Personality Disorders in Children and Adolescents

Carla Sharp

Efrain Bleiberg

Introduction

The revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV— TR) (1) defines personality disorder (PD) as “an enduring pattern of inner experiences and behavior that deviates markedly from the expectations of the individual’s culture.” This pattern is manifested in two or more of the following areas: cognition; affectivity; interpersonal functioning; and impulse control. The enduring pattern is characterized as “inflexible and pervasive across a broad range of personal and social situations” and as a pattern that leads to “clinically significant distress or impairment in social, occupational or other important areas of functioning.” Finally, DSM-IV-TR states that the pattern is “stable and of long duration” and that its onset can be traced back “at least to adolescence or early adulthood.”

PD represent a staggering burden to society. Surveys document that they affect a significant percentage of the general population, with a prevalence estimated between 10% and 13% 2,3. Merikangas and Weissman (4) found that approximately half of those receiving mental health treatment suffer from a personality disorder. Yet the significance of the personality disorders extends far beyond the suffering of the affected individuals and their families. Personality disorders involve patterns of maladjustment associated with extraordinary social costs: Individuals with personality disorder experience high rates of divorce, unemployment, and homelessness (5); accidents (6); violence, assaultive behavior, and homicide 7,8; self-injurious and parasuicidal behavior (9); attempted and completed suicide (10); increased need for medical care and hospitalization and visits to the emergency room (11); and criminality, alcoholism and drug abuse (12). Personality disorders are associated with disability, underachievement, family disruption, child abuse and neglect, illegitimacy, STDs, delayed recovery from medical illness, malpractice suits, medical and judicial recidivism, and dependency on the public (13).

Patients with PD present formidable challenges to clinicians and psychiatric treatment settings as they display characteristically maladaptive patterns of coping and relating in their relationships with their treaters. The presence of a personality disorder accounts for a significant degree of the treatment failures or delayed recoveries in the treatment of comorbid axis I psychiatric disorders such as depression (14), bipolar disorder (15), or obsessive compulsive disorder (16), as well as with dissatisfaction and disruption of psychiatric treatment. Clinicians treating patients with PD struggle with their own emotional reactions as the treatment process strains their competence, sensitivity, integrity and commitment to ethical standards and professional behavior.

Not surprisingly, the study of PD, as Millon and Davis (17) noted, is fraught with more controversy than any other area of psychopathology. The controversies are particularly pronounced regarding the child and adolescent antecedents of the PD of adulthood. Questions can indeed be raised regarding whether we can make the diagnosis of personality disorder in a child or an adolescent. PD is defined as relatively enduring and pervasively maladaptive patterns of coping, thinking, feeling, and relating. Children and adolescents, whether suffering from psychiatric disorders or not, are engaged in
dramatic and highly fluid developmental processes in which every aspect of their bodies and personalities affecting their patterns of coping, thinking, feeling, and relating are constantly changing at different rates, creating new equilibriums and disequilibriums within the children and in their relations with the environment.

Such fluidity challenges the categorical approach to PD enshrined in DSM-IV-TR, which defines PD as a discrete diagnosis with clear boundaries. Yet, as Cicchetti and Cohen (18), among others, have noted, the developmental trajectories of specific patterns of adjustment and maladjustment, including the patterns of coping, thinking, feeling, and relating that define personality and underlie adjustment or maladjustment, may be categorized and classified just as “disorders” are. Along these lines, Kernberg, Weiner and Bardenstein (19) contend that children exhibit distinctive patterns of perceiving reality and thinking about themselves and the environment that endure across time and situation and that these patterns warrant the designation of personality disorder, regardless of the children’s age, when they become inflexible, maladaptive, and chronic; cause significant impairment, and produce severe subjective distress. A developmental approach to the investigation of personality and PD is thus crucial not only conceptually but also as a path to early identification, treatment and prevention. Early intervention appears essential in PD in order to preclude the development of the relatively enduring traits and patterns of maladjustment associated with the enormous personal and family suffering and massive social burden outlined above.

As Shapiro (20) cautions, however, empirical data supporting the validity and reliability of the construct and diagnosis of PD in children and adolescents are largely lacking. Given the significant stigma associated with a diagnosis of personality disorder, particularly in regard to diagnoses such as psychopathy (21) or borderline personality, diagnostic circumspection is clearly warranted, particularly in the absence of solid empirical evidence of diagnostic validity and reliability.

Not surprisingly, there has been growing interest in the empirical investigation of personality disorders in children and adolescents over the last two decades. Most research has focused on Borderline Personality Disorder (BPD) and antisocial personality disorder 22,23.

This chapter will review BPD, the most extensively studied personality disorder in children, adolescent and adults, as illustrative of the challenges and the importance of understanding PD as it unfolds and becomes organized in childhood and adolescence and as a window into the developmental processes in which biological and psychosocial risk and protective factors interact to shape developmental trajectories and patterns of adjustment and maladjustment.

Borderline Personality Disorder (BPD)

Definition

DSM-IV-TR includes BPD in the cluster B of the personality disorders, which also comprises the histrionic, narcissistic, and antisocial personality disorders. DSM-IV provides criteria for BPD unmodified by developmental considerations (Table 5.14.1).

However, the fourth edition of the DSM suggests, for the first time, that BPD can be diagnosed in children and adolescents when maladaptive traits have been present for at least 1 year (in contrast to 2 years for adult BPD) and the traits are pervasive, persistent, and unlikely to be limited to a particular developmental stage or an episode of Axis I disorder.

TABLE 5.14.1 DSM-IV-TR CRITERIA FOR BORDERLINE PERSONALITY DISORDER

A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts, as indicated by five (or more) of the following:

Frantic efforts to avoid real or imagined abandonment
Note: Do not include suicidal or self-mutilating behavior covered in criterion 5.
A pattern of unstable and intense interpersonal relationships characterized by altering between extremes of idealization and devaluation
Identity disturbance: markedly and persistently unstable self-image or sense of self
Impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse, reckless driving, binge eating)
Note: Do not include suicidal or self-mutilating behavior covered in criterion 5.
Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior
Affective instability due to a marked reactivity of mood (e.g., intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days)
Chronic feelings of emptiness
Inappropriate, intense anger or difficulty controlling anger (e.g., frequent displays of temper, constant anger, recurrent physical fights)
Transient, stress-related paranoid ideation or severe dissociative symptoms

To diagnose a personality disorder in an individual under age 18 years, the features must have been present for at least 1 year.

History

Clinical descriptions of BPD in childhood, beginning in the late 1940s, formulated these children’s symptoms within a psychoanalytic framework (24). Margaret Mahler and colleagues (25) suggested the term borderline psychosis to refer to children at the milder end of a proposed continuum that extended to the most severe psychotic conditions of childhood. Ekstein and Wallerstein (26) used the term borderline to describe children who were not mildly or incipiently psychotic but presented, instead, a stable condition, paradoxically defined by its persistent instability, and characterized by rapid and ongoing shifts in levels of ego functioning, including reality testing, relationships with others, and defense mechanisms. Such formulations defined borderline children as less severely disturbed than psychotic children but more seriously impaired than neurotic children. In a similar vein, Kernberg (27) characterized “borderline” as a level of development and organization underlying several personality disorders. This developmental pattern, according to Kernberg, included limitations in the capacity to differentiate self from others, reliance in primitive defenses and attainment of reality testing, without the achievement of object constancy and identity integration.

Such formulations of borderline pathology in children used diverse clinical criteria, and likely described a heterogeneous population (28), but laid the foundation for the development of formal criteria for BPD in children and adolescents, as summarized in Table 5.14.2.

TABLE 5.14.2 EFFORTS TO DESCRIBE FORMAL DIAGNOSTIC CRITERIA OF BPD IN CHILDREN AND ADOLESCENTS

Lofgren, Bemporad, et al. 63	Vela, Gottlieb, et al. 98	Golman, D’Angelo, et al. 18
Paradigmatic fluctuation of functioning, with rapid shifts between psychotic-like urotic levels of reality testing A lack of “signal anxiety” and a proneness to states of panic dominated by overwhelming concerns of body dissolution, annihilation, or abandonment A disruption in thought processes and content that shifts rapidly into loose, idiosyncratic thinking An impairment in relationships, with much difficulty, when under stress, in distinguishing self from others, in appreciating other people’s needs, or in integrating disparate emotional experiences into a coherent relationship A lack of impulse control with an inability to contain intense affects, delay gratification, control rage, or modulate destructive an self-destructive tendencies	Disturbances in interpersonal relationships Disturbances in the sense of reality Excessive anxiety Severe impulse problems “Neurotic-like” symptoms Uneven or distorted development	A pattern of unstable and intense interpersonal relationships characterized by alternation between extremes of overidealization and devaluation and/or marked distortion of the nature of the relationship Example: Describing teacher as a “girlfriend,” chronic inability to maintain friendships despite wish to do so Impulsiveness in at least two areas that are potentially self-damaging (e.g., reckless risk taking, running away, stealing, substance abuse, sex, binge eating) Example: Walking across railroad bridge railing; sniffing glue Affective instability: marked, rapid shifts from baseline mood to depression, irritability, or anxiety lasting less than a few hours and only rarely more than a few days; episodes may include transient distortions of reality Example: Early-afternoon anxiety attached with persecutory delusions, followed by successful participation in soccer game in late afternoon Inappropriate, intense anger or lack of control of anger (e.g., frequent displays of temper, constant anger, recurrent physical fights) Example: Easily provoked, frequent fights, threatens and attempts to throw therapist out window Recurrent suicidal threats, gestures, or behavior or self-mutilating or self-endangering acts Example: Carves boyfriend’s name into arm, multiple episodes of being struck by car Marked and persistent disturbance in self-perception and self-presentation characterized by confusion regarding two of the following: gender identity or roles, friendships, socially appropriate behaviors, school or career plans, self-image Example: Chronic cross-dressing, running for class president despite having no friends Chronic feelings of emptiness or boredom Example: Chronic complaints of boredom, unable to invest in appropriate activities Frantic efforts to avoid, or major preoccupation with, real or imagined abandonment (do not include suicidal or self-mutilating behavior covered in item 5). Example: Continual concern that therapist will not be there at next appointment, refusal to leave house while parent is at work

Goldman and colleagues (29) were the first to adapt standardized adult DSM criteria for BPD in children and adolescents (see third column, Table 5.14.2), thus allowing for the comparison of findings from different studies and the application of adult assessment tools to child and adolescent samples.

Epidemiology

Reliable epidemiological data on prevalence rates of BPD in children and adolescents are limited, with rates varying depending on the population sampled.

Inpatient Settings

Studies that have investigated rates of BPD in adolescents’ inpatients with histories of depression and suicide attempts points to higher prevalence rates in adolescents compared to adults 30,31,32. Similarly, Levy et al. (33) showed a BPD rate of 43% in 165 adolescent inpatients (mean age 15.5 years). Grilo and colleagues (34) demonstrated nonsignificant differences in rates of BPD for adolescents (49%) versus young adults (43%) using the same measures for both samples.

Community Settings

The Toronto Adolescent Longitudinal Study (35) by Korenblum and colleagues pioneered the study of BPD in children and adolescents in community settings in a small community sample (n = 72), where 42% of adolescents showed some degree of personality disturbance, of which 40% fell into a cluster B disorder. In a second community sample (n =63) the same investigators found that 46% of 13-year old school children met criteria for BPD. The largest community based study of juvenile BPD to date (the Children in the Community Study), assessed a sample of 733 children between the ages of 9 and 19 years, and found a prevalence of 3%.

The inconsistency in prevalence rates likely resulted from variations in the design of the studies, the measures employed and the populations studied. Clearly, large-scale, community-based, epidemiological studies, utilizing reliable measures, are needed in order to ascertain the true prevalence rates of juvenile BPD.

Etiology

Models are emerging that seek to integrate biological and psychosocial factors interacting with one another to generate a developing organization of capacities, attitudes, values and goals, coping strategies, relationship patterns and ways of feeling, processing experience and responding across contexts. A selective review of investigations of genetic-biological and psychosocial factors in the etiology of BPD will be followed by an examination of these emerging interactional models.

Genetic Factors

Studies investigating genetic factors associated with BPD have included family, adoption, and twin studies. Family studies of BPD point to a morbidity risk of 11.5% in first-degree relatives (36). A twin study reported concordances rates for BPD of 35% for dizygotic twins and 7% for monozygotic pairs (37).

Studies taking a dimensional approach have combined phenotypic factor analyses of personality disorder questionnaires with multivariate genetic analyses. Using this methodology, several genetic factors underlying personality disturbance have been identified. One factor includes affective liability and instability in cognitive functioning, sense of self, and interpersonal relationships, a cluster of traits closely resembling the diagnostic criteria for BPD. This factor has shown heritability estimated at 47% (38).

This and other studies point to a genetic role in the etiology of BPD, but verification in child and adolescent samples is lacking. Recent reports confirm the role of genetic factors in psychopathy in children as young as 7 years old (39). Such data are not yet available for other PDs, including juvenile BPD.

Biological Factors

A robust body of evidence supports the linkage between a broad array of neuropsychiatric vulnerabilities and BPD (40). Some authors proposed that at least a subgroup of borderline patients have a vulnerability to affective dysregulation, which gives rise to mood lability and heightened sensitivity to rejection and abandonment (41). Klein hypothesized that manipulative relations result from affective dysregulation rather than causing it.

A number of studies demonstrate significantly higher rates of depression, mood disorders, and substance abuse in first-degree relatives of individuals with personality disorder, but no increase in schizophrenia spectrum disorders (42). The linkage between these disorders and BPD, however, is neither uniform nor strong.

A linkage has also been established between BPD and impulse-control disorders. A clear overlap exists between the disruptive behavior disorders— particularly ADHD, conduct disorder, and BPD (43). Studies of delinquent adolescents document a high prevalence of learning disorders and ADHD in this population. Studies of delinquent and conduct-disordered adolescents suggest that at least a subset of these youngsters present BPD associated with ADHD and learning disorders.

Empirical research (44) has focused on impulsive aggression and affective instability as psychobiologic domains relevant to the ethiopathogenesis of BPD. The last decade has seen an explosion of studies investigating these domains in BPD through structural neuroimaging, positron emission tomography (PET), functional neuroimaging (fMRI), neuropsychological tests, EEG and SPECT 45,46,47,48,49,50.

Studies of serotonergic metabolites, such as 5-hydroxyindoleaacetic acid (5-HIAA) in cerebrospinal fluid (CSF) have demonstrated serotonergic involvement in impulsive aggression 51,52,53. Neuroimaging data have confirmed reduced serotonergic neurotransmission in cortical inhibitory areas that are usually associated with regulating or dampening the release of aggression (54). Such studies have paved the way for the search of serotonergic candidates genes 55,56,57, suggesting that individual genetic differences may contribute to reduced serotoninergic involvement in the impulsive aggression associated with BPD.

Functional neuroimaging of affective processing in BPD have shed light on the psychobiology of affective instability. In response to affective stimuli, BPD patients show bilateral increases in activation of the amygdala, suggesting an increased reactivity to emotionally relevant stimuli (58). BPD patients also display increased left amygdala activation to facial expressions of emotion (59), further supporting the notion of deficient affective processing in BPD. In addition, several studies using structural MRI have demonstrated reduced amygdala and hippocampal volume in BPD.

Taken together, studies of the neurobiological correlates of BPD converge in pointing to a dysfunctional fronto-limbic network that could account for both symptoms of impulsive aggression and affective instability and the characteristic hyperreactivity of BPD individuals to loss, abandonment, or frustration. The neural circuit implicated in such dysfunction includes the anterior cingulate cortex (ACC), the orbitofrontal and dorsolateral prefrontal cortex, the hippocampus, and the amygdala (Figure 5.14.1).

Studies of neurobiological correlates of BPD in adults enhance diagnostic specificity and offer the potential of more reliable predictors of treatment response as well as novel targets for therapeutic interventions. However, its etiopathogenic relevance to childhood and adolescent BPD is unclear, as similar neurobiological correlates have not been demonstrated in children and adolescents, except for studies that show that children with significant precursors of BPD precursors present difficulties in executive functioning similar to those demonstrated in adult BPD 61,62.

Psychosocial Factors

A large body of research into psychosocial predictors of BPD has suggested a range of adverse and traumatic childhood experienced as etiological factors. Most of the studies have been retrospective in nature, thus calling for cautious interpretation. Adult patients with BPD report higher rates of abuse and neglect during childhood 63,64,65,66,67,68, experiences of disturbed parental involvement during childhood (69), problems tolerating separations and frustration (70); childhood attachment problems (71); parental separation and loss 72,73 and symptoms of externalizing disorder combined with abnormal neuropsychological functioning, physical abuse, and separations (74).

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