Journal of Abnormal Psychology Copyright 2005 by the American Psychological Association 2005, Vol. 114, No. 4, 505–521 0021-843X/05/$12.00 DOI: 10.1037/0021-843X.114.4.505 Temperament as a Unifying Basis for Personality and Psychopathology Lee Anna Clark University of Iowa Personality and psychopathology long have been viewed as related domains, but the precise nature of their relations remains unclear. Through most of the 20th century, they were studied as separate fields; within psychopathology, clinical syndromes were separated from personality disorders in 1980. This division led to the revelation of substantial overlap among disorders both within and across axes and to the joint study of normal and abnormal personality. The author reviews these literatures and proposes an integrative framework to explain personality–psychopathology relations: Three broad, innate tempera- ment dimensions—negative affectivity, positive affectivity, and disinhibition—differentiate through both biologically and environmentally based developmental processes into a hierarchical personality trait structure and, at their extremes, are risk factors (diatheses) for psychopathology, especially given adverse life experiences (stress). Keywords: temperament, psychopathology, personality, taxonomy, DSM–V The first model of personality–psychopathology relations may only half the story. The other half is their division, both between have been the doctrine of the four humors, attributed to Hip- psychiatry (with its major focus on abnormal processes) and psy- pocrates and Galen (Maher & Maher, 1994). The balance of these chology (which generally emphasizes the study of normal func- four humors—blood (sanguis), phlegm, bile (choler), and black tioning) and also within each field. One sign of the split within bile (melancholer)—determined one’s temperament: sanguine, psychology was the separation in 1965 of the Journal of Abnormal phlegmatic, choleric, or melancholic, respectively. Temperament, and Social Psychology into the Journal of Abnormal Psychology in turn, determined vulnerability to illness, and a humoral imbal- and the Journal of Personality and Social Psychology. ance led to physical or mental illness. Balance—and thus health— was restored by such techniques as bleeding and purging. With the advent of modern science, which in psychology began The Advent of the DSM: An Atheoretical Model in the late 19th century, theories of personality–psychopathology In mid-20th century, psychiatry systematized its accumulated relations were based on Darwinian concepts (Maher & Maher, knowledge of psychopathology in the Diagnostic and Statistical 1994). One basic theme was that all types of mental illness Manual of Mental Disorders (DSM–I, DSM–II; American Psychi- reflected a general character deficiency that was genetically based, atric Association, 1952, 1968). In these DSMs, personality pathol- and the specific forms of which reflected biological and/or per- ogy was considered alongside other disorders with little attention sonal development. Freud’s well-known theory of the stages of to their potential interrelations. However, with the advent of DSM– character development, each with its associated psychopathology, III (American Psychiatric Association, 1980), personality disor- is the most elaborate and influential of these views. ders were given their own “Axis II,” which reopened the door for In the early 20th century, Kraepelin posited that personality the systematic study of the two domains in relation to each other. disorders were formes frustes of the major psychoses. Kretschmer The DSMs were intended as descriptive documents to aid both went a step further, hypothesizing a single continuum from per- research and treatment planning. Whereas prevailing theories no sonality (schizothyme) through personality disorder (schizoid) to doubt influenced each of the DSMs, theory per se was not a clinical syndrome (schizophrenia; Livesley, Schroeder, Jackson, & guiding principle in their development, and DSM–III explicitly Jang, 1994). Interestingly, Pavlovian conditioning theorists reju- declared its atheoretical intent. However, the creation of separate venated the ancient four-humoral theory, substituting variation in axes clearly indicated that personality disorders were considered a neuronal responses for the strength and balance of humors (Maher distinct type of psychopathology, which also invited study of their & Maher, 1994), and Eysenck explicitly related his three-factor interrelation. personality model to Pavlovian concepts. Whereas Eysenck’s di- A notable phenomenon of the successive DSMs was the increase mensions still play a major role in the field, the link to conditioning in diagnoses, as well as in subtypes and specifiers to address theories, for the most part, does not. within-diagnosis heterogeneity (Watson, 2003). Some of the diag- This precis suggests that personality and psychopathology have nostic increase was due to new disorders (e.g., cyclothymia), but a been studied in relation to each other since antiquity, but that is substantial proportion resulted from subdivison (e.g., bipolar dis- order into Bipolar I and Bipolar II disorders). These changes also were based largely on descriptive studies rather than theory-driven Correspondence concerning this article should be addressed to Lee Anna research. Clark, Department of Psychology, University of Iowa, 111 Jessup Hall, Virtually without offering either a theoretical rationale or em- Iowa City, IA 52242-1316. E-mail: [email protected] pirical justification, DSM–III included hierarchical exclusion rules 505 506 CLARK affecting 60% of all disorders (Boyd et al., 1984), prohibiting indicating the presence of broad latent factors underlying certain Diagnosis A if it was “due to” Diagnosis B. Both clinicians and sets of comorbid disorders. researchers chafed at these strictures because (a) they prevented Insofar as the Widiger and Clark (2000) review indicates that full diagnostic representation of patients’ symptom sets, (b) they these various literatures are not entirely distinct, but have overlap- made it difficult to study disorders lower in the hierarchy, and (c) ping elements, it points to the possibility of a more comprehensive the “due to” rule was difficult to apply in that it required a integration. Suggesting the form that this broader integration might subjective and inferential judgment regarding causal primacy of take is the primary purpose of this article. To that end, I first the relevant disorders in the absence of empirical data or clear examine briefly the literatures on comorbidity among Axis I dis- guidance from the DSM.1 Consequently, some adopted the more orders, among Axis II disorders, and across the axes. I then straightforward rule of simply not diagnosing A if B was present, examine the literatures concerning overlap of normal-range per- whereas others, researchers in particular, ignored the rules in order sonality with first Axis II and then Axis I disorders. In both cases, to study their effects. In response to these twin pressures, the I focus on recent trends and important issues that these literatures exclusion rules were largely removed from DSM–III–R (American raise. I then propose an overarching framework to integrate the Psychiatric Association, 1987). broad domains of personality and psychopathology and the various literatures they subsume. I present an initial view of the form and Diagnostic Comorbidity structure of this framework and consider the various challenges that such a framework needs to address. The most obvious and immediate effect of removing the exclu- sion rules was the well-known revelation of a high degree of Etiological Models diagnostic co-occurrence both within and across axes, which pre- sented a challenge for a taxonomy in which, ideally, diagnoses are In considering the broad literature on diagnostic comorbidity, it distinct entities. The usual term in the literature for this phenom- is useful to keep in mind the four major etiological models of enon is comorbidity, but as Lilienfeld, Waldman, and Israel (1994) comorbidity that have been proposed. These models fall into two discussed, there are problems with that term, including that it does major types based on whether they attribute causal significance to not distinguish between mere overlap and statistical covariation. temporal order (for discussions, see Maser & Cloninger, 1990; Nonetheless, I will use the term comorbidity because of its near Lilienfeld et al., 1994; Mineka et al., 1998). The predisposition or universal usage in the literature, begging the readers’ understand- vulnerability model postulates that a prior disorder increases the 2 ing that in some places it may be imprecise. likelihood that a person will experience a later onset disorder, Clark, Watson, and Reynolds (1995) reviewed the emerging whereas the pathoplasty model posits that a prior disorder influ- comorbidity literature and discussed various factors that affect ences the severity, course, or treatment response of a later onset comorbidity rates, such as time frame (i.e., concurrent or lifetime disorder. The other two models posit that comorbid disorders diagnoses), range of inclusion (i.e., only clear cases or also sub- reflect the same underlying process or etiological factor, so that clinical varieties), diagnostic method (i.e., paper-and-pencil self- neither can be viewed as clearly causing the other. The common/ report or interview), and sample type (e.g., clinic or community shared cause, liability,