Anhedonia - a common feature of depression and other neuropsychiatric disorders - encompasses a reduction in the subjective experience and anticipation of rewarding events, and a reduction in the motivation to seek out such events. The presence of anhedonia often predicts or accompanies treatment resistance, and as such better interventions and treatments are important. Yet the mechanisms giving rise to anhedonia are not well understood. In this chapter, we briefly review existing computational conceptualisations of anhedonia. We argue that they are mostly descriptive and fail to provide an explanatory account of why anhedonia may occur. Working within the framework of reinforcement learning, we examine two potential computational mechanisms that could give rise to anhedonic phenomena. First, we show how anhedonia can arise in multi-dimensional drive-reduction settings through a trade-off between different rewards or needs. We then generalise this in terms of model-based value inference and identify a key role for associational belief structure. We close with a brief discussion of treatment implications of both of these conceptualisations. In summary, computational accounts of anhedonia have provided a useful descriptive framework. Recent advances in reinforcement learning suggest promising avenues by which the mechanisms underlying anhedonia may be teased apart, potentially motivating novel approaches to treatment.

Mammalian species form unique bonds between mothers and infants. Maternal care, including suckling, is necessary for infant survival, and the mother and, sometimes, the father require a lot of effort in nurturing infants. An infant's probability of survival depends on the extent of the investment of care by the mother. In parallel, mothers must identify their offspring and invest only in those who possess their genes to achieve evolutionary benefits. Therefore, they need to recognize their offspring and show a strong preference for them. For this reason, bond formation between mothers and infants is important. The mother monitors her offspring's physical condition and stays close to them. The offspring also form strong bonds with their mothers. Therefore, a separation between the mother and infant causes severe stress for both parties. Although it was initially thought that such bonds between mother and infant are limited to the same species, we have also observed a similar phenomenon in the human-dog relationship. In this article, we discuss the neuroendocrine mechanisms that underlie bond formation and separation based on findings of neurobiological research in mice and the relationship between humans and dogs.

Functional [psychogenic nonepileptic/dissociative] seizures (FND-seiz) and related functional neurological disorder subtypes were of immense interest to early founders of modern-day neurology and psychiatry. Unfortunately, the divide that occurred between the both specialties throughout the mid-twentieth century placed FND-seiz at the borderland between the two disciplines. In the process, a false Cartesian dualism emerged that labeled psychiatric conditions as impairments of the mind and neurological conditions as disturbances in structural neuroanatomy. Excitingly, modern-day neuropsychiatric perspectives now consider neurologic and psychiatric conditions as disorders of both brain and mind. In this article, we aim to integrate neurologic and psychiatric perspectives in the conceptual framing of FND-seiz. In doing so, we explore emerging relationships between symptoms, neuropsychological constructs, brain networks, and neuroendocrine/autonomic biomarkers of disease. Evidence suggests that the neuropsychological constructs of emotion processing, attention, interoception, and self-agency are important in the pathophysiology of FND-seiz. Furthermore, FND-seiz is a multi-network brain disorder, with evidence supporting roles for disturbances within and across the salience, limbic, attentional, multimodal integration, and sensorimotor networks. Risk factors, including the magnitude of previously experienced adverse life events, relate to individual differences in network architecture and neuroendocrine profiles. The time has come to use an integrated neuropsychiatric approach that embraces the closely intertwined relationship between physical health and mental health to conceptualize FND-seiz and related functional neurological disorder subtypes.

Obsessive-compulsive disorder (OCD) sits at the epicenter of a spectrum of related conditions (often referred to as obsessive-compulsive related disorders (OCRD) or obsessive-compulsive spectrum disorders (OCSD)) that can be as disabling as they are varied in presentation. Research in the field now encompasses diverse disciplines ranging from inflammatory mechanisms to computational psychiatry, to neurocognitive endophenotypes to functional imaging to pharmacogenomics to brain stimulation approaches. As these disorders become more clearly elucidated, there is a need to continually re-evaluate the implications of research findings and to incorporate these findings into new treatment approaches that benefit both patients and clinicians. Even the Diagnostic and Statistical Manual of Mental Disorders 5th Edition (DSM-5) is intended to be flexible and to incorporate validated and reliable biomarkers and neuroscience findings as they become available. This concluding chapter highlights just a few areas of study that promise to influence our understanding of the pathophysiology and clinical practice of OCRD. These include patient-centered outcomes research, the study of developmental brain trajectories in spectrum conditions, robot models of OCRDs, goal-directed versus habit-based behaviors, pharmacogenomics, problematic use of the Internet, and digital interventions. For example, digital medicine may become increasingly useful by identifying patients early on in the course of their illness; providing biomarkers to subtype patients; predicting treatment response; serving as a more proximal outcome measure of treatment response; or providing easily accessible and less costly forms of care. In order to address unmet clinical needs in OCRD, it is helpful to take an interdisciplinary perspective, and the work described in this collection of articles is likely to be invaluable in shaping the future of the field.

The evaluation and treatment of patients with epilepsy is not limited to the type of epilepsy, but it must incorporate the common comorbid neurologic, psychiatric, and medical disorders, as the latter can bare an impact on the course and response to treatment of the seizure disorder and vice versa. In this article we review the bidirectional relations among epilepsy and two of its most common comorbidities, mood disorders and migraine and examine the implications of these relations on the selection of therapies of these three disorders and their response to treatment. We also review the most salient common pathogenic mechanisms that may explain such relations.

Adolescence is an exquisitely sensitive period of development during which pathways branch toward success in school and prosocial pursuits or, conversely, toward behavior problems and involvement in high-risk activities and systems, such as juvenile justice (JJ). Adverse childhood experiences (ACEs) such as poverty, family dysfunction, and child maltreatment, have been strongly and repeatedly associated with JJ involvement. A significant body of research from neuroscience has established that ACEs can alter facets of neurodevelopment that undergird self-regulation throughout childhood and adolescence, thereby increasing susceptibility to behaviors that attract attention of the JJ system. Because the ability to intervene prior to system-entrenchment is crucial to disrupting an adverse developmental pathway, we look toward neuroscience to offer insights into how to do so more effectively. In this chapter, evidence is summarized that informs an understanding of how neurodevelopmental pathways may lead to JJ involvement. Because neurodevelopment is malleable in response to both detrimental and positive experiences, there is potential for well-targeted interventions to normalize brain and cognitive development, especially during sensitive periods of maturation. This discussion is followed by a proposed research agenda to determine how to exploit these critical windows of opportunity to divert youth from persistent antisocial behavior and JJ involvement. Lastly, a review of neuroscience findings regarding the ability of intervention to strengthen brain systems that modulate self-regulation is presented. This research has direct practical significance with potential to be translated into meaningful policy change.

This chapter aims to familiarise the reader with a diverse and fast-growing literature concerning the role that habits play in obsessive-compulsive disorder (OCD). Core concepts will be introduced, including how the balance between habits and a more deliberate form of action selection (goal-directed control) has traditionally been measured and how cross-species translation, neuroscience tools, and computational modelling have been used to build on these basic principles and reveal core mechanisms under study today. Next, the application of these methods to the study of OCD and related disorders will be detailed, converging on a theory that enhanced habit expression, and indeed compulsions in OCD, might arise from deficits in goal-directed control systems. These basic findings will be contextualised in terms of major tide changes in the field, including the shift from categorical disease frameworks to dimensional ones. Mechanistically, recent research concerning how goal-directed deficits arise, perhaps through failures in the construction of a mental model, are discussed along with studies critically evaluating our ability to measure habits in humans, in a laboratory setting. The chapter ends with a nod to the future, focusing on the need for clinically oriented, longitudinal, and intervention-based research that aim to translate what is now a wealth of cross-sectional mechanistic insights to the clinic.

The caregiving environment that children and adolescents experience is critically important for their social-emotional development. Parenting may affect child social-emotional outcomes through its effects in shaping the child's developing brain. Research has begun to investigate effects of parenting on child and adolescent brain function in humans using functional magnetic resonance imaging (fMRI). Here we review these initial studies. These studies find associations between parenting behavior and child and adolescent functional activation in neural networks involved in emotional arousal, emotion regulation (ER), reward processing, cognitive control, and social-emotional information processing. Findings from these studies suggest that higher negative parenting and lower positive parenting are generally associated with heightened activation in emotional arousal networks in response to negative emotional stimuli in youth. Further, findings indicate that lower positive parenting is associated with higher response in reward processing networks to monetary reward in youth. Finally, findings show that lower positive parenting predicts lower activation in cognitive control networks during cognitive control tasks and less adaptive neural responses to parent-specific stimuli. Several studies found these associations to be moderated by child sex or psychopathology risk status and we discuss these moderating factors and discuss implications of findings for children's social-emotional development.

Patients with epilepsy can experience different neuropsychiatric symptoms related (peri-ictal) or not (interictal) with seizures. Peri-ictal symptoms can precede (pre-ictal) or follow (post-ictal) the seizure, or even be the expression of the seizure activity (ictal). Neuropsychiatric symptoms, such as irritability and apathy, are among the most frequent pre-ictal manifestations. Ictal fear is reported by around 10% of patients with focal seizures, and sometimes can be difficult to differentiate from panic attacks. Post-ictal anxiety, mood and psychotic symptoms are also frequently reported by patients. Peri-ictal phenomena can occur as isolated symptom or as a cluster of symptoms, sometimes resembling a full-blown psychiatric syndrome. Actually, peri-ictal and interictal neuropsychiatric manifestations seem to be closely associated.

Social support (SS), or having people to depend on during times of stress, may offer an emotional and neurological buffer to problem drinking. Specifically, SS may modulate reward and stress-related brain responses to mitigate perceptions of alcohol reward and stress. There is limited evidence, however, on this topic and specifically on brain networks that may modulate SS effects on stress and alcohol reward. Here we present a review of the current literature on this topic as well as data from a large community sample of 115 social drinkers. Findings from a novel fMRI task viewing alcohol cue, stress, and neutral images, in separate blocks, while providing ratings on subjective feelings of alcohol craving, stress, and arousal are included. Lower SS significantly predicted greater alcohol craving during alcohol cue and stress conditions, higher baseline levels of stress, and greater arousal in the alcohol cue, relative to neutral condition. Remarkably, individuals with low SS showed greater reward activation (ventral medial prefrontal cortex (VmPFC) and ventral striatum) during alcohol cue exposure, while those with high SS showed no such activation (p<0.001, family wise error corrected at 0.05). Furthermore, individuals with lower SS showed greater stress circuit (VmPFC, dorsal striatum, and periaqueductal gray) activation not observed in the high SS groups. Both groups showed increased amygdala activation under stress condition. The findings support the notion that SS is a powerful modulator of stress response and reward motivation. High SS buffers neural and subjective stress responses, while low SS potentiates greater reward seeking with higher alcohol craving and greater brain activation during alcohol cue exposure. Previous research and current results suggest the need to further explore the role of SS in those at risk of developing alcohol use disorder and assess novel prevention strategies to boost SS in at-risk drinkers.