Mechanisms For The Cooccurrence Of Mood Disorders And

Although a well-documented relationship exists between BPD and mood disorders, the exact nature of this relationship has been a subject of much speculation and controversy. Farmer and Nelson-Gray (1990) summarized eight hypotheses that have been advanced regarding relations between PDs and depression. Four of these (the orthogonal, overlapping symptoms, heterogeneity, and modification hypotheses) are primarily descriptive and do not propose a particular mechanism or suggest that no such mechanism exists. Four hypotheses, described below, do propose a causal mechanism to account for co-occurrence.

The characterological predisposition hypothesis suggests that individuals with personality disorders engage in maladaptive behaviors that result in stressful life events and difficulties, which in turn increase vulnerability to depression, or that individuals with BPD are susceptible to depression because of a "bad self" or anger turned inward, or "abandonment depression" (Gunderson & Elliott, 1985). There is no direct prospective evidence regarding this hypothesis for BPD, but some maladaptive personality traits, such as dependency, do predict the first onset of major depression (e.g., Hirschfeld et al., 1989).

Conversely, the complication hypothesis suggests that depression, particularly chronic or recurrent depression, can lead to the development of PD

characteristics, either only during a depressive episode (e.g., increased dependency that may decline again when depression remits) or as a more enduring "scar" effect.

The attenuation hypothesis suggests that personality disorders are an attenuated form of mood disorders and have the same causes (e.g., genetics). Akiskal (2004), one of the more prominent proponents of the attenuation hypothesis with regard to BPD, notes the high rate of comorbidity with mood disorders, particularly the bipolar spectrum, shared family history, and similarities in sleep electroencephalographs (EEG) and neuroendocrine findings. However, others (e.g., Gunderson & Elliott, 1985; Gunderson & Phillips, 1991) have noted important differences between BPD and mood disorders, and have suggested that co-occurrence is best explained as chance association (the orthogonal hypothesis). This question remains the subject of heated debate. Among 16 patients with BPD, 32% reported spontaneous mania or hypomania, and 81% had "soft" signs of bipolarity, such as a bipolar temperament, pharmacological response pattern, or family history of bipo-larity (Deltito et al., 2001). Interestingly, in dialectical behavior therapy (DBT, Linehan, 1993a), emotion dysregulation, a cardinal feature of bipolar disorders, is viewed as the core difficulty of persons with BPD, from which the other characteristics largely emerge over time as the individual interacts with an environment that often responds poorly to such dysregulation. Linehan has never suggested that BPD is a bipolar spectrum disorder, but this would not be inconsistent with her model.

Klein and Schwartz (2002) compared the fit between several causal models and data from a 5-year longitudinal study of outpatients with dysthymic disorder. Results suggested that BPD features and depressive symptoms are influenced by partially overlapping processes, consistent with what Farmer and Nelson-Gray (1990) refer to as the "coeffect" hypothesis.

It is likely that several mechanisms contribute to the co-occurrence of BPD and depressive disorders, including shared biological and psychosocial causal influences, the effects of BPD on depression, and the influence of recurrent depression on development of BPD.

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