A number of hypotheses have been suggested to account for the high comorbidity rate. Each hypothesis aligns with certain theoretical orientations to psychopathology and suggests, accordingly, what might be the appropriate treatment (De-vanand, 2002).
The "predisposition hypothesis" posits that one condition (either the Axis I or Axis II condition) predisposes the individual to develop the "other" condition. This corresponds well to theories of genetic loading, or diathesis, with regard to the development of psychopathology.
The "subclinical or prodrome hypothesis" posits that the personality disorder is a prodrome of the Axis I disorder, both of which share a common biogenetic substrate—having a personality disorder puts the individual selectively at risk for developing an Axis I condition. A possible flaw with this hypothesis relates to a temporal concern. How can we account for the presentation of a mood or anxiety disorder in childhood, before the Axis II condition becomes evident?
The "life events hypothesis" suggests that stressors early in life (e.g., attachment insults or trauma) lead to the development of both Axis I and Axis II disorders, especially mood disorders. This is consistent with a psychodynamic orientation.
The "scarring hypothesis" suggests that, with severe and recurring Axis I episodes, a scarring of the personality occurs, which results in the development of a personality disorder.
Again, this raises a temporal concern. Current diagnosis criteria require the personality disorder to be established by adulthood, and many individuals with a personality disorder do not have an Axis I episode until later. Have we missed identifying earlier Axis I episodes—specifically, symptoms of mood and anxiety disorders in childhood or adolescence?
Perhaps, the hypothesis with the greatest support (at least anecdotally) is the "modifier/pathoplasty hypothesis." This suggests that, with the high comorbidity rate of Axis I and Axis II disorders, each one modifies the expression of the other. This hypothesis recognizes the bidirectionality and the interrelated-ness (not causality) of both types of clinical conditions, albeit this process is not yet well understood. This hypothesis also supports the likelihood that Axis II personality disorders and Axis I clinical disorders share common aspects of psychopathology (Shea & Yen, 2003).
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