stages should be more thoroughly explored through longitudinal studies and explorations focused on other alcohol-consumption patterns related to socio-emotional impairments—for example, binge drinking (Maurage, Bestelmeyer, Rouger, Charest, & Belin, 2013). 4. The inclusion of social cognition deficits in AUD models: The dominant dual-process models have not integrated emotional and social functions, which are still considered as mere side-products of the imbalance between automatic and controlled systems. A subsequent theoretical proposal, the triadic model (Noe¨l, Brevers, & Bechara, 2013), postulates a third insula-based system involved in the detection of interoceptive signals and in their conversion in affective feelings. This model, while having received limited empirical support as yet, might constitute a foundation to integrate socioemotional deficits in AUD models. Finally, these research results should urgently be integrated into clinical practices, where social cognition deficits are totally under-evaluated and undertreated, despite repeated clinical observations underlining their importance in the detoxification process. Centrally, proposals regarding the implementation of
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MINI-DICTIONARY OF TERMS
379 FIGURE 39.5 Proposal for future research avenues. Graphical synthesis of the main research perspectives proposed to deepen the understanding of social cognition in patients with AUD.
cognitive remediation in addictive disorders have recently bloomed (Verdejo-Garcia, 2016), but these programs have been focused on cognitive variables. In line with what has been proposed in schizophrenia (Grant, Lawrence, Preti, Wykes, & Cella, 2017), a structured neuropsychological training program focusing on the evaluation and training of social cognition in patients with AUD should urgently be tested in care structures as it could improve socio-emotional abilities, but also positively impact clinical outcomes of patients by breaking the vicious cycle linking social cognition deficits, social isolation, and alcohol consumption.
MINI-DICTIONARY OF TERMS Attributional bias The propensity to consider that the personal and interpersonal events occurring in one’s life are mostly due to internal (i.e., individual responsibility) or external (i.e., others’ responsibility or contextual variables) causes.
Emotional processing The efficient perception, interpretation, and reaction to the emotional states expressed by other individuals through their facial expression, voice prosody, or body posture, as well as the correct decoding and regulation of one’s own affective states. Empathy The capacity to understand other individuals’ cognitive or affective perspectives and to propose a verbal or behavioral answer adapted to the emotions, feelings, or thoughts they expressed. Social cognition The psychological processes related to the identification and interpretation of social signals sent by other individuals in interpersonal contexts, as well as the skills needed to effectively respond to these signals. Social knowledge The awareness and understanding of the rules and conventions to be followed during social interactions, and of the role assigned to each participant in social contexts. Social perception The aptitude to interpret verbal and nonverbal stimuli to infer individuals’ role and current relationships in equivocal or intricate interpersonal contexts. Theory of mind The ability to use the interpersonal signals produced by other individuals to infer their mental states, thoughts, or emotions, and to anticipate their behaviors or actions.
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KEY FACTS Social Cognition in Alcohol Use Disorders • Severe alcohol use disorders (AUD) are the most frequent psychiatric disorder, affecting 5% 10% of adults in Western countries. • AUD are associated with cognitive deficits, as indexed by altered perceptive motor, attentional and memory capacities, but also reduced executive functions (e.g., inhibition, flexibility, problem solving). • Social cognition impairments have more recently been identified in patients with AUD, encompassing reduced performance in Theory of Mind (i.e., the inference of others’ mental states based on the interpersonal signals they send) and emotion decoding (i.e., the decoding of others’ emotional states expressed through their face, voice, or body)—two central abilities for efficient social interactions. • These social cognition deficits might favor the persistence of AUD in patients by creating a vicious cycle: impaired social cognition would lead to social isolation, itself leading to increased alcohol consumption used as a coping strategy, which would, in turn, aggravate social cognition impairments due to alcohol neurotoxicity. • Social cognition should, thus, be further investigated in AUD, and more globally in addictive states, notably to specify its role in the emergence and stabilization of excessive alcohol consumption and its evolution during the disease’s course.
SUMMARY POINTS • This chapter reviews social cognition impairments in alcohol use disorders (AUD). • Beyond the well-established cognitive deficits, AUD are also characterized by large-scale impairments to detect, interpret, and use social signals in interpersonal contexts. • Reduced abilities have been repeatedly found for Theory of Mind and emotion processing among patients with AUD. • The potential deficit for other social cognition subcomponents (social perception, social knowledge, and attributional bias) has still to be thoroughly evaluated. • Future studies should also explore the causal links between AUD and social cognition deficits, as well as their interactions with cognitive deficits and their variation across individuals with AUD.
• In view of the massive alterations observed for socio-emotional processes in patients with AUD, these factors should be taken into account in clinical settings, centrally, by proposing a specific social cognition evaluation and training.
Acknowledgments Pierre Maurage is research associate at the Fund for Scientific Research (F.R.S.-FNRS, Belgium). This chapter was supported by a grant from the “Fondation pour la Recherche en Alcoologie” (FRA, France).
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39 Socio-Emotional Deficits in Severe Alcohol Use Disorders Pierre Maurage1, Benjamin Rolland2,3 and Fabien D’Hondt4,5 1
Laboratory for Experimental Psychopathology, Psychological Science Research Institute, Universite´ catholique de Louvain, Louvain-la-Neuve, Belgium 2UCBL, CRNL, INSERM U1028, CNRS UMR5292, Universite of Lyon, Lyon, France 3UPMOPHA Department, Le Vinatier Hospital Centre, University Service of Addictology of Lyon (SUAL), Bron, France 4University of Lille, CNRS, UMR 9193, SCALab - Sciences Cognitives et Sciences Affectives, Lille, France 5CHU Lille, Clinique de Psychiatrie, CURE, Lille, France
LIST OF ABBREVIATIONS AUD ToM
alcohol use disorders theory of mind
THE IMPORTANCE OF SOCIOEMOTIONAL FACTORS IN SEVERE ALCOHOL USE DISORDERS Severe alcohol-use disorders (AUD, following DSM5 nomenclature, Hasin et al., 2013) are a widespread pathology affecting 5% 10% of adults in Western countries, and constitute the most frequent psychiatric disorder (Rehm et al., 2010). In view of their omnipresence and large-scale negative consequences, they have emerged as a central experimental and clinical research field for a wide range of scientific disciplines during the past few decades, among which are psychology and neurosciences. Neuropsychological models of AUD have mostly conceptualized this disorder as characterized by a strongly increased attraction toward the substance, combined with a progressive loss of cognitive control over consumption. This consensual view is illustrated in the currently dominant theoretical proposals, namely the dual-process models (Stacy & Wiers, 2010), stating that AUD relies on the imbalance between an over-activated limbic-automatic system (involved in the appetitive responses towards alcohol-related stimuli) and an under-activated
Neuroscience of Alcohol. DOI: https://doi.org/10.1016/B978-0-12-813125-1.00039-8
prefrontal-cognitive system (involved in cognitive evaluation and behavioral control). This theoretical framework has received strong empirical support: on the one hand, the excessive activation of the automatic system has been documented by studies showing intense craving and attentional biases toward alcohol in AUD (Field & Cox, 2008); on the other hand, AUD is obviously characterized by impaired performance in a wide range of cognitive abilities, these impairments being particularly massive for inhibition and underpinned by large-scale frontal lobe dysfunctions (Stavro, Pelletier, & Potvin, 2013). Following this view, therapeutic programs should, thus, centrally aim at reestablishing an equilibrium between these two systems, by reducing automatic attraction, and/or increasing cognitive control. While offering a reliable conceptualization of AUD leading to fruitful experimental and clinical implications, dual-process models have neglected other key processes involved in the emergence and maintenance of AUD, among which are emotional and interpersonal disorders. Indeed, patients with AUD cannot only be defined as “dysregulated machines” presenting an automatic-control imbalance. As repeatedly reported in clinical observations, AUD is also an affective and relational disease: firstly, the comorbidity between AUD and mood disorders has long been established, most patients with AUD presenting intense negative emotionality, as well as depressive and anxious symptoms (Schuckit, 2006). Secondly, AUD is associated
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with familial, professional, and social difficulties, a majority of patients with AUD presenting reduced social networking, limited social support, or even persistent social isolation. Centrally, these socio-emotional disturbances should not be considered as secondary variables in AUD treatment as empirical studies have identified social support as a major factor for abstinence (Gordon & Zrull, 1991), and as 40% of relapses are directly attributed to persistent negative effects or reduced social networking (Zywiak, Westerberg, Connors, & Maisto, 2003). Negative emotionality and disrupted interpersonal functioning are, thus, at the heart of the addictive pathology, and a more inclusive conceptualization of AUD should include socioemotional impairments. However, evidence-based studies have long neglected these factors and their experimental exploration in AUD has only emerged during the past two decades. To underline the importance of social cognition in AUD, this chapter will propose a typology-based description of the currently available data regarding socio-emotional abilities in patients with AUD, and then identify the main fundamental and therapeutic perspectives in this field to encourage an in-depth experimental exploration of these factors, as well as their implementation in clinical evaluation and remediation settings.
A TYPOLOGICAL REVIEW OF SOCIAL COGNITION IN PATIENTS WITH AUD Social cognition is the ability to use psychological and cognitive resources to efficiently detect, understand, regulate, and react to stimulations emerging from interpersonal environments and social interactions (Green, Horan, & Lee, 2015). Although recent, the psychological and neuroscience exploration of social cognition in AUD constitutes a blooming research field. To offer the clearest possible description of this literature, this chapter’s review will use a classification of social cognition subcomponents proposed in schizophrenia research (Green et al., 2008), dividing these abilities into five subcategories (Fig. 39.1): Theory of Mind (ToM), social perception, social knowledge, attributional bias, and emotional processing. While these categories present some overlap and while several tasks simultaneously assess multiple categories, data will be described following this typology. First, ToM constitutes a complex social cognition component repeatedly shown as impaired in several psychopathological states, such as schizophrenia or depression (Bora, Bartholomeusz, & Pantelis, 2016). In AUD, several paradigms have been used to explore ToM abilities, from quite large batteries (Bosco, Capozzi, Colle, Marostica, & Tirassa, 2014) to more
specific investigations using the false-beliefs task (Fig. 39.2; Maurage, de Timary, Tecco, Lechantre, & Samson, 2015) or the faux-pas task (Thoma, Winter, Juckel, & Roser, 2013). These works led to coherent results documenting reduced ToM abilities in AUD; this deficit being present for all subcomponents of ToM (first-/third-person perspective taking, first-/ second-order inferences). Moreover, beyond this generalized deficit, other studies have explored the dissociation between cognitive and affective ToM, suggesting that the affective component (i.e., others’ emotions or feelings) is more strongly impaired (Nandrino et al., 2014). Beyond these dissociations, patients with AUD, thus, present significantly reduced ToM abilities, as clearly confirmed by meta-analyses (Bora & Zorlu, 2017; Onuoha, Quintana, Lyvers, & Guastella, 2016). Additionally, a social cognition component strongly associated with ToM is empathy. The links between ToM and empathy are still being debated (Green et al., 2015), but empathy is clearly a key component to develop and maintain efficient social interactions, and this ability is impaired in AUD: a first study observed lower empathy levels in AUD (Martinotti, Di Nicola, Tedeschi, Cundari, & Janiri, 2009), while later explorations (Maurage et al., 2011) showed a dissociation between impaired affective (i.e., detecting and feeling others’ emotional states) and preserved cognitive (i.e., understanding others’ nonemotional, mental states) empathy subcomponents. Second, social perception is evaluated by tasks presenting pictures or videos of social interactions, based on which the participant has to interpret verbal and nonverbal content to understand multifaceted interpersonal relations. This subcomponent had already been partly measured in the ToM tasks (Nandrino et al., 2014), but the measure of social perception abilities in AUD has been more directly conducted in two studies: A recent one (Maurage et al., 2016) used the “Movie for Assessment of Social Cognition task” (Fig. 39.3; Dziobek et al., 2006), requiring the participant to detect and categorize the thoughts, affects, and actions of four characters, and to infer their intentions and interpersonal relations. Patients with AUD were impaired in understanding the emotions expressed by the characters, but remained able to comprehend their nonemotional thoughts or behaviors. This result thus extends, on the basis of a more direct measure of the interpersonal relationships’ perception, the proposal of a dissociation between an impaired emotional subcomponent of social cognition and a preserved cognitive one. Another study, using neuroimaging measures, went one step beyond this by exploring the cerebral correlates of social perception in AUD, but also the self-related consequences of negative social interactions (Maurage et al., 2012). This study used the
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FIGURE 39.1 Subcomponents of social cognition. Graphical presentation of the five subcomponents related to social cognition, as defined by Green et al. (2008).
cyberball paradigm (Williams & Jarvis, 2006), a balltossing game in which a situation of social rejection is created by leading two other computer-guided players to exclude the participant from the game. When confronted with rejection, patients with AUD presented an increased social perception of this ostracism (indexed by more intense ostracism feelings and insula/cingulate cortex activities). These results, thus, suggest that, regarding social perception, AUD is associated with: (1) a reduced ability to take into account others’ emotional states during tasks in which the participant is not involved; (2) conversely, an increased sensitivity to the social perception of others thoughts and behaviors when these are directed toward the participant, threatening their social integration. Third, preliminary results suggest that AUD is associated with abnormalities in social knowledge, which might constitute a core deficit provoking a cascade of negative consequences for social interactions. Specifically, patients
with AUD have a reduced ability to correctly perform a humor detection task based on written jokes involving interpersonal contexts (Uekermann, Channon, Winkel, Schlebusch, & Daum, 2007). This indexes a difficulty to use social knowledge to identify the humoristic break of social rules provoked by an incongruity in the described interactions. It has also been shown that AUD is related to a reduced detection of irony (Amenta, Noe¨l, Verbanck, & Campanella, 2013), witnessing a reduced knowledge of the social rules and roles underlying human interactions. Another social knowledge facet measured in patients with AUD is the presence of maladaptive self-beliefs related to social standards: patients with AUD present a specific tendency to over-evaluate the standards required in social interactions (Maurage et al., 2013). In other words, AUD is related to an exaggerated estimation of the requested interpersonal performance to obtain a satisfactory social outcome. This biased social knowledge, strongly correlated with interpersonal difficulties, could, thus, contribute to the emergence of a
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FIGURE 39.2 False-beliefs task. Schematic illustration of the events’ sequence in the false-beliefs task used to explore ToM in AUD. (A) Track-Task (spontaneous tracking of the other person’s perspective): (1) The woman (right) watches in which box the green object is located (while the participant cannot see it); (2) She leaves the room and the man (left) switches boxes; (3) She returns and gives a hint by placing the pink object on one of the boxes to help finding the green object. At this point, the participant has to point to the box containing the green cube; (B) Inhibit-Task (self-perspective inhibition): (1) The woman watches in which box the green object is located. The participant can also see the object‘s location; (2) The woman leaves the room and the man changes the object‘s location; (3) The woman returns and the participant has to indicate which of the two boxes the woman will open first. Note: for description’s clarity, the green cube is visible in the illustration whereas it is hidden in the box during the experiment.
FIGURE 39.3 Movie for Assessment of Social Cognition task. Illustration of an item of the Movie for Assessment of Social Cognition task used to explore social perception in AUD. The upper part describes the critical sequences of the video. The lower part gives the four possible answers proposed to the participant.
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vicious cycle: the exaggerated standards may lead to negative feelings during social interactions, which might, in turn, increase social isolation. Fourth, attributional bias is the only subcomponent of social cognition still to be explored in patients with AUD. Many studies have been conducted on attentional or cognitive biases among patients (Field & Cox, 2008), but this approach has not yet been applied to interpersonal biases. Several studies have identified attributional biases in other psychiatric states, and these results should encourage future works to explore these processes in patients with AUD by using attributional bias tasks (e.g., Combs, Penn, Wicher, & Waldheter, 2007). Fifth and finally, numerous studies have been conducted to explore emotional processing in patients with AUD. After a seminal study (Philippot et al., 1999) describing a reduced ability to identify the emotional states expressed by human faces, a large variety of experimental designs have been used (Donadon & Oso´rio, 2014) presenting various facial emotions by means of numerous procedures, most results confirming the presence of this deficit: patients with AUD need more emotional intensity to detect others’ affective states (Fig. 39.4; D’Hondt, de Timary, Bruneau, & Maurage, 2015). Importantly, this deficit appears specific for emotional states and more intense for negative emotions (Bora & Zorlu, 2017). However, it is generalized to all emotional stimulations, including voice prosody or body posture (Maurage et al., 2009). As the aptitude to decode emotional cues offered by others is crucial to efficiently understand their state-of-mind and affective feelings, it has been suggested that this global emotion decoding difficulty in patients with AUD plays a role in the reduction of interpersonal bonds and in the social isolation frequently observed
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in this population (D’Hondt, Campanella, Kornreich, Philippot, & Maurage, 2014). Moreover, the impaired capacity to identify others’ emotions in patients with AUD also extends towards the identification of one’s own emotions, as AUD is related to increased alexithymia, that is, an impaired ability to feel, identify, and express internal affective states (Stasiewicz et al., 2012).
TOWARDS A DEEPER UNDERSTANDING OF SOCIAL COGNITION IN PATIENTS WITH AUD Overall, the large majority of studies exploring social cognition in AUD have documented substantial impairments, particularly for ToM and emotional processing. In view of the key role played by these aptitudes in interpersonal relations, these impairments might contribute to the personal, professional, and societal difficulties reported in patients with AUD (Kornreich et al., 2002) and should, thus, be further considered in clinical settings beyond the classical focus on cognitive functions. In this respect, it is noteworthy that the correlation between AUD-related deficits in social cognition and standard clinical features of AUD severity—for example, DSM-5 AUD criteria (Hasin et al., 2013), “Alcohol Use Disorder Identification Test” score (Bohn, Babor, & Kranzler, 1995), or features of AUD outcomes like postdetoxification relapse rates—have hardly been explored, as only one study (Rupp, Derntl, Osthaus, Kemmler, & Fleischhacker, 2017) showed that reduced emotional processing abilities at the start of treatment is associated with higher relapse rates, thus, confirming the involvement of social cognition in clinical outcomes.
FIGURE 39.4 Emotional processing paradigm. Example of stimuli illustrating the various emotional valences and intensities used to explore emotion processing in AUD. (A) Example of a realistic face depicting four different prototypical emotional facial expressions (neutral, happy, angry, and sad); (B) Example of a morphing continuum (angry sad) for one identity. The percentage of each emotion contained in each of the 10-morph step is mentioned at the bottom of the figure (e.g., 95% 5% means that this stimulus contains 95% of anger and 5% of sadness).
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Furthermore, future studies should also couple the neuropsychological assessment of social cognition with more clinically-focused tools used to assess social functioning—for example, Measurement in Addictions for Triage and Evaluation, whose assessment is partly based on the WHO international classification of functioning (Schippers, Broekman, Buchholz, Koeter, & van den Brink, 2010). Another challenge regarding future studies is that this research field suffers from a lack of theoretical background and experimental coherence, as studies have not been integrated into a clear fundamental model. The present attempt to offer a typology of social cognition data in patients with AUD, based on the proposals emerging in other psychiatric states, has clearly shown that, while ToM and emotional processing have been largely studied (using scattered and often multidetermined paradigms), other components of social cognition have not been thoroughly measured. A first major research perspective would, thus, be to capitalize on the typology presented here to develop a coherent research program which would propose, for each identified social cognition subcomponent, an in-depth exploration based on controlled and component-specific tasks, as initiated in schizophrenia (Green et al., 2015), as well as on a strict control of AUD characteristics and comorbid psychopathological states. Recent papers (Kwako, Momenan, Litten, Koob, & Goldman, 2016) have initiated this ambitious program by proposing a neuroscience-grounded battery to explore key variables in AUD, among which are some measures of emotional and social processing. This constitutes an important first step towards a rational evaluation of social cognition in patients with AUD, despite a still quite imprecise specification of the processes to be evaluated. Beyond the needed clarification and deepening of the core socio-emotional processes at stake in patients with AUD, other crucial research questions should be addressed (Fig. 39.5), among which: 1. The interactions between socio-emotional and cognitive processes: Most studies have explored social cognition in AUD in an isolated fashion, but these abilities might strongly interact with other AUD deficits, and centrally cognitive functions. Preliminary results have indicated that social cognition in AUD is influenced by working (Uekermann et al., 2007) or autobiographical (Nandrino et al., 2014) memory, and that socioemotional difficulties might be partly caused by visuo-perceptive impairments (D’Hondt, Lepore, & Maurage, 2014), but these proposals should be confirmed using more controlled joint explorations of socio-emotional and cognitive abilities.
2. The interindividual variability of socio-emotional deficits: All presented studies have capitalized on a groupbased approach, considering patients with AUD as a homogeneous population. However, when going one step beyond this to analyze individual performances, it appeared that only 50% of patients with AUD present a genuine ToM deficit (Maurage et al., 2015). Moreover, this heterogeneity in socioemotional disorders has been specifically explored using a cluster analytic approach (Maurage, de Timary, & D’Hondt, 2017), which clearly showed that AUD is a constellation of individuals with a wide variety of socio-emotional profiles. Future studies should, thus, systematically complement the classical group approach by individual analyses specifying the interindividual variation of the deficits, as well as the differential role played by psychopathological and addictive comorbidities. 3. The causal relation between AUD and social cognition deficits, and their evolution: Previous studies have focused on recently detoxified patients with AUD. This focus did not allow determining whether socioemotional impairments are a consequence of the neurotoxicity provoked by repeated excessive alcohol use or, at least partly, a causal factor involved in AUD development. More globally, the evolution of social cognition deficits during the course of the disease (e.g., after long-term abstinence) and in its successive stages should be more thoroughly explored through longitudinal studies and explorations focused on other alcohol-consumption patterns related to socio-emotional impairments—for example, binge drinking (Maurage, Bestelmeyer, Rouger, Charest, & Belin, 2013). 4. The inclusion of social cognition deficits in AUD models: The dominant dual-process models have not integrated emotional and social functions, which are still considered as mere side-products of the imbalance between automatic and controlled systems. A subsequent theoretical proposal, the triadic model (Noe¨l, Brevers, & Bechara, 2013), postulates a third insula-based system involved in the detection of interoceptive signals and in their conversion in affective feelings. This model, while having received limited empirical support as yet, might constitute a foundation to integrate socioemotional deficits in AUD models. Finally, these research results should urgently be integrated into clinical practices, where social cognition deficits are totally under-evaluated and undertreated, despite repeated clinical observations underlining their importance in the detoxification process. Centrally, proposals regarding the implementation of
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MINI-DICTIONARY OF TERMS
379 FIGURE 39.5 Proposal for future research avenues. Graphical synthesis of the main research perspectives proposed to deepen the understanding of social cognition in patients with AUD.
cognitive remediation in addictive disorders have recently bloomed (Verdejo-Garcia, 2016), but these programs have been focused on cognitive variables. In line with what has been proposed in schizophrenia (Grant, Lawrence, Preti, Wykes, & Cella, 2017), a structured neuropsychological training program focusing on the evaluation and training of social cognition in patients with AUD should urgently be tested in care structures as it could improve socio-emotional abilities, but also positively impact clinical outcomes of patients by breaking the vicious cycle linking social cognition deficits, social isolation, and alcohol consumption.
MINI-DICTIONARY OF TERMS Attributional bias The propensity to consider that the personal and interpersonal events occurring in one’s life are mostly due to internal (i.e., individual responsibility) or external (i.e., others’ responsibility or contextual variables) causes.
Emotional processing The efficient perception, interpretation, and reaction to the emotional states expressed by other individuals through their facial expression, voice prosody, or body posture, as well as the correct decoding and regulation of one’s own affective states. Empathy The capacity to understand other individuals’ cognitive or affective perspectives and to propose a verbal or behavioral answer adapted to the emotions, feelings, or thoughts they expressed. Social cognition The psychological processes related to the identification and interpretation of social signals sent by other individuals in interpersonal contexts, as well as the skills needed to effectively respond to these signals. Social knowledge The awareness and understanding of the rules and conventions to be followed during social interactions, and of the role assigned to each participant in social contexts. Social perception The aptitude to interpret verbal and nonverbal stimuli to infer individuals’ role and current relationships in equivocal or intricate interpersonal contexts. Theory of mind The ability to use the interpersonal signals produced by other individuals to infer their mental states, thoughts, or emotions, and to anticipate their behaviors or actions.
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KEY FACTS Social Cognition in Alcohol Use Disorders • Severe alcohol use disorders (AUD) are the most frequent psychiatric disorder, affecting 5% 10% of adults in Western countries. • AUD are associated with cognitive deficits, as indexed by altered perceptive motor, attentional and memory capacities, but also reduced executive functions (e.g., inhibition, flexibility, problem solving). • Social cognition impairments have more recently been identified in patients with AUD, encompassing reduced performance in Theory of Mind (i.e., the inference of others’ mental states based on the interpersonal signals they send) and emotion decoding (i.e., the decoding of others’ emotional states expressed through their face, voice, or body)—two central abilities for efficient social interactions. • These social cognition deficits might favor the persistence of AUD in patients by creating a vicious cycle: impaired social cognition would lead to social isolation, itself leading to increased alcohol consumption used as a coping strategy, which would, in turn, aggravate social cognition impairments due to alcohol neurotoxicity. • Social cognition should, thus, be further investigated in AUD, and more globally in addictive states, notably to specify its role in the emergence and stabilization of excessive alcohol consumption and its evolution during the disease’s course.
SUMMARY POINTS • This chapter reviews social cognition impairments in alcohol use disorders (AUD). • Beyond the well-established cognitive deficits, AUD are also characterized by large-scale impairments to detect, interpret, and use social signals in interpersonal contexts. • Reduced abilities have been repeatedly found for Theory of Mind and emotion processing among patients with AUD. • The potential deficit for other social cognition subcomponents (social perception, social knowledge, and attributional bias) has still to be thoroughly evaluated. • Future studies should also explore the causal links between AUD and social cognition deficits, as well as their interactions with cognitive deficits and their variation across individuals with AUD.
• In view of the massive alterations observed for socio-emotional processes in patients with AUD, these factors should be taken into account in clinical settings, centrally, by proposing a specific social cognition evaluation and training.
Acknowledgments Pierre Maurage is research associate at the Fund for Scientific Research (F.R.S.-FNRS, Belgium). This chapter was supported by a grant from the “Fondation pour la Recherche en Alcoologie” (FRA, France).
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