Avoidant Personality Disorder: Boundaries of a Diagnosis
A discussion of the epidemiology, assessment, diagnostic dilemmas, and treatment of avoidant personality disorder.
Avoidant personality disorder (APD) is characterized by a general tendency to fear and avoid social interactions-even interactions with persons who are well known to the individual. In addition to deserving our clinical and research attention in its own right, APD highlights some of the key controversies with our current classification system. These debates include the "horizontal" boundaries between different Axis I and Axis II conditions as well as the "vertical" boundaries between a clinical disorder and certain personality or temperamental traits. In pediatric psychiatry, use of the diagnosis underscores the conflict between the motivation to avoid Axis II diagnoses in children and adolescents and the motivation toward early identification and early intervention of psychiatric illness.
In this article, I will briefly summarize some of the key components of APD, with a focus on epidemiology, assessment, diagnostic dilemmas, and treatment.
Background and epidemiology
DSM-IV defines APD as "a pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to negative evaluation that begins by early adulthood and is present in a variety of contexts." In persons with APD, the avoidance of, and restraint during, social contact is the result of fears of rejection and humiliation.
APD is one of the cluster C personality disorders, along with dependent and obsessive-compulsive personality disorders. The level of impairment associated with APD is high; employment, interpersonal relationships, and global functioning are all negatively affected. The morbidity associated with APD rivals and even exceeds that associated with such Axis I disorders as major depressive disorder.1
APD is relatively common; the prevalence is about 5% in the community2 and nearly 15% among psychiatric outpatients.3 As such, APD is one of the most-if not the most-prevalent personality disorders. APD occurs about equally between males and females.
Clinical course
The symptoms of APD often appear early and the disorder can be distinguished from other personality disorders by elementary school or even earlier. Adults with APD reported less involvement in extracurricular activities and sports, and were less popular than adults with another personality disorder or major depression.4 Kagan5 and Hirshfeld and colleagues6 have characterized a temperamental trait labeled behavioral inhibition that applies to children who have a strong tendency to be shy and restrained in novel situations. Behavioral inhibition-a potential precursor to later social anxiety and avoidance-has been reliably assessed in children 2 years old and perhaps even younger.5,7
Longitudinal research has demonstrated detectable, although certainly not inevitable, links between behavioral inhibition and many disorders in childhood and adolescence. These include social anxiety disorder and avoidant disorder (as defined in DSM-III-R).7,8 Emotional disorders, such as anxiety, depression, and eating disorders, in adolescence predict cluster C personality disorders in adulthood in women.9
While there appears to be at least some continuity between adult APD and childhood symptoms, accumulating research is beginning to demonstrate a more waxing and waning course of APD symptoms through adulthood than had originally been expected. A 2-year prospective study from the Collaborative Longitudinal Personality Disorders Study found that over time, feelings of inadequacy and social ineptness and the need to be certain of being liked before entering into social situations were more stable than worries about shame and risks of exposure in one's employment.10
Considerably less is known about APD as affected persons age. The disorder is scarcely studied in geriatric psychiatry.
Diagnosis in children and adolescents
The finding in APD and other personality disorders that there is an onset of symptoms in childhood and adolescence represents a dilemma for many clinicians. On one hand, our training dictates the general principal of early identification and intervention to help avoid or reduce long-term suffering. At the same time, clinicians tend to avoid diagnosing personality disorders in children and adolescents.11 While the reasons for this practice are not entirely clear, the tendency may be based in part on the notion that a child's personality is still "in progress" and thus he or she should not be labeled as "disordered" for fear of stigmatization.
While this concept has some merit, it is also flawed. Symptoms of Axis I disorders, such as attention-deficit/hyperactivity disorder, also tend to undergo change through the course of the person's development, yet this does not prevent clinicians from making a diagnosis at a particular point to allow for the amelioration of impairing symptoms.
Furthermore, personality development does not stop when a patient reaches age 18. As for stigmatization, it is not intuitively obvious why a diagnosis of APD carries a higher burden than many other conditions that can be diagnosed before adulthood, such as social anxiety disorder.
A final obstacle to diagnosing APD in children is the criterion that a cause for social avoidance be identified (eg, fear or shame or embarrassment). Such a cause may be difficult to detect in younger children, whose self-consciousness is still developing.
Etiology and neurobiology
There has been little research into the cause and pathophysiology of APD per se, although much literature exists about related Axis I conditions or traits, such as shyness. Behavioral inhibition and other temperament traits like it (eg, harm avoidance) are thought to be related to overactivity of regions of the brain that are involved in the fear response. One recent study found evidence that high levels of harm avoidance were related to decreased coupling between the amygdala and the anterior cingulate gyrus which, in turn, may be related to genes involved in serotonin transmission.12
The heritability of behavioral inhibition ranges from 25% to 44%, as measured in toddlers.13 Interestingly, there is some evidence to support stronger genetic associations with the personality dimensions that may underlie APD than with the specific APD symptoms themselves.14
Assessment
The differential diagnosis of APD (or its "horizontal" boundaries) includes mainly other psychiatric disorders. While there may be theoretical distinctions between APD and related diagnoses, these differences can be very difficult to untangle in practice, especially if one takes a developmental perspective of the patient. The Table lists some features that may distinguish other traits and disorders from APD.
The main theoretical distinction between APD and both schizoid personality disorder and an autistic spectrum disorder is the notion that persons with APD very much want social contact-but are afraid to seek it out, while those with schizoid personality disorder or an autistic spectrum disorder are less intrinsically interested in social contact. However, many individuals with an autistic spectrum disorder do seek out human contact but struggle with how to achieve it. It is thus advisable to obtain a good developmental history if both of these disorders are being considered as alternatives to APD.
Developmentally, it is also possible that over time a person with APD who initially craves social contact will begin to settle into a pattern in which this contact is no longer sought. Another point of divergence between APD and an autistic disorder relates to social cues. Children with an autistic spectrum disorder tend to ignore these cues, while those with APD are hypersensitive to them.
Perhaps the greatest diagnostic dilemma pertains to the boundaries between APD and the general subtype of social anxiety disorder (GSAD). The diagnostic criteria overlap considerably. Attempts to find distinguishing characteristics in the epidemiology, physiology, and response to treatment have yielded little in the way of qualitative differences.15 Indeed, there may be more differentiation between the specific and generalized form of GSAD than between generalized GSAD and APD, despite their existence on different axes.
Researchers have similarly been interested in the "vertical" boundaries between APD and established personality or temperamental traits, such as shyness. There certainly appears to be significant overlap between certain disorders, such as APD, and specific personality dimensions. Nevertheless, the increasingly popular hypothesis that APD simply represents the extreme end of a normally distributed trait such as shyness appears to be overly simplistic.
Studies of the relationship between shyness and generalized social phobia show that many people with very high levels of shyness do not meet criteria for GSAD.16 This lack of continuity has stimulated researchers to begin looking for other features that could moderate the relationship between shyness and psychiatric disorders. These include other personality or temperament traits (such as emotion regulation) or specific cognitive factors that may exacerbate shyness into full-fledged APD.
Assessment for APD is part of a general psychiatric evaluation; the condition should be suspected in patients in whom social avoidance, fear of embarrassment, and intimacy difficulties are uncovered. Instruments to aid in the diagnosis of APD and other personality disorders continue to be refined, although their use in routine practice remains limited.17
As with most personality disorders, most patients who meet criteria for APD will meet criteria for other Axis I and Axis II conditions. Notable among these are Axis I anxiety and affective disorders, other cluster C disorders, and substance abuse.
Treatment
Treatment of APD involves psychotherapy and/or medication. Unfortunately, treatment studies rarely focus primarily on APD and instead analyze patients with APD as a subset of those with GSAD or other personality disorders.18 Given this limitation, multiple types of psychotherapy have been shown to be effective in adult APD, including cognitive- behavioral, psychodynamic, and supportive-expressive therapy.19-21
No medications have been specifically approved for the management of APD. However, research has documented improvement in patients who meet criteria for both APD and social anxiety disorder when treated with selected serotonin reuptake inhibitors and benzodiazepines.22,23 Current recommendations include consideration of pharmacotherapy in APD, regardless of whether a patient meets criteria for a comorbid Axis I disorder,24,25 although additional research in this area is sorely needed. Given the risk of substance use in APD, physicians should be cautious in prescribing benzodiazepines.
Regardless of treatment modality, however, one of the keys to treatment success (as with other anxiety conditions) is exposure. Patients who simply take a medication or who speak with a therapist are not likely to report symptom relief before they take the risk of confronting their feared situations.
Greater success can be anticipated if the therapist supports patients and encourages them to confront their fears. This can take the shape of a specific homework assignment within a cognitive-behavioral format or therapist support of the patient's willingness to risk intimacy and no longer be the "perfect patient" within a psychodynamically oriented framework.
The bottom line
APD is a relatively common condition that is associated with significant impairment in multiple domains. The boundaries of the disorder-both horizontally with other psychiatric diagnoses and vertically with personality dimensions such as shyness-continue to be blurry and not well established. In particular, there seems to be little to qualitatively distinguish APD from the generalized type of social anxiety disorder.
Research into the course of APD demonstrates the disorder's origin in early temperamental traits. Increasing data exist to suggest that during adulthood APD may be more changeable over time than originally thought. These data suggest that positive responses can occur with psychotherapy and/or medications.
Dr Rettew is assistant professor of psychiatry and pediatrics at the University of Vermont College of Medicine in Burlington.
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