Annual Review of Clinical Psychology - Volume 9, 2013

Enormous progress in the field of clinical science has been made over the past 50 years, with advances in our understanding of psychopathology and more sophisticated research methodology leading to the development of more efficacious psychological treatments for a variety of behavioral disorders. Despite these advances, the public health impact of well-established psychological treatments is less than it should be. After an overview of the current status of the field, we identify barriers that must be overcome to maximize the public health impact and propose that to breach these barriers we must (a) augment the efficacy of treatments, (b) broaden the impact of treatments across diagnoses to include temperamental variables, (c) attend more closely to mechanisms of action of treatments, and (d) learn the best methods for disseminating and implementing psychological interventions. We conclude by proposing new directions in both research and clinical practice to accomplish these goals.

According to the idea that addiction is a chronic relapsing disease, remission is at most a temporary state. Either addicts never stop using drugs, or if they do stop, remission is short lived. However, research on remission reveals a more complex picture. In national epidemiological surveys that recruited representative drug users, remission rates varied widely and were markedly different for legal and illegal drugs and for different racial/ethnic groups. For instance, the half-life for cocaine dependence was four years, but for alcohol dependence it was 16 years, and although most dependent cocaine users remitted before age 30, about 5% remained heavy cocaine users well into their forties. Although varied, the remission results were orderly. An exponential growth curve closely approximated the cumulative frequency of remitting for different drugs and different ethnic/racial groups. Thus, each year a constant proportion of those still addicted remitted, independent of the number of years since the onset of dependence.

Integrative data analysis (IDA), a novel framework for conducting the simultaneous analysis of raw data pooled from multiple studies, offers many advantages including economy (i.e., reuse of extant data), power (i.e., large combined sample sizes), the potential to address new questions not answerable by a single contributing study (e.g., combining longitudinal studies to cover a broader swath of the lifespan), and the opportunity to build a more cumulative science (i.e., examining the similarity of effects across studies and potential reasons for dissimilarities). There are also methodological challenges associated with IDA, including the need to account for sampling heterogeneity across studies, to develop commensurate measures across studies, and to account for multiple sources of study differences as they impact hypothesis testing. In this review, we outline potential solutions to these challenges and describe future avenues for developing IDA as a framework for studies in clinical psychology.

In network approaches to psychopathology, disorders result from the causal interplay between symptoms (e.g., worry → insomnia → fatigue), possibly involving feedback loops (e.g., a person may engage in substance abuse to forget the problems that arose due to substance abuse). The present review examines methodologies suited to identify such symptom networks and discusses network analysis techniques that may be used to extract clinically and scientifically useful information from such networks (e.g., which symptom is most central in a person's network). The authors also show how network analysis techniques may be used to construct simulation models that mimic symptom dynamics. Network approaches naturally explain the limited success of traditional research strategies, which are typically based on the idea that symptoms are manifestations of some common underlying factor, while offering promising methodological alternatives. In addition, these techniques may offer possibilities to guide and evaluate therapeutic interventions.

Researchers use multiple informants' reports to assess and examine behavior. However, informants' reports commonly disagree. Informants' reports often disagree in their perceived levels of a behavior (“low” versus “elevated” mood), and examining multiple reports in a single study often results in inconsistent findings. Although researchers often espouse taking a multi-informant assessment approach, they frequently address informant discrepancies using techniques that treat discrepancies as measurement error. Yet, recent work indicates that researchers in a variety of fields often may be unable to justify treating informant discrepancies as measurement error. In this review, the authors advance a framework (Operations Triad Model) outlining general principles for using and interpreting informants' reports. Using the framework, researchers can test whether or not they can extract meaningful information about behavior from discrepancies among multiple informants' reports. The authors provide supportive evidence for this framework and discuss its implications for hypothesis testing, study design, and quantitative review.

Ambulatory assessment (AA) covers a wide range of assessment methods to study people in their natural environment, including self-report, observational, and biological/physiological/behavioral. AA methods minimize retrospective biases while gathering ecologically valid data from patients' everyday life in real time or near real time. Here, we report on the major characteristics of AA, and we provide examples of applications of AA in clinical psychology (a) to investigate mechanisms and dynamics of symptoms, (b) to predict the future recurrence or onset of symptoms, (c) to monitor treatment effects, (d) to predict treatment success, (e) to prevent relapse, and (f) as interventions. In addition, we present and discuss the most pressing and compelling future AA applications: technological developments (the smartphone), improved ecological validity of laboratory results by combined lab-field studies, and investigating gene-environment interactions. We conclude with a discussion of acceptability, compliance, privacy, and ethical issues.

Endophenotypes for psychopathology have been conceived as latent, unobserved, but measureable manifestations of phenomena that causally connect genetic liability to clinical disorder. Several decades of research have led to refinement of the construct and identification of some candidate endophenotypes, but rather limited progress on finding the genes involved or the mechanisms by which endophenotypes are driven by genetic and environmental factors and in turn drive psychopathology. Currently promising avenues for research involve development of transdiagnostic concepts not limited to traditional diagnostic categories, measures of endophenotypic and manifest psychopathology that have higher validity than those categories, and methods for modeling complex relationships among diverse contributors to etiology. With more grounding in animal neuroscience and other aspects of basic biological and psychological science, exemplified in the Research Domain Criteria initiative, there is every reason to anticipate that the endophenotype concept will grow more central in the psychopathology literature.

Exposure-based treatments for clinical anxiety generally are very effective, but relapse is not uncommon. Likewise, laboratory studies have shown that conditioned fears are easy to extinguish, but they recover easily. This analogy is striking, and numerous fear extinction studies have been published that highlight the processes responsible for the extinction and return of acquired fears. This review examines and integrates the most important results from animal and human work. Overall, the results suggest that fear extinction is relatively easy to “learn” but difficult to “remember.” It follows that treatments will benefit from an enhanced focus on the long-term retrieval of fear extinction. We review the available studies on the prevention of return of fear and the prospects of weakening fear memories forever. We show that the behavioral principles outlined in learning theory provide a continuous inspiration for preclinical (neurobiological) and clinical research on the extinction and return of fear.

Research on social anxiety and social anxiety disorder has proliferated over the years since the explication of the disorder through cognitive-behavioral models. This review highlights a recently updated model from our group and details recent research stemming from the (a) information processing perspective, including attention bias, interpretation bias, implicit associations, imagery and visual memories, and (b) emotion regulation perspective, including positive emotionality and anger. In addition, we review recent studies exploring the roles of self-focused attention, safety behaviors, and post-event processing in the maintenance of social anxiety. Within each area, we detail the ways in which these topics have implications for the treatment of social anxiety and for future research. Finally, we conclude with a discussion of how several of the areas reviewed contribute to our model of social anxiety disorder.

Generalized anxiety disorder (GAD) is associated with substantial personal and societal cost yet is the least successfully treated of the anxiety disorders. In this review, research on clinical features, boundary issues, and naturalistic course, as well as risk factors and maintaining mechanisms (cognitive, biological, neural, interpersonal, and developmental), are presented. A synthesis of these data points to a central role of emotional hyperreactivity, sensitivity to contrasting emotions, and dysfunctional attempts to cope with strong emotional shifts via worry. Consistent with the Contrast Avoidance model, evidence shows that worry evokes and sustains negative affect, thereby precluding sharp increases in negative emotion. We also review current treatment paradigms and suggest how the Contrast Avoidance model may help to target key fears and avoidance tendencies that serve to maintain pathology in GAD.

The rationale, research literature, and proposed changes to the dissociative disorders and conversion disorder in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) are presented. Dissociative identity disorder will include reference to possession as well as identity fragmentation, to make the disorder more applicable to culturally diverse situations. Dissociative amnesia will include dissociative fugue as a subtype, since fugue is a rare disorder that always involves amnesia but does not always include confused wandering or loss of personality identity. Depersonalization disorder will include derealization as well, since the two often co-occur. A dissociative subtype of posttraumatic stress disorder (PTSD), defined by the presence of depersonalization or derealization in addition to other PTSD symptoms, is being recommended, based upon new epidemiological and neuroimaging evidence linking it to an early life history of adversity and a combination of frontal activation and limbic inhibition. Conversion disorder (functional neurological symptom disorder) will likely remain with the somatic symptom disorders, despite considerable dissociative comorbidity.

During the past two decades, research in the field of depression and cardiovascular disorders has exploded. Multiple studies have demonstrated that depression is more prevalent in populations with cardiovascular disease, is a robust risk factor for the development of cardiovascular disease in healthy populations, and is predictive of adverse outcomes (such as myocardial infarction and death) among populations with preexisting cardiovascular disease. Mechanistic studies have shown that poor health behaviors, such as physical inactivity, medication nonadherence, and smoking, strongly contribute to this association. Small randomized trials have found that antidepressant therapies may improve cardiac outcomes. Based on this accumulating evidence, the American Heart Association has recommended routine screening for depression in all patients with coronary heart disease. This review examines the key epidemiological literature on depression and cardiovascular disorders and discusses our current understanding of the mechanisms responsible for this association. We also examine current recommendations for screening, diagnosis, and management of depression. We conclude by highlighting new research areas and discussing therapeutic management of depression in patients with cardiovascular disorders.

Humans have an intrinsic need for social connection; thus, it is crucial to understand depression in an interpersonal context. Interpersonal theories of depression posit that depressed individuals tend to interact with others in a way that elicits rejection, which increases their risk for future depression. In this review, we summarize the interpersonal characteristics, risk factors, and consequences of depression in the context of the relevant theories that address the role of interpersonal processes in the onset, maintenance, and chronicity of depression. Topics reviewed include social skills, behavioral features, communication behaviors, interpersonal feedback seeking, and interpersonal styles as they relate to depression. Treatment implications are discussed in light of the current research on interpersonal processes in depression, and the following future directions are discussed: developing integrative models of depression, improving measurement of interpersonal constructs, examining the association between interpersonal processes in depression and suicide, and tailoring interventions to target interpersonal processes in depression.

Postpartum depression (PPD) is a common and serious mental health problem that is associated with maternal suffering and numerous negative consequences for offspring. The first six months after delivery may represent a high-risk time for depression. Estimates of prevalence range from 13% to 19%. Risk factors mirror those typically found with major depression, with the exception of postpartum-specific factors such as sensitivity to hormone changes. Controlled trials of psychological interventions have validated a variety of individual and group interventions. Medication often leads to depression improvement, but in controlled trials there are often no significant differences in outcomes between patients in the medication condition and those in placebo or active control conditions. Reviews converge on recommendations for particular antidepressant medications for use while breastfeeding. Prevention of PPD appears to be feasible and effective. Finally, there is a growing movement to integrate mental health screening into routine primary care for pregnant and postpartum women and to follow up this screening with treatment or referral and with follow-up care. Research and clinical recommendations are made throughout this review.

Translational research on emotion in schizophrenia has revealed deficits in emotion perception and expression, as well as intact areas, including emotional experience and brain activation in the presence of emotionally evocative material. Yet, a closer look at emotional experience reveals that all is not well in the experience domain. People with schizophrenia have difficulty anticipating emotional events and maintaining or savoring their emotional experiences, as evidenced in behavioral, psychophysiological, and brain imaging studies. Furthermore, people with schizophrenia have difficulty integrating emotion perception with context and reporting on feelings that are differently valenced than presented emotional stimuli. Differences in brain activation are typically observed in areas tightly coupled with cognitive control, such as the dorsolateral prefrontal cortex, and thus the latest research on emotion in schizophrenia explicitly integrates emotion and cognition. Translational research holds promise to identify when in the course of the disorder emotion deficits emerge and to develop more effective interventions for schizophrenia.

Several important paradigm shifts have occurred in the field of schizophrenia treatment, including an increased focus on early detection, the development of preemptive interventions, and the view of schizophrenia as a neurodevelopmental disease characterized by decreased efficiency and abnormal connectivity in cortical and subcortical neural networks. In this review, we briefly describe some of the neural impairments that contribute to the development of schizophrenia, with an emphasis on the impact of stress and trauma on cognitively vulnerable neural systems. We then present current data on two behavioral interventions that target these critical risk factors and that aim to preempt the onset of schizophrenia in vulnerable individuals or improve the clinical course in recent-onset schizophrenia: cognitive therapy and computerized cognitive training.

The current state of the literature regarding psychosocial treatments for schizophrenia is reviewed within the frameworks of the recovery model of mental health and the expanded stress-vulnerability model. Interventions targeting specific domains of functioning, age groups, stages of illness, and human service system gaps are classified as evidence-based practices or promising practices according to the extent to which their efficacy is currently supported by meta-analyses and individual randomized controlled trials (RCTs). Evidence-based practices include assertive community treatment (ACT), cognitive behavior therapy (CBT) for psychosis, cognitive remediation, family psychoeducation, illness self-management training, social skills training, and supported employment. Promising practices include cognitive adaptive therapy, CBT for posttraumatic stress disorder, first-episode psychosis intervention, healthy lifestyle interventions, integrated treatment for co-occurring disorders, interventions targeting older individuals, peer support services, physical disease management, prodromal stage intervention, social cognition training, supported education, and supported housing. Implications and future directions are discussed.

Stability is thought to be one of the major distinguishing features between personality disorders (PDs) and other forms of psychopathology. The development of more reliable PD assessments and the implementation of four major longitudinal studies on PD stability have provided critical data with which to evaluate the stability of PD features. Results from these and other studies reveal significant complexity in the interpretation of PD stability because of several issues that can impact stability estimates. Such estimates will vary as a function of the type of constructs being assessed, the type of stability being considered, the modality and reliability of the assessments being used, and the impacts of sampling. In this article, longitudinal research on PD stability is reviewed in the context of these issues. It is concluded that no single answer can be given to the question, “How stable are PDs?” and that future research and classification need to consider carefully and account for the complexity of this question.

The purpose of this review is (a) to study and systematically review the recent literature examining the co-occurrence and relationships between Axis I psychiatric disorders and Axis II personality disorders, specifically the six originally proposed for the Diagnostic and Statistical Manual of Mental Disorders (DSM)-5, and (b) to consider the clinical utility of the current Axis I and Axis II approach in the DSM-IV-TR and apply findings to state a position on the issue of collapsing together Axis I and Axis II. Community surveys or prospective cohort studies were reviewed as a priority. Our review indicates that the associations between clinical disorders and personality disorders clearly varied within each disorder and across the six personality disorders. Our understanding has advanced, particularly related to the clinical utility of comorbidity, and there may be sufficient evidence to support moving borderline personality disorder to Axis I. However, it seems premature to conclude that comorbidity is best conceptualized by having all disorders in a single category or by deleting disorders so that comorbidity is reduced. Our review suggests some priorities for future research into comorbidity, such as including personality disorders in future multivariate comorbidity models.

Schizophrenia and autism have been linked since their earliest descriptions. Both are disorders of cerebral specialization originating in the embryonic period. Genetic, molecular, and cytologic research highlights a variety of shared contributory mechanisms that may lead to patterns of abnormal connectivity arising from altered development and topology. Overt behavioral pathology likely emerges during or after neurosensitive periods in which resource demands overwhelm system resources and the individual's ability to compensate using interregional activation fails. We are at the threshold of being able to chart autism and schizophrenia from the inside out. In so doing, the door is opened to the consideration of new therapeutics that are developed based upon molecular, synaptic, and systems targets common to both disorders.

Over the past decade, considerable advances have been made in understanding genetic influences on eating pathology. Eating disorders aggregate in families, and twin studies reveal that additive genetic factors account for approximately 40% to 60% of liability to anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Molecular genetics studies have been undertaken to identify alterations in deoxyribonucleic acid sequence and/or gene expression that may be involved in the pathogenesis of disordered eating behaviors, symptoms, and related disorders and to uncover potential genetic variants that may contribute to variability of treatment response. This article provides an in-depth review of the scientific literature on the genetics of AN, BN, and BED including extant studies, emerging hypotheses, future directions, and clinical implications.

The goal of this review is to provide an overview of biomarkers for Alzheimer's disease (AD), with emphasis on neuroimaging and cerebrospinal fluid (CSF) biomarkers. We first review biomarker changes in patients with late-onset AD, including findings from studies using structural and functional magnetic resonance imaging (MRI), advanced MRI techniques (diffusion tensor imaging, magnetic resonance spectroscopy, perfusion), positron emission tomography with fluorodeoxyglucose, amyloid tracers, and other neurochemical tracers, and CSF protein levels. Next, we evaluate findings from these biomarkers in preclinical and prodromal stages of AD including mild cognitive impairment (MCI) and pre-MCI conditions conferring elevated risk. We then discuss related findings in patients with dominantly inherited AD. We conclude with a discussion of the current theoretical framework for the role of biomarkers in AD and emergent directions for AD biomarker research.

Currently, 8.5% of the US population meets criteria for alcohol use disorders, with a total cost to the US economy estimated at $234 billion per year. Alcohol and tobacco use share a high degree of comorbidity and interact across many levels of analysis. This review begins by highlighting alcohol and tobacco comorbidity and presenting evidence that tobacco increases the risk for alcohol misuse and likely has a causal role in this relationship. We then discuss how knowledge of alcohol and tobacco interactions can be used to reduce alcohol use, focusing on whether (a) smoking status can be used as a clinical indicator for alcohol misuse, (b) tobacco policies reduce alcohol use, and (c) nicotinic-based medications can be used to treat alcohol use disorders.

Around 19% of US adults smoke cigarettes, and smoking remains the leading avoidable cause of death in this country. Without treatment only ∼5% of smokers who try to quit achieve long-term abstinence, but evidence-based cessation treatment increases this figure to 10% to 30%. The process of smoking cessation comprises different pragmatically defined phases, and these can help guide smoking treatment development and evaluation. This review evaluates the effectiveness of smoking interventions for smokers who are unwilling to make a quit attempt (motivation phase), who are willing to make a quit attempt (cessation phase), who have recently quit (maintenance phase), and who have recently relapsed (relapse recovery phase). Multiple effective treatments exist for some phases (cessation), but not others (relapse recovery). A chronic care approach to treating smoking requires effective interventions for every phase, especially interventions that exert complementary effects both within and across phases and that can be disseminated broadly and cost-effectively.

This review examines neuroimaging and neurocognitive findings on alcohol-related toxicity in adolescents. Teens who meet criteria for alcohol use disorders, as well as those who engage in subdiagnostic binge drinking behaviors, often show poorer neurocognitive performance, alterations in gray and white matter brain structure, and discrepant functional brain activation patterns when compared to nonusing and demographically matched controls. Abnormalities are also observed in teens with a family history of alcoholism, and such differences in neuromaturation may leave youths at increased risk for the development of an alcohol use disorder or increased substance use severity. More prospective investigations are needed, and future work should focus on disentangling preexisting differences from dose-dependent effects of alcohol on neurodevelopment. Intervention strategies that utilize neuroimaging findings (e.g., identified weaknesses in particular neural substrates and behavioral correlates) may be helpful in both prevention and intervention campaigns for teens both pre- and postinitiation of alcohol use.

Health disparities (differences in health by socioeconomic groups) are a pressing issue in our society. This article provides an overview of a multilevel approach that seeks to understand the mechanisms underlying health disparities by considering factors at the individual, family, and neighborhood levels. In addition, we describe an approach to connecting these factors to various levels of biological processes (systemic inflammation, cellular processes, and genomic pathways) that drive disease pathophysiology. In the second half of the article, we address the question of why some low-socioeconomic-status (low-SES) individuals manage to maintain good physical health. We identify naturally occurring psychosocial factors that help buffer these individuals from adverse physiological responses and pathogenic processes leading to chronic disease. What is protective for low-SES individuals is not the same as what is protective for high-SES individuals, and this needs to be taken into account in interventions aimed at reducing health disparities.

After sketching how my own interest and research into bullying problems began, I address a number of potentially controversial issues related to the definition and measurement of such problems. The importance of maintaining the distinctions between bullying victimization and general victimization and between bullying perpetration and general aggression is strongly emphasized. There are particular problems with the common method of peer nominations for purposes of prevalence estimation, comparisons of such estimates and mean levels across groups and time, and measurement of change. Two large-scale projects with time series data show that several recent claims about cyber bullying made in the media and by some researchers are greatly exaggerated and lack scientific support. Recent meta-analyses of the long-term outcomes for former bullies and victims provide convincing evidence that being involved in such problems is not just a harmless and passing school problem but something that has serious adjustment and public health consequences that also entail great costs to society. Another section presents my view of why the theme of bullying took quite some time to reach the peer relations research community in the United States and the role of a dominant research tradition focusing on “likeability” in this account. In a final section, I summarize some reasons why it may be considered important and interesting to focus both research and intervention on bully/victim problems.

Recovery (also known as the “recovery orientation,” “recovery vision,” or “recovery philosophy”) has been the dominant paradigm shaping current mental health policy for the past decade. It is claimed to be a revolutionary departure from the past and a guide to policy that will transform outcomes of severe mental illness. This review looks critically at the history of recovery and examines the ways in which this history has shaped the values, beliefs, and practices of current recovery-based policies. Recovery is a treatment philosophy that emerged from the ruins of deinstitutionalization and the psychopharmaceutical revolution. Yet paradoxically, recovery reflects many of the same ideas that made deinstitutionalization and the era of psychopharmacology possible. Further, history reveals how the recovery movement is deeply indebted to and embedded within the sociocultural values of neoliberalism that have shaped public policy since the presidential election of Ronald Reagan in 1980.