This is the first study, to our knowledge, to investigate the longitudinal associations between personality disorders and Axis I disorders using a prospective design and continuous measures of course for both. For subgroups of AVPD and BPD participants with the relevant Axis I disorders, the findings provided partial support for the predictions derived from the crosscutting dimensional model (Siever & Davis, 1991
). The predicted associations for OCPD were not significant.
BPD course over follow-up showed associations with MDD, consistent with the affective instability dimension proposed to underlie the mood disorders on Axis I and the Cluster B (dramatic–erratic) personality disorders. Failure to remit from MDD was associated with a substantially reduced likelihood of remitting from BPD, and the time-varying associations showed that changes in status for these disorders were closely linked in time. These findings, despite the difference in approach, are consistent with those of Klein & Schwartz (2002)
, who examined longitudinal associations between BPD and early onset dysthymia. Outpatients with dysthymia were assessed three times over 5 years through the use of semistructured interviews. Using structural equation modeling, the authors tested multiple models of the associations (no association, direct effects in both directions over short periods of time, lagged direct effects in which one condition influenced the other over a longer period, and a fixed common factor underlying both disorders). The fixed common factor model was the best fitting of the models, with an excellent fit to the data. The authors noted that the latent fixed common factor could reflect several possible etiologies, including a shared genetic substrate, a shared temperamental vulnerability such as neuroticism, or environmental events such as early abuse or neglect (Klein & Schwartz, 2002
BPD changes were also linked, as predicted, with changes in PTSD. BPD participants with PTSD that remitted over follow-up were more likely to remit from BPD than those with nonremitting PTSD, or than those without PTSD at baseline. Improvement in BPD increased the likelihood of subsequent remission from PTSD in the time-varying analyses, although the time-varying association was not significant in the opposite direction. One possible explanation is that BPD is a more complex disorder, sharing some but not all dimensions with PTSD. Improvement in BPD predicting proximal remission from PTSD could reflect the improvement of one or more shared dimensions (for example, affect dysregulation or brief dissociative episodes). On the other hand, remission from PTSD was associated with increased probability of remission from BPD in the analyses in which we examined associations over the interval as a whole not restricted to the 1-month interval. This discrepancy might suggest that remission from PTSD could over time (i.e., when not restricted to the 1-month interval) lead to improvement in nonshared dimensions of BPD. Alternatively, our methods and data may have been insufficiently sensitive to the associations in both directions, meaning the discrepancy is due to measurement error.
An unpredicted association was found for BPD and panic disorder: BPD participants with unremitting panic disorder were less likely to remit from BPD. Associations between BPD and panic disorder were not found in the time-varying analyses, however, meaning that the changes are not occurring in close proximity. Similarly, a possible reason for the discrepancy may be that conditions facilitating the remission from panic disorder, and/or changes resulting from panic disorder remission, may over a longer period of time effect improvement in BPD, in contrast to a dimension of psychopathology shared by the two disorders.
AVPD showed significant associations with the broad group of anxiety disorders, consistent with the anxiety/inhibition dimension. In terms of specific anxiety disorders, associations were found for social phobia and OCD. AVPD showed unpredicted associations with major depression, but this association disappeared in the time-varying analysis when BPD was controlled. Thus, when both BPD and AVPD were present and both improved, it was the improvement in BPD that had the strongest link with remission from MDD. This finding speaks to the importance of examining the possible influence of co-occurring personality disorder diagnoses when associations between personality disorders and Axis I disorders are found.
OCPD did not show the predicted changes with anxiety disorders, failing to support a crosscutting anxiety/inhibited dimension underlying OCPD. Of note in this regard are findings from studies examining the factor structure of dimensional scores from the 11 DSM–III
personality disorders. Although a factor structure consistent with the three Axis II clusters has typically been found, the exception has been for OCPD, which has either not loaded on any factors (Zimmerman & Coryell, 1990
) or formed its own factor (Kass et al., 1985
). These findings suggest that OCPD may not be well characterized as a disorder of the anxious–inhibited cluster.
Although the findings support some of the hypotheses, it is important to emphasize that the associations found in the time-varying analyses apply only to subsets of the BPD and AVPD participants: those with the co-occurring Axis I diagnosis at baseline. Fewer than half (45%) of the BPD participants had MDD at baseline, and 38% had PTSD. Of the AVPD participants, less than one third (31%) had social phobia, and only 14% had OCD at baseline. This reflects the heterogeneity and multidimensional nature of the personality disorders, that is, not all individuals meeting criteria for a given personality disorder are characterized by disturbances on all of the dimensions underlying the criteria (Shea, 1992
). BPD, in particular, has been shown in several studies to consist of multiple dimensions. Confirmatory factor analyses of BPD criteria from CLPS assessments supported a three-factor model, labeled disturbed relatedness, behavioral dysregulation (impulsivity), and affective dysregulation (Sanislow et al., 2002
). Two of these (impulsivity and affective dysregulation) correspond to the Siever and Davis (1991)
dimensions. The findings of correlated changes in course for the BPD and AVPD subgroups with the respective Axis I disorders does not mean that the disorders are synonymous, but rather that they may share some dimensions of psychopathology.
Research on biological abnormalities has shown both similarities and differences between BPD and depression. Most biological studies of BPD have not controlled for the presence of major depression, which may contribute to the inconsistent findings (Koenigsberg et al., 1999
). It may be that the biological similarities are stronger in those BPD patients with affective dysregulation. A further question to consider in terms of a shared psychobiological dimension of affective dysregulation is the differences in quality of the mood disturbance. Major depression typically involves a more fixed depressed mood, whereas depression in BPD tends to be characterized by more mood reactivity. One hypothesis is that low serotonergic activity and high cholinergic sensitivity may be common to both BPD and depression, but different abnormalities in noradrenergic function, which modulates the extent of engagement with the social environment, may result in the differences in reactivity of mood (Koenigsberg et al., 1999
). Though this work is preliminary and far from definitive, it illustrates the more general point, which is that two disorders (BPD and depression, in this case) may share some etiologic mechanisms and differ on others. Furthermore, the shared mechanisms may apply only to a subset of individuals given the multidimensional nature of the personality disorder diagnoses.
The current findings, though consistent with the notion of shared dimensions of psychopathology across Axis I for subgroups of individuals with BPD and AVPD, clearly do not rule out other mechanisms that may contribute to Axis I co-occurrence for these as well as for other personality disorders. Indeed, it is likely that multiple mechanisms contribute to the co-occurrence of the personality and Axis I disorders. The interpersonal difficulties that are the hallmark of personality disorders, for example, put affected individuals at high risk for the kinds of chronic and acute life events (failures and losses) that then increase the risk of the onset and/or maintenance of depressive or anxiety disorders. In the current study, we examined the co-varying associations in improvement across disorders. A vulnerability model would predict that one disorder precedes the other but would not necessarily predict that both disorders would improve together. Thus the current data are not well suited for testing a vulnerability model, which are ideally tested in studies allowing prospective observation of the first onset of disorders. Other methodological approaches are essential to a more definitive understanding of the nature and mechanisms involved in the associations. More intensive study of the timing (sequence) and psychosocial context, including stressors and precipitants, surrounding the onset or recurrence of the disorders would be informative. Studies of neurobiological correlates would be a valuable strategy to shed light on the extent to which mechanisms may be shared or distinct. For example, time-varying associations of repeated measures of serotonergic activity, with the status of BPD and MDD symptoms over time could be used to test the hypothesis of a shared mechanism for BPD and MDD.
BPD does not show the predicted association with substance use or eating disorders, which are representative of the impulsive aspect of the impulsive/aggressive dimension. This suggests that despite their frequent co-occurrence, changes in the manifestations of these disorders are not closely linked in time. Again, the absence of longitudinal associations does not rule out the possibility of causal associations (for example, vulnerability, complication, or other risk models). Several models have been articulated to explain the high rates of co-occurrence between BPD and substance use disorders (Trull et al., 2000
). These include the use of substances to cope with negative affective states in BPD, consistent with a vulnerability or risk model, or that both disorders may be mediated by common constitutional and family environmental factors. Despite likely causal associations in the development of these disorders, the current findings of no associations in course are inconsistent with the notion that both are manifestations of the same currently operative mechanisms.
Another explanation for the current findings is that the associations found are artifacts of a state effect. That is, participants who were in an episode of depression or anxiety disorder at baseline gave a distorted report of their longer term personality as a result of the coloring of their perceptions by their mood state. This would mean that such personality disorder diagnoses were false positives and that the apparent correlation in improvement was really the result of just the depression (or anxiety) and the associated distorted perceptions remitting. However, if this were the case, the personality disorder criteria falsely reported as characteristic when depressed (or anxious), should be denied for the entire assessment interval once the individual is remitted from the Axis I disorder. This would mean, for example, that for participants with major depression that remitted by the 6-month assessment, the personality disorder remission should occur in Month 1 of the follow-up. This did happen in some cases (see Gunderson et al., 2003
, for a description and discussion of early remissions), but the improvement in the personality disorder status in relation to the Axis I remission (and vice versa) generally occurred over a period of several months.
A limitation of the current study is the collection of data on four personality disorders, which precludes examinations of other possible personality disorder–Axis I associations. Furthermore, the study exclusion of a history of schizophrenia or schizoaffective disorder precludes examination of personality disorder associations (notably STPD) with Axis I psychotic disorders. Also, the number of cases naturally varied for different pairs of disorders, influencing the statistical power to find associations. For example, the risk ratio of .77 for MDD predicting BPD remission, on the basis of 90 participants, reaches our significance level of .05, whereas the risk ratio of .54 for OCD predicting BPD remission, on the basis of 28 participants, does not. Thus, some relationships may be underestimated. On the other hand, the differences in the size of the pairs is also meaningful, as larger numbers reflect associations among the specific pairs of personality disorders and Axis I disorders.
An additional issue concerns the ability to determine precisely the timing of the symptomatic improvements across the disorders. Interviews covered the prior 6 or 12 months, and despite efforts to determine as precisely as possible the timing of symptoms and criteria changes, the interviewers necessarily relied on participants’ memories of these changes. Although our reliability study of retrospective ratings described above suggested good concordance over time, more frequent assessments would provide a better test of the timing of the changes. Additionally, given that the same interviewers assessed the course of the personality disorders and Axis I disorders, it is possible that interviewer bias influenced the results. However, it is unlikely that the interviewers had a specific bias in terms of personality disorder-Axis I relationships; the fact that associations were found for only two of the personality disorders, and for a minority of Axis I disorders, argues against interviewer bias as a major factor in the findings. An advantage of nonblind interviews is increased knowledge of the study participant and thus perhaps the ability to make more valid judgments.
In summary, our findings support some of the hypothesized associations. BPD shows a significant association with MDD and with PTSD. AVPD shows a significant association with anxiety disorders, and specifically with social phobia and OCD. The findings for BPD and AVPD are consistent with the model of crosscutting dimensions (Siever & Davis, 1991
) for subsets of individuals with these disorders. Other models, however, may also be applicable. Future reports should examine associated disorders in more depth, including the role of specific personality disorder criteria in the associations found and the investigation of longer time lags. Longer follow-up should also allow for an examination of time-varying associations between the personality disorders and recurrence and new onsets of Axis I disorders. Other studies are needed to address the associations of other personality disorders with Axis I disorders.