Abstract

Anxiety disorders are the most prevalent mental health conditions. Although they are less visible than schizophrenia, depression, and bipolar disorder, they can be just as disabling. The diagnoses of anxiety disorders are being continuously revised. Both dimensional and structural diagnoses have been used in clinical treatment and research, and both methods have been proposed for the new classification in the Diagnostic and Statistical Manual of Mental Disorders IV (DSM-5). However, each of these approaches has limitations. More recently, the emphasis in diagnosis has focused on neuroimaging and genetic research. This approach is based partly on the need for a more comprehensive understanding of how biology, stress, and genetics interact to shape the symptoms of anxiety.

Anxiety disorders can be effectively treated with psychopharmacological and cognitive–behavioral interventions. These interventions have different symptom targets; thus, logical combinations of these strategies need to be further studied in order to improve future outcomes. New developments are forthcoming in the field of alternative strategies for managing anxiety and for treatment-resistant cases. Additional treatment enhancements should include the development of algorithms that can be easily used in primary care and with greater focus on managing functional impairment in patients with anxiety.

INTRODUCTION

Anxiety disorders are present in up to 13.3% of individuals in the U.S. and constitute the most prevalent subgroup of mental disorders. The extent of their prevalence was first revealed in the Epidemiological Catchments Area study about 26 years ago. Despite their widespread prevalence, these disorders have not received the same recognition as other major syndromes such as mood and psychotic disorders; in addition, the primary care physician is usually the principal assessor and treatment provider. As a result of this management environment, anxiety disorders can be said to account for decreased productivity, increased morbidity and mortality rates, and the growth of alcohol and drug abuse in a large segment of the population.

 

Advances in anxiety research over the previous decade are likely to be reflected in modifications of diagnostic criteria in the upcoming DSM-5,planned for publication in May 2013. For instance, post-traumatic stress disorder (PTSD) and obsessive–compulsive disorder (OCD) have been reclassified in the separate domains of Trauma and Stressor Related Disorders and Obsessive–Compulsive and Related Disorders, respectively.

In this article, we review the challenges to the diagnosis of anxiety disorders, provide a model that explains how anxiety symptoms occur and change over time, highlight the neurotransmitter systems affected by these disorders, and discuss the roles and relative efficacy of pharmacological and non-pharmacological interventions.

DIAGNOSTIC DILEMMAS

In patients with some disorders such as generalized anxiety disorder (GAD) and social anxiety disorder (SAD), the presence of comorbidities is a rule rather than the exception. In clinical practice and in research, it is not unusual to find the coexistence of two or more diagnosable conditions in the same patient or at least symptomatic overlap with several subsyndromal states. This is particularly true for symptom overlap between different anxiety disorders, depression, and alcohol and drug abuse.

Another significant problem with the present classification of anxiety disorders is the absence of known etiological factors and of specific treatments for different diagnostic categories. Studying the genetic underpinnings of anxiety disorders using molecular biological techniques has failed to produce a single gene or a cluster of genes implicated as an etiologic factor for any single anxiety disorder, even though some genetic findings exist for OCD and panic .

Despite these diagnostic ambiguities, the emergence of efficacious serotonergic medications that cut across a variety of categorical disorders (e.g., mood and anxiety) has led many to suggest that a dimensional model might be more applicable in the study and treatment of these conditions. In this view, the disorder is seen as a complex set of coexisting symptom dimensions (e.g., panic, social awkwardness, and obsessiveness). Each of these dimensions can vary, depending on hypothetical, biological, or genetic factors, which may dictate separate biological or psychological treatment approaches .The usefulness of the dimensional versus the categorical approach remains a highly debatable topic in research and in clinical practice and is one of the bases for the introduction of DSM-5.

THE ‘ABC’ MODEL OF ANXIETY

Understanding how emotional reactivity, core beliefs, and coping strategies interact in time should lead to more precise diagnoses and better management of anxiety disorders. We recently applied a mathematical model using nonlinear dynamics to describe these processes and further developed this model to cover diagnostic presentations and their underlying processes. The model that we, for simplicity, call the “ABC model of anxiety” could be viewed as an interaction in space and time of alarms, beliefs and coping strategies .

Within psychiatry, similarities between distinct disorders has led to the emergence of the term “spectrum” disorders, a concept initially developed for OCD. This approach, although useful, can be overly inclusive and misleading because it sometimes lumps together disorders that have little in common, such as placing pathological gambling and body dysmorphic disorder (BDD) in the same OCD spectrum. So far, few genetic or neural-circuitry investigations have validated this concept.

Dimensional and categorical diagnosis in the DSM-IV-TR is usually produced by cross-sectional comparisons of distinct subject samples. However, diagnostic presentations in clinical practice occur in individuals treated sequentially and may therefore be better understood as part of a psychopathological process that unfolds over time. For example, although a patient might meet criteria for OCD purely on the basis of obsessions or compulsions, the latter usually arise later in the disorder as if to counteract the threat and anxiety associated with obsessive thoughts.

In recent years, scientists and clinicians have begun to realize that the processes underlying anxiety and fear might be similar among the various disorders. This has resulted in the implementation of uniform treatment regimens in primary care and in the development of the unified theory of anxiety.

Interplay Between Biological and Psychological Factors

One possibility is that abnormal cognition could be the inherited factor. Cognitive theory assigns a primary importance to abnormal or “catastrophic” cognition as an underlying mechanism of all anxiety disorders. Most cognitive strategies for treatment and research were developed in earlier years.

The ABC model focuses on the interaction of information processing and emotional and cognitive processes that are controlled by overlapping circuits and compete for the same brain resources.

In most anxiety disorders, patients usually process fear-inducing information in excessive detail that overwhelms their ability to appraise it properly. They cope by separating the information into “good” and “bad” with no gray area in between. As a result, they consider the worst-case scenario (i.e., by catastrophizing about the situation) and then act to protect themselves against the perceived danger.