Anxiety disorders range in severity from common, mild phobias (e.g., fear of insects, heights, or storms) to chronic, disabling conditions such as panic disorder or obsessive–compulsive disorder (OCD). Anxiety diagnoses are made according to the specific symptomatic manifestation of each disorder. Table 19–1 lists the anxiety disorder diagnoses included in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, Text Revision (DSM-IV-TR). Posttraumatic stress disorder and acute stress disorder are covered in Chapter 20, and OCD is covered in Chapter 21.
Table 19–1. DSM-IV-TR Anxiety Disorders ||Download (.pdf)
Table 19–1. DSM-IV-TR Anxiety Disorders
Panic disorder (with or without agoraphobia)
Generalized anxiety disorder
Acute stress disorder
Posttraumatic stress disorder
Anxiety disorder due to medical condition
Substance-induced anxiety disorder
Anxiety is characterized by heightened arousal (i.e., physical symptoms such as tension, tachycardia, tachypnea, tremor) accompanied by apprehension, fear, obsessions, or the like. Anxiety disorders are different from normal fears, although the symptoms can be similar. Generally speaking, normal fears represent emotional reactions to real, external threats, and the emotional response is appropriately related to the actual danger. In contrast, the symptoms of anxiety disorders occur either without obvious external threat or when the response to the threat is excessive. When an extreme or inappropriate fear or worry is present and is coupled with some degree of life impairment, the diagnosis of anxiety disorder should be considered.
Anxiety disorders are among the most common of psychiatric disorders, affecting up to 15% of the general population at any time. Individual anxiety disorders occur frequently. Phobic disorders (i.e., specific or social phobia) may affect as much as 8–10% of the population, generalized anxiety disorder (GAD) about 5%, and OCD and panic disorder each about 1–3%. Although posttraumatic stress disorder appears common, its specific frequency is unknown (see Chapter 20). The comorbidity of anxiety disorders with other psychiatric disorders is high. For example, about 40% of patients with primary anxiety disorders will have a lifetime history of a DSM-IV-TR depressive disorder. Further, in patients who have other psychiatric disorders, significant anxiety symptoms often are associated with those disorders. Therefore, clinically significant anxiety symptoms will occur frequently in patients seen in clinical practice.
Traditional psychoanalytic theory describes anxiety disorders as being rooted in unconscious conflict. Freud originally used the term “Angst” (literally, “fear”) to describe the simple intrapsychic response to either internal or external threat. He later derived the concept of the pleasure principle, which describes the tendency of the psychic apparatus to seek immediate discharge of impulses. In his earliest organized theory of anxiety, Freud postulated that conflicts or inhibitions result in the failure to dissipate libidinal (i.e., sexual) drives. These restrictions on sexual expression could occur because of external threat and would subsequently result in a fear of the loss of control of the drive. The damming-up of the impulses, along with the fear of loss of control, would result in anxiety.
Freud soon began to see the limitations of this theory and later proposed that anxiety was central to the concept of neurosis. He acknowledged that anxiety was a natural, biologically derived response mechanism required for survival. He abandoned the concept of the transformation of sexual drive (energy) into anxiety and accepted the prevailing notion of the time: anxiety was a result of threat. He recognized two sources of such threat. The first, termed traumatic situations, involved stimuli that were too severe for the person to manage effectively and could be considered the common or natural fear response. The second, called danger situations, resulted from the recognition or anticipation of upcoming trauma, whether internal (by loss of control of drives) or external. The response to these threats resulted in what was called signal anxiety, which was an attenuated and therefore more manageable anxiety response not directly related to trauma. Signal anxiety could be seen as anxiety that resulted from the avoidance of threat.
The structural hypothesis of mental function—which includes the id as the seat of drives, the superego as the location of inhibitions, and the ego as the apparatus for managing drives and inhibitions—evolved during this time period. Central to this hypothesis is the concept of defense mechanisms. Psychological defenses are thought to be primarily a function of the ego, which uses these defenses to manage id impulses and superego demands. Repression is formulated as the primary defense mechanism, in which unacceptable drive states are maintained largely outside of awareness. Failure of repression could result in anxiety and the use of secondary mechanisms to maintain intrapsychic stability.
The concept of the primacy of the defense mechanism to both generate and manage the anxiety has remained central to psychoanalysis for much of its history. Further, psychoanalytic treatment has focused on the need to uncover childhood trauma, releasing unnecessary defensive inhibitions and developing psychological competence. A number of schools of thought have been elaborated from classical Freudian psychoanalysis, including ego psychology, object relations theory, and self psychology (see Chapter 11).
The basic principles of learning theory as they relate to human development are rooted in the work of developmental psychologists, especially Jean Piaget (see Chapter 8). Piaget's observations of children led to an understanding of the progress of development through a series of predictable stages, referred to as epigenesis. Developmental milestones represent an interaction between the maturing brain substrate and environmental influences. Hence children learn according to both the capacity of the brain to manage incoming stimuli and the nature of the stimuli themselves. Appropriate environmental responses facilitate a normal learning process, and aberrant reactions produce problems in development.
As stimuli are assimilated and processed, learning takes place. Learning theory proposes two forms of learning: classical conditioning and operant conditioning (see Chapter 8). The classical conditioning model depends on the pairing of a stimulus that evokes a response (the unconditioned stimulus) with a neutral environmental object or event (the conditioned stimulus). The repeated pairing of the two stimuli would lead to the ability of the conditioned stimulus to elicit the same response as the unconditioned stimulus (the conditioned response).
Whereas classical conditioning views the organism as a relatively passive participant in the learning process, operant conditioning views stimuli as a series of either positive or negative events that influence subsequent behavior. Positive reinforcement occurs when a particular behavior results in a reward. Alternatively, negative reinforcement results when a specific behavior leads to the successful avoidance of an aversive event (i.e., punishment). Positive or negative reinforcements would then enhance the likelihood that the behavior would be repeated. Reinforcements of behaviors, whether they are achievements of rewards or avoidance of pain, underlie learning.
According to learning theory, an anxiety disorder develops when environmental cues become associated with anxiety-producing events during development. Within the construct of GAD, for example, worry and fear become conditioned and are repeated in order to avoid intermittent negative reinforcement. Hence the periodic successful avoidance of a negative outcome reinforces the behavior. For example, an individual's fear (and subsequent avoidance) of air travel would be enhanced by reading about occasional air disasters.
Traditional behavioral therapy of anxiety involves the uncoupling of the unconditioned response from the associated stimulus. Wolpe postulated that actions that inhibited anxiety (i.e., relaxation) in the face of the conditioned stimulus would reduce symptoms. Behavioral treatment of anxiety uses systematic desensitization (progressive exposure to an anxiety-evoking stimulus). This type of treatment has been used successfully to treat anxiety disorders such as phobias and OCD, but it has had limited systematic study in other anxiety disorders.
In a subsequent elaboration of learning theory, a cognitive theory of the etiology of depressive and anxiety disorders has evolved (see Chapter 8, 10). Although several theories have been advanced, Beck's concept of the cognitive triad has gained the broadest acceptance and application. In this view, abnormal emotional states, such as anxiety and depression, are a result of distorted beliefs about the self, the world, and the future. Anxiety disorders, therefore, involve incorrect beliefs that interpret events in an exaggeratedly dangerous or threatening manner. These fundamental belief systems, or schema, result in automatic thought responses to external or internal cues that trigger anxiety. As such, anxiety disorders consistently involve abnormalities of information processing that result in symptom formation.
Cognitive–behavioral therapy involves elements of classical behavioral approaches such as systematic desensitization; however, treatment is extended to the discovery and correction of distorted cognitive schema. The absence of exaggerated misinterpretations of cues leads to a reduction in symptom formation. Cognitive–behavioral psychotherapy has been used successfully to treat a variety of anxiety disorders, including panic disorder, phobias, and OCD.
From a biological standpoint, anxiety and fear have high adaptive value in all animals by increasing the animal's capacity for survival. The emotion of anxiety drives a number of highly adaptive behaviors, including escape from threat. The normal brain functions that underlie the anxiety response have been elucidated gradually over the past 50 years. The current understanding of the biological nature of anxiety has been prompted in part by an elucidation of the actions of drugs that reduce the symptoms of anxiety disorders. These observations can be divided into three broad areas: the gamma amino butyric acid (GABA) receptor/benzodiazepine receptor/chloride channel complex; the noradrenergic nucleus locus coeruleus and related brain stem nuclei; and the serotonin system, especially the raphe nuclei and their projections. Abnormalities in the functioning of these areas have been associated with various anxiety disorders.
Gray and colleagues have developed a general theory of a neural behavioral-inhibition system that mediates anxiety. The purpose of this system is to evaluate stimuli—consistent with punishment, non-reward, novelty, or fear—that simultaneously produce behavioral inhibition and increase arousal and attention. Antianxiety drugs inhibit responses in these areas. Using pharmacologic and lesioning studies, researchers have related anxiety to several interconnected anatomical areas. Sensory stimuli activate the hippocampus, especially the entorhinal cortex, which secondarily produces habituation by actions on the lateral and medial septal areas. Behavioral inhibition is achieved by projections to the cingulate gyrus. These areas are then influenced by noradrenergic activity of the locus coeruleus and are modulated both by serotonergic innervations from the raphe and by GABAA-receptor activity. Antianxiety drugs work via mechanisms that influence these areas and receptors. These mechanisms include noradrenergic activation (e.g., tricyclic antidepressants), serotonergic activity (e.g., selective serotonin reuptake inhibitors or buspirone), or benzodiazepine interactions with GABA receptors.
Acute threat results in fear, activating the “fight or flight” response. This, in turn, is mediated by brain regions such as the locus coeruleus and the amygdala. The amygdala participate in the encoding of fearful memory and aversive conditioning; they are therefore involved in both acute fear and negative anticipatory expectation (i.e., anxiety).
Acute fear activates the sympathetic nervous system via the locus coeruleus, resulting in physical symptoms such as tachycardia, tremor, and diaphoresis. Awareness of fear occurs in the cortex, especially the frontal cortex that registers fear and responds with adaptive survival behaviors. The cingulate gyrus is also involved in the mediation of information between cortical and subcortical structures.
Controlled family studies of the major subtypes of anxiety disorders including panic disorder, phobic disorders, GAD, and OCD reveal that all of these anxiety subtypes are familial, and twin studies suggest that the familial aggregation is attributable in part to genetic factors. Panic disorder and its spectrum show the strongest genetic determinants; half or more of persons with panic disorder have a family history of the disorder. Although there has been a plethora of studies designed to identify genes underlying these conditions, to date, no specific genetic loci have been identified and replicated in independent samples.
Anxiety is a normal emotion, a common reaction to the stresses of everyday life. At what point does anxiety become pathologic? In order to make this distinction, one must define the key characteristics of the disorders and recognize that in pathologic anxiety normal psychological adaptive processes have been overwhelmed to the point that daily functioning has been impaired. Anxiety disorders begin at the point of impairment. For example, everyone worries occasionally. When this worry begins to preoccupy a person's thoughts to the point that psychosocial functioning is impeded, an anxiety disorder may be diagnosed.
Anxiety is commonly associated with other medical or psychiatric conditions. Other conditions that give rise to anxiety have their own diagnostic categories: anxiety disorder due to medical condition and substance-induced anxiety disorder.
Psychological testing has not been shown to be useful in aiding the diagnosis of anxiety disorders.
There are no laboratory findings suggesting or supporting the diagnosis of anxiety disorders, though there is evidence that a family or personal history of panic disorder may convey a liability to experience anxiety with carbon dioxide (CO2) exposure.
Functional neuroimaging studies in patients with anxiety disorders have shown neurophysiological abnormalities during symptom provocation tests, implicating limbic, paralimbic and sensory association regions.
The often-chronic course of anxiety disorders, and its frequent comorbidity with other psychiatric conditions, especially mood disorders, are delineated in more detail (i.e., as they pertain to specific subtypes of anxiety disorders) in the paragraphs below.
Differential Diagnosis (Including Comorbid Conditions)
These differential diagnoses, along with other psychiatric disorders that can manifest significant anxiety, are listed in Table 19–2.
Table 19–2. Differential Diagnosis of Anxiety Disorders ||Download (.pdf)
Table 19–2. Differential Diagnosis of Anxiety Disorders
Obstructive pulmonary disease
Mitral valve prolapse
Developmental disorders (e.g., Autism, Williams Syndrome)
Premenstrual dysphoric disorder
Schizophrenia (and other psychotic disorders)
Psychostimulants (e.g., methylphenidate, amphetamine)
Steroids (corticosteroids, anabolic steroids)
Stimulant abuse (e.g., cocaine)
Sympathomimetics (e.g., pseudoephedrine
Transient ischemic attack