Annual Review of Clinical Psychology - Volume 11, 2015

Our article reviews and celebrates Susan Nolen-Hoeksema's remarkable contributions to psychological and clinical science, focusing on her vast body of theoretical and empirical work and her influence on colleagues and students. Susan spent her career trying to understand how and why a style of regulating emotions called rumination increases vulnerability to depression and exacerbates and perpetuates negative moods. More broadly, we describe research by Susan and her colleagues on the predictors of depression in childhood and adolescence; gender differences in depression and rumination in adolescence and adulthood; roots, correlates, and adverse consequences of ruminative response styles; and rumination as a transdiagnostic risk factor for not only depression but also a host of psychological disorders, including anxiety, substance abuse, and eating disorders. Susan's intellectual legacy is evident in her impressive publication and citation record, the clinical applications of her work, and the flourishing careers of the students she mentored.

I describe the development and course of my research in studying clinical dysfunction among children, adolescents, and adults. This is an autobiographical account that highlights programs of research, career moves, and experiences along the way that were particularly influential. Research on specific topics and the methods to study them were inherently fascinating but invariably led me to broader issues well beyond what I was studying. The research alerted me to how and why current methods, assumptions, and research practices might be constraining and perhaps slightly misguided. My research and specific findings in a given area were not necessarily part of any particular breakthrough but rather helped me see how more, different, and better work was needed. Collaborations with a diverse set of colleagues and models from other disciplines than psychology helped me conceptualize the goals of research on a given topic (e.g., developing evidence-based treatments, reducing the burden of mental illness, promoting a sustainable environment to mitigate climate change) and propose a shift from current practices as a means to obtain them.

This article provides a selective review of advances in scientific knowledge about autism spectrum disorder (ASD), using DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, fifth edition) diagnostic criteria as a framework for the discussion. We review literature that prompted changes to the organization of ASD symptoms and diagnostic subtypes in DSM-IV, and we examine the rationale for new DSM-5 specifiers, modifiers, and severity ratings as well as the introduction of the diagnosis of social (pragmatic) communication disorder. Our goal is to summarize and critically consider the contribution of clinical psychology research, along with that of other disciplines, to the current conceptualization of ASD.

We present a revision of latent state-trait (LST-R) theory with new definitions of states and traits. This theory applies whenever we study the consistency of behavior, its variability, and its change over time. States and traits are defined in terms of probability theory. This allows for a seamless transition from theory to statistical modeling of empirical data. LST-R theory not only gives insights into the nature of latent variables but it also takes into account four fundamental facts: Observations are fallible, they never happen in a situational vacuum, they are always made using a specific method of observations, and there is no person without a past. Although the first fact necessitates considering measurement error, the second fact requires allowances for situational fluctuations. The third fact implies that, in the first place, states and traits are method specific. Furthermore, compared to the previous version of LST theory (see, e.g., Steyer et al. 1992, 1999), our revision is based on the notion of a person-at-time-t. The new definitions in LST-R theory have far-reaching implications that not only concern the properties of states, traits, and the associated concepts of measurement errors and state residuals, but also are related to the analysis of states and traits in longitudinal observational and intervention studies.

Postpartum depression (PPD) adversely affects the health and well being of many new mothers, their infants, and their families. A comprehensive understanding of biopsychosocial precursors to PPD is needed to solidify the current evidence base for best practices in translation. We conducted a systematic review of research published from 2000 through 2013 on biological and psychosocial factors associated with PPD and postpartum depressive symptoms. Two hundred fourteen publications based on 199 investigations of 151,651 women in the first postpartum year met inclusion criteria. The biological and psychosocial literatures are largely distinct, and few studies provide integrative analyses. The strongest PPD risk predictors among biological processes are hypothalamic-pituitary-adrenal dysregulation, inflammatory processes, and genetic vulnerabilities. Among psychosocial factors, the strongest predictors are severe life events, some forms of chronic strain, relationship quality, and support from partner and mother. Fully integrated biopsychosocial investigations with large samples are needed to advance our knowledge of PPD etiology.

Most youth psychotherapy research involves conditions quite unlike the clinical practice it is designed to strengthen. Most studies have not tested interventions with clinically referred youths and practicing clinicians in clinical care settings, nor have they tested whether new treatments produce better outcomes than usual practice. Limited exposure to real-world conditions and questions may partially explain why empirically supported treatments show such modest effects when tested under more representative conditions, against usual care. Our deployment-focused model calls for intervention development and testing with the kinds of participants (e.g., clients and clinicians) and in the contexts (e.g., clinics) for which the interventions are ultimately intended, and for randomized comparisons to usual clinical care. Research with the Child STEPs (system and treatment enhancement projects) treatment approach illustrates the methods and potential benefits of the deployment-focused model. Findings supporting Child STEPs are but one part of a rich research matrix needed to shrink the gap between intervention research and clinical practice.

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders includes a new class of obsessive-compulsive and related disorders (OCRDs) that includes obsessive-compulsive disorder (OCD) and a handful of other putatively related conditions. Although this new category promises to raise awareness of underrecognized and understudied problems, its empirical validity and practical utility are questionable. This article reviews the phenomenology of OCD and then presents a critical analysis of the arguments underlying the new OCRD class. This analysis leads to a rejection of the OCRD classification on both scientific and logical grounds. The article closes with a discussion of the treatment implications of the OCRDs approach.

In the past two decades, research advances have enhanced our understanding of the clinical features, cognitive biases, and treatment of body dysmorphic disorder (BDD). In this review, we critically examine the current state of the evidence on the proposed cognitive and emotional processing mechanisms of BDD. We describe how major findings in these areas made unique contributions to the development of an empirically informed cognitive-behavioral model of BDD, which in turn facilitated the translation of research to treatment strategies. Finally, we outline important areas of future research.

In this article, we present and review the evidence for two major biopsychosocial theories of the onset and course of bipolar spectrum disorders (BSDs) that integrate behavioral, environmental, and neurobiological mechanisms: the reward hypersensitivity and the social/circadian rhythm disruption models. We describe the clinical features, spectrum, age of onset, and course of BSDs. We then discuss research designs relevant to demonstrating whether a hypothesized mechanism represents a correlate, vulnerability, or predictor of the course of BSDs, as well as important methodological issues. We next present the reward hypersensitivity model of BSD, followed by the social/circadian rhythm disruption model of BSD. For each model, we review evidence regarding whether the proposed underlying mechanism is associated with BSDs, provides vulnerability to the onset of BSDs, and predicts the course of BSDs. We then present a new integrated reward/circadian rhythm (RCR) dysregulation model of BSD and discuss how the RCR model explains the symptoms, onset, and course of BSDs. We end with recommendations for future research directions.

This review examines the history of psychiatric nosology, with particular reference to the nineteenth-century origins of the concepts of manic-depressive illness and schizophrenia as distinct clinical syndromes and their evolution and diagnostic refinement over time. I document how the terminology applied to these entities has generated controversy, and discuss the ways in which the resulting diagnostic entities as defined by pure phenomenological symptom descriptors fail to capture discrete diagnostic distinctions, leading some researchers to posit an illness continuum rather than separate disorders. Furthermore, the two syndromes overlap substantially on multiple biologic measures, and clarity is lacking as to the underlying etiology and pathology necessary to move from descriptions of clinical syndromes to diseases. I next examine how biologically based classifications agnostic to conventional diagnostic schemes may be useful and how these are being implemented in practice, and conclude by summarizing where such approaches are likely to lead.

This review uses a levels-of-analysis framework to summarize the current understanding of developmental dyslexia's etiology, brain bases, neuropsychology, and social context. Dyslexia is caused by multiple genetic and environmental risk factors as well as their interplay. Several candidate genes have been identified in the past decade. At the brain level, dyslexia is associated with aberrant structure and function, particularly in left hemisphere reading/language networks. The neurocognitive influences on dyslexia are also multifactorial and involve phonological processing deficits as well as weaknesses in other oral language skills and processing speed. We address contextual issues such as how dyslexia manifests across languages and social classes as well as what treatments are best supported. Throughout the review, we highlight exciting new research that cuts across levels of analysis. Such work promises eventually to provide a comprehensive explanation of the disorder as well as its prevention and remediation.

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is most often identified in postmortem autopsies of individuals exposed to repetitive head impacts, such as boxers and football players. The neuropathology of CTE is characterized by the accumulation of hyperphosphorylated tau protein in a pattern that is unique from that of other neurodegenerative diseases, including Alzheimer's disease. The clinical features of CTE are often progressive, leading to dramatic changes in mood, behavior, and cognition, frequently resulting in debilitating dementia. In some cases, motor features, including parkinsonism, can also be present. In this review, the historical origins of CTE are revealed and an overview of the current state of knowledge of CTE is provided, including the neuropathology, clinical features, proposed clinical and pathological diagnostic criteria, potential in vivo biomarkers, known risk factors, and treatment options.

This review provides an overview of the relationship between depression and cognition in the elderly, with an emphasis on psychotherapies and nonpharmacologic approaches. We first review the clinical presentation of late-life depression and comorbid cognitive impairment, as well as the epidemiology and risk factors for cognitive impairment in late-life depression and the temporal relationship between depression and cognitive impairment. Next, we discuss the salient topic of elderly suicide and cognitive impairment. We then touch briefly on the neuropsychological deficits, biomarkers, and neuroimaging findings in late-life depression with comorbid cognitive impairment. We then focus most of this review on psychotherapies and nontraditional treatments for late-life depression with comorbid cognitive impairment and examine what evidence, if any, exists of the cognitive and functional benefits of these treatments. Finally, we examine the cognitive effects of pharmacologic treatments and brain stimulation therapies.

The exponential rise in the number of functional brain connectivity studies, particularly those examining intrinsic functional connectivity (iFC) at rest, and the promises of this work for unraveling the ontogeny of functional neural systems motivate this review. Shortly before this explosion in functional connectivity research, developmental neuroscientists had proposed theories based on neural systems models to explain behavioral changes, particularly in adolescence. The current review presents recent advances in imaging in brain connectivity research, which provides a unique tool for the study of neural systems. Understanding the potential of neuroimaging for refining neurodevelopmental models of brain function requires a description of various functional connectivity approaches. In this review, we describe task-based and resting-state functional magnetic resonance imaging (fMRI) analytic strategies, but we focus on iFC findings from resting-state data to describe general developmental trajectories of brain network organization. Finally, we use the example of drug addiction to frame a discussion of psychopathology that emerges in adolescence.

Emotional problems figure prominently in many clinical conditions. Recent efforts to explain and treat these conditions have emphasized the role of emotion dysregulation. However, emotional problems are not always the result of emotion dysregulation, and even when emotional problems do arise from emotion dysregulation, it is necessary to specify precisely what type of emotion dysregulation might be operative. In this review, we present an extended process model of emotion regulation, and we use this model to describe key points at which emotion-regulation difficulties can lead to various forms of psychopathology. These difficulties are associated with (a) identification of the need to regulate emotions, (b) selection among available regulatory options, (c) implementation of a selected regulatory tactic, and (d) monitoring of implemented emotion regulation across time. Implications and future directions for basic research, assessment, and intervention are discussed.

Over the past two decades, research examining the impact of self-reported experiences of discrimination on mental and physical health has increased dramatically. Studies have found consistent associations between exposure to discrimination and a wide range of Diagnostic and Statistical Manual of Mental Disorders (DSM)-diagnosed mental disorders as well as objective physical health outcomes. Associations are seen in cross-sectional as well as longitudinal studies and persist even after adjustment for confounding variables, including personality characteristics and other threats to validity. However, controversies remain, particularly around the best approach to measuring experiences of discrimination, the significance of racial/ethnic discrimination versus overall mistreatment, the need to account for “intersectionalities,” and the importance of comprehensive assessments. These issues are discussed in detail, along with emerging areas of emphasis including cyber discrimination, anticipatory stress or vigilance around discrimination, and interventions with potential to reduce the negative effects of discrimination on health. We also discuss priorities for future research and implications for interventions and policy.