Identifying Latent Trajectories of Personality Disorder Symptom Change: Growth Mixture Modeling in the Longitudinal Study of Personality Disorders

Although clinical thinking about personality pathology can be traced to the nineteenth-century idea of “moral insanity” (Vaillant & Perry, 1985) and subsequent psychoanalytic studies of character pathology (Freud, 1959), the modern conception of personality disorders (PDs) originated with the introduction of the DSM-III in 1980. This nomenclature established explicit diagnostic criteria for 11 PDs putatively characterized by inflexible and maladaptive personality traits that are expressed pervasively across interpersonal situations (American Psychiatric Association, 1980). The notion that PDs are trait-like and enduring over time was largely untested at the time of the DSM-III, although contemporaneous personality research suggested a high degree of within-individual consistency over time (Costa, McCrae, & Arenberg, 1980). To explore the stability of PD diagnoses and symptoms over time, several research groups undertook major longitudinal studies in the 1990s (Grilo, McGlashan, & Skodol, 2000; Lenzenweger, 1999; Paris, Brown, & Nowlis, 1987; Zanarini, Frankenburg, Hennen, Reich, & Silk, 2006). Accumulating evidence from these studies indicates that the mean number of symptoms for nearly all PDs declines over time and that these disorders are much less stable than previously thought (Lenzenweger, Johnson, & Willett, 2004; Skodol et al., 2005). For example, Zanarini and colleagues (2006) found that 88% of psychiatric patients with Borderline PD no longer met the diagnostic threshold ten years after diagnosis (and 39% of the sample remitted within two years). Furthermore, the stability of the diagnostic criteria that define certain PDs varies widely over relatively brief time intervals, suggesting that some criteria capture dysfunctional personality traits whereas others may be more sensitive to stress-related behaviors or state-dependent symptoms (McGlashan et al., 2005). Although reports from the Collaborative Longitudinal Personality Disorders Study (CLPS; Skodol et al., 2005) and the McLean Study of Adult Development (Zanarini, Frankenburg, Hennen, Reich, & Silk, 2005) have observed symptom remission for each of the PDs studied, they are potentially limited by the fact that participants were receiving psychiatric treatment at the initial study assessment and had high levels (above diagnostic threshold) of personality pathology, which raises a concern that PD symptom remission may partly reflect regression toward the mean (Campbell & Kenny, 1999). A limitation of several longitudinal PD research reports to date (Gunderson et al., 2011; Johnson et al., 2000; Sanislow et al., 2009), including previous reports from the Longitudinal Study of Personality Disorders (LSPD; Lenzenweger, 1999), is that they have used statistical methods that characterize changes in the mean level of symptoms over time based either on group averages or individual growth curves. Such methods are insensitive to the possibility of latent subgroups mixed within the study sample whose symptoms change at different rates or who have qualitatively different symptom levels at baseline (Muthen, 2004). Thus, it remains unknown whether there are subgroups of individuals whose PD symptoms do not remit over time or affected persons whose symptoms remit especially rapidly. Even less is known about the potential development of PD symptoms among individuals who are initially asymptomatic (Cohen, Crawford, Johnson, & Kasen, 2005). Clarifying heterogeneity in the course of PDs is an important topic because persistent PD symptomatology is associated with poor treatment response (Newton-Howes, Tyrer, & Johnson, 2006) and psychosocial impairment (Gunderson et al., 2011). Thus, identifying the characteristics of individuals who experience chronic PD symptoms versus those whose symptoms remit rapidly over time may have direct implications for clinical assessment. Moreover, characterizing such heterogeneity may inform an understanding of the development and pathogenesis of personality pathology, which remains largely opaque to date. Growth mixture modeling (GMM), a synthesis of latent growth curve modeling and finite mixture modeling, is a longitudinal data analytic approach that provides leverage on the question of whether change trajectories in a sample are homogeneous (with variation around mean parameters) or whether latent subgroups with distinct trajectories are commingled within the observed variation (Muthen & Shedden, 1999). This approach is ideally suited to parse heterogeneity in the longitudinal course of PD symptoms and has been used effectively to study the course of other forms of psychopathology (Lincoln & Takeuchi, 2010; Malone, Van Eck, Flory, & Lamis, 2010). In particular, GMM is an optimal technique for testing whether mean-level declines in PD symptoms occur universally or whether the longitudinal course of PDs is more heterogeneous than previously described. The present study examined whether distinct latent trajectories of PD symptom change were evident in the LSPD, a multi-wave prospective study designed to examine change in PD symptoms in early adulthood (Lenzenweger, 1999). Our study builds on the LSPD research corpus by focusing specifically on heterogeneity in the longitudinal trajectories of PD symptoms, whereas previous analyses of this dataset have addressed mean-level stability in the sample (Lenzenweger, 1999; Lenzenweger et al., 2004) and the associations among PDs and personality variables (e.g., Lenzenweger & Willett, 2007). Two groups of participants were observed in the LSPD: symptomatic individuals who met a diagnostic threshold for at least one DSM-III-R PD on a self-report screening instrument (PPD), and asymptomatic individuals who were drawn from a pool of subjects that did not the meet diagnostic threshold for any PD (NoPD). In the initial selection of LSPD subjects, no attempt was made to exclude participants with comorbid PDs. Thus, it is likely that symptom change at the disorder level represents a mixture of individuals with and without particular PD features, rather than a homogeneous, single-PD group. In addition, the NoPD group may have included persons at risk to develop a PD at baseline who developed personality pathology during the four-year follow-up period. Because the NoPD and PPD groups were sampled for the relative absence or presence, respectively, of any form of personality pathology, our primary analyses focused on identifying latent trajectories of growth in the total number of PD symptoms. This approach aligns with a large literature describing the core features of personality disorder that span diagnostic constructs (Livesley, 1998) and that are crucial in clinical decision making (Pilkonis, Hallquist, Morse, & Stepp, 2011). Furthermore, the notion of a general PD dimension is a primary component of current proposals for PD nomenclature in DSM-5 (Krueger, Skodol, Livesley, Shrout, & Huang, 2007). Separate GMMs were estimated for the NoPD and PPD groups (which varied considerably in their composition) so that the number and form of latent trajectories were not constrained by the study design. To explore heterogeneity in the course of specific PDs, we also conducted exploratory GMMs for each of the 11 DSM-III-R PDs in each group. Personality disorders are often comorbid with each other and with Axis I psychopathology (Grilo et al., 2000; Zimmerman & Mattia, 1999), and greater comorbidity is associated with functional impairment and poor treatment response (Fournier et al., 2008; Newton-Howes et al., 2006). Moreover, personality traits may represent a common substrate that is related to many forms of psychopathology (Krueger, 2005; Krueger & Markon, 2006; Lahey, 2009). Thus, to characterize the covariation among PD symptoms, personality traits, and psychopathology, we compared PD latent trajectory classes in terms of person-specific estimates of the initial level and rate of change for all other PDs, depression, anxiety, and four major personality traits. For the PPD group, we hypothesized that two latent trajectories would be evident for the total number of PD symptoms: 1) those whose symptoms were moderate to high at baseline and decreased little over time; 2) those with similar levels of baseline symptomatology who experienced significant remission. We further predicted that the persistent class would have greater Axis II comorbidity, anxiety, and depressive symptoms at baseline and that these comorbidities would remain higher over time than in the remitting class (Zanarini, Frankenburg, Vujanovic, et al., 2004; Zanarini, Frankenburg, Hennen, Reich, & Silk, 2004). For the NoPD group, we hypothesized that two trajectories would be observed for total PD symptoms: 1) those who exhibited minimal to subclinical symptomatology over time (consistent with the sampling strategy of the LSPD), and 2) those whose symptoms increased over time, suggesting the development of personality pathology in someone with low initial risk (Cohen, Chen, et al., 2005). Analyses of individual PDs were undertaken within a context of discovery and, therefore, we did not have specific hypotheses about the number or form of latent trajectories at the disorder level.