This study provides the first examination of the naturalistic, 7-year course of six anxiety disorders in a clinical group with a high rate of PDs. Remission estimates in this study group indicate that by year 7, between 73% and 94% of individuals had anxiety disorders remit and between 34% and 67% of those individuals had anxiety disorders relapse. When compared with findings from the HARP study (37–82% remission and 39–56% relapse; Bruce et al. 2005
), these high rates of remission and relapse suggest that anxiety disorders are remitting and relapsing more frequently in a clinical group with a high rate of PD diagnoses. Our findings highlight the complex and variable course of anxiety disorders, characterized by frequent remissions and relapses over time as well as the occurrence of new onsets of anxiety disorders in patient groups with high rates of PDs. Our findings also highlight the negative prognostic significance of PDs on the course of anxiety disorders. These findings underscore the importance of considering both anxiety disorders and PDs by researchers and clinicians who work with either patient group.
The high rates of PD diagnoses in this study group allowed examination of specific PD associations with the course of specific anxiety disorders while controlling for the effects of age, gender, number of Axis I disorders and the other study PD diagnoses. OCPD was associated with increased risk for new onset of OCD, GAD and agoraphobia episodes, increased risk of GAD relapse and decreased risk of PTSD relapse over and above other factors. AVPD was associated with decreased likelihood of SP remission, increased likelihood of new SP and OCD episode onset and greater chronicity in SP episodes. AVPD was also associated with decreased risk for relapse of panic disorder with agoraphobia. BPD was associated with increased risk of new episode onsets for GAD and panic disorder with agoraphobia, as well as an increased risk of relapse of OCD. STPD was associated with decreased remission rates in PTSD, increased risk for relapse of SP and greater chronicity in GAD episodes.
Several of these findings replicate associations identified in prior studies conducted over shorter duration or without continuous follow-up. This study replicates findings that AVPD is predominately associated with the course of SP (Massion et al. 2002
) and corroborates speculation that these two disorders share a common dimension (Ralevski et al. 2005
; Reich, 2009
). Prior research reviewed by Reich (2000)
also associated cluster A PDs, such as STPD, with SP, although this finding has been dismissed by the authors as an erroneous assignment of paranoid fears to social anxiety. However, the present findings that STPD increases risk for SP in a carefully diagnosed clinical group suggest that either the prior findings may have been accurate or, alternatively, that the criteria for SP are constructed in a manner that makes it difficult to ascertain the differences in pathological mechanisms underlying the symptomatic expression. We replicated findings associating BPD with increased risk for new onsets of anxiety disorder episodes (Alnæs & Torgersen, 1999
), specifically panic disorder and GAD. The BPD and STPD associations with GAD in this study group replicate the findings from a large epidemiological survey (Grant et al. 2009
). Our finding associating BPD with increased risk of OCD relapse is consistent with prior findings that individuals with a BPD diagnosis and self-mutilation exhibited significantly greater OCD symptomatology (McKay et al. 2000
). The present finding that PDs were not associated with remission from panic disorder also replicates prior research (Massion et al. 2002
). Contrary to prior findings, we did not identify OCPD as a risk factor for new onsets or chronicity of panic disorder (Alnæs & Torgersen, 1999
), although it was associated with new onsets of OCD (Maina et al. 2008
) and with relapse of GAD (Grant et al. 2009
). Consistent with theoretical assertions in OCPD regarding control of worry, individuals with OCPD may have increased vulnerability for worry when they find their perfectionistic motives are unattainable or their rigid standards are unmet.
These findings have several clinical and research implications. Treatment planning for individuals with co-occurring PDs and anxiety disorders may need to take into account these findings when considering the course of symptoms. In particular, individuals who present for treatment with PD diagnoses and who have a history of a co-occurring anxiety disorder (BPD with OCD, or AVPD with SP) may warrant additional treatment focus on preventing the recurrence of symptoms associated with anxiety disorder. Further research is needed to examine whether existing treatments for anxiety disorders are equally effective in samples with co-occurring PDs. In addition, the associations in course between disorders may be mechanistically explained by personality traits, which underlie both disorders. Future directions should consider whether maladaptive personality traits increase vulnerability for course of anxiety disorders.
Several potential limitations should be considered when interpreting our findings. One limitation is the absence of a comparison group with no PD for each anxiety disorder. However, this study group did contain a MDD with no PD comparison group, a diagnosis that is frequently co-morbid with anxiety disorders. This MDD control group expands the potential variance in ways that serve to strengthen the analytic approach in lieu of a purified contrast group. In addition, the study was a naturalistic study of treatment- seeking individuals, yielding greater variability among participants than a controlled treatment protocol and thereby increasing the generalizability of these findings to patients with PDs. However, these findings may not generalize to non-treatment-seeking individuals or to individuals who are treatment seeking but do not express interest in participating in research. In addition, although the LIFE methodology is well validated and reliable, it is potentially vulnerable to bias or participant difficulties in recall of symptoms. Weekly assessment of symptoms may result in different associations than were identified in the current study.
The moderating influence of PDs on anxiety disorder course may represent differential stylistic approaches that use cognitive, affective and behavioral mechanisms to differentially mitigate dispositional anxiety, increasing risk for relapse, delaying remission and increasing chronicity for anxiety disorders and decreasing risk for relapse for other anxiety disorders. For example, a diagnosis of BPD may make individuals predisposed to OCD tendencies more vulnerable to mitigating increasing anxiety resulting from affective and interpersonal instability through compulsive or impulsive behaviors, such as self-harm. Alternatively, individuals with AVPD may establish a lifestyle in which they effectively avoid social, work and recreational situations, resulting in little opportunity to experience situations in which agoraphobic responses may occur, thus ‘protecting ’ against relapse of the panic disorder. AVPD and panic disorder with agoraphobia may have a synergistic, or pathoplastic, relationship such that the presence of personality trait tendencies and anxious predispositions interact to promote the presence of one or the other disorder. Future research will need to examine the prospective interactive effects of these disorders to determine the risk, protective and/or pathoplastic mechanisms underlying these findings. In particular, future studies will need to examine the concurrent course of PDs and anxiety disorders and consider whether alternative definitions of remission, relapse and chronicity, or whether an alternative construal of the disorders (e.g. changes within diagnostic categories in the DSM), affect findings. These data not only raise questions but also inform the boundaries of these classes of disorder relevant to the development of the DSM-V.