Objectives

• Understand the relevance of developmental pathogenesis to the study of personality.

• Understand interplay of necessary, sufficient, and contributory causes for the development of personality pathology.

• Gain insight into how personality dynamics interact in relation to their environment.

• Learn about the hypothesized relationship between some personality disorder expressions and more acute pathology, such as schizophrenia.

• Explain how different temperaments at birth may contribute to vastly different life experiences and ultimate expressions of personality.

• Explain the term pathogenic, and list the three types of events that may contribute to pathogenesis.

• Identify parental behaviors and inconsistencies that are thought to cause difficulty in later adaptation.

• Describe the role of traumatic experiences in personality development.

• Explain the importance of early learning.

• Explain how culture, with its values, ideals, and institutions, interfaces with personality development.

Tracing the developmental history of personality and its disorders is one of the most difficult but rewarding phases in the study of medical and psychological science. This study of causation is frequently termed etiology in medicine and developmental patho-genesis in psychology. It attempts to establish the relative importance of a number of determinants of personality pathology and seeks to demonstrate how overtly unrelated determinants interconnect to produce a clinical picture. Methods such as laboratory tests, case histories, clinical observation, and experimental research are combined in an effort to unravel this intricate developmental sequence.

Most people have been conditioned to think of causality in a simple format in which a single event, known as the cause, results in a single effect. Scientists have learned, however, that particular end results usually arise from the interaction of a large number of causes. Furthermore, it is not uncommon for a single cause to play a part in a variety of end results. Each of these individual end results may set off an independent chain of events that will progress through different intricate sequences.

Thus, study of developmental etiology is complicated by the fact that a particular end result, such as a physical disease, may be produced by any one of a number of different and, on occasion, even mutually exclusive causal sequences; for example, you can get cancer from smoking or from radiation. It should be obvious that causation is not a simple matter of a single cause leading to a single effect. Disentangling the varied and intricate pathways to personality pathology is an especially difficult task indeed.

In philosophy, causes are frequently divided into three classes: necessary, sufficient, and contributory. A necessary cause is an event that must precede another event for it to occur. For example, certain theorists believe that individuals who do not possess a particular genetic defect will not become schizophrenic; they usually contend that this inherent defect must be supplemented by certain detrimental experiences before the schizophrenic pattern will emerge. In this theory, the genetic defect is viewed as a necessary but not a sufficient cause of the pathology.

A sufficient condition is one that is adequate in itself to cause pathology; no other factor need be associated with it. However, a sufficient condition is neither a necessary nor an exclusive cause of a particular disorder. For example, a neurosyphilitic infection may be sufficient in itself to produce certain forms of psychopathology, but many other causes can result in these disorders as well.

Contributory causes are factors that increase the probability that a disorder will occur, but are neither necessary nor sufficient to do so. These conditions, such as economic deprivation or racial conflict, add to a welter of other factors that, when taken together, shape the course of pathology. Contributory causes usually influence the form in which the pathology is expressed and play relatively limited roles as primary determinants.

In personality, causes are divided traditionally into predisposing and precipitating factors.

Predisposing factors are contributory conditions that usually are neither necessary nor sufficient to bring about the disorder but that serve as a foundation for its development. They exert an influence over a relatively long time span and set the stage for the emergence of the pathology. Factors such as heredity, socioeconomic status, family atmosphere, and habits learned in response to early traumatic experiences are illustrations of these predispositions.

No hard-and-fast line can be drawn between predisposing and precipitating causes, but a useful distinction may be made between them. Precipitating factors refer to clearly demarcated events that occur shortly before the onset of the manifest pathology. These factors either bring to the surface or hasten the emergence of a pathological disposition; that is, they evoke or trigger the expression of established, but hidden, dispo-sitional factors. The death of a parent, a severe car accident, the sudden breakup of a romantic relationship, and so on illustrate these precipitants.

The premise that early experience plays a central role in shaping personality attributes is one shared by numerous theorists. Stating this premise, however, is not to agree as to which specific factors during these developing years are critical in generating particular attributes, nor is it to agree that known formative influences are either necessary or sufficient. Psychoanalytic theorists almost invariably direct their etiologic attentions to the realm of early childhood experience. Unfortunately, they differ vigorously among themselves as to which aspects of nascent life are crucial to development.

There is reason to ask whether etiologic analysis is even possible in personality pathology in light of the complex and variable character of developmental influences. Can this most fundamental of scientific activities be achieved given that we are dealing with an interactive and sequential chain of causes composed of inherently inexact data of a highly probabilistic nature in which even the very slightest variation in context or antecedent condition, often of a minor or random character, produces highly divergent outcomes? Because this looseness in the causal network of variables is unavoidable, are there any grounds for believing that such endeavors could prove more than illusory? Further, will the careful study of individuals reveal repetitive patterns of symptomatic congruence, no less consistency among the origins of diverse clinical attributes such as overt behavior, intrapsychic functioning, and biophysical disposition? And will etio-logic commonalities and syndromal coherence prove to be valid phenomena, that is, not merely imposed on observed data by virtue of clinical expectation or theoretical bias?

Among other concerns, the hard data, the unequivocal evidence from well-designed and well-executed research, are sorely lacking. Consistent findings on causal factors for specific clinical entities would be extremely useful were such knowledge only in hand. Unfortunately, our etiologic database is both scanty and unreliable. As noted, it is likely to remain so because of the obscure, complex, and interactive nature of influences that shape psychopathologic phenomena. The yearning among theorists of all viewpoints for a neat package of etiologic attributes simply cannot be reconciled with the complex philosophical issues, methodological quandaries, and difficult-to-disentangle subtle and random influences that shape mental disorders. In the main, almost all etiologic theses today are, at best, perceptive conjectures that ultimately rest on tenuous empirical grounds, reflecting the views of divergent schools of thought positing their favorite hypotheses. These speculative notions should be conceived as questions that deserve empirical evaluation, rather than promulgated as the gospel of confirmed fact.

Inferences drawn in the clinical consulting room concerning past experiences, especially those of early childhood, are of limited, if not dubious, value by virtue of having only the patient as the primary, if not the sole, source of information. Events and relationships of the first years of life are notably unreliable because of the lack of clarity of retrospective memories. The presymbolic world of infants and young toddlers comprises fleeting and inarticulate impressions that remain embedded in perceptually amorphous and inchoate forms—forms that cannot be reproduced as the growing child's cognitions take on a more discriminative and symbolic character. What is recalled, then, draws on a highly ambiguous palette of diffuse images and affects, a source whose recaptured content is readily subject both to direct and subtle promptings from contemporary sources, for example, a theoretically oriented therapist.

Arguments pointing to thematic or logical continuities between the character of early experience and later behaviors, no matter how intuitively rational or consonant with established principles they may be, do not provide unequivocal evidence because their causal connections are different; equally convincing developmental hypotheses can be and are posited. Each contemporary explication of the origins of most personality disorders is persuasive, yet remains but one among several plausible possibilities.

Among other troublesome aspects of contemporary etiologic proposals are the diverse syndromal consequences attributed to essentially identical causes. Although it is not unreasonable to trace different outcomes to similar antecedents, there is an unusual inclination among theorists to assign the same "early conflict" or "traumatic relationship" to all varieties of psychological ailment. For example, an almost universal experiential ordeal that ostensibly undergirds varied syndromes such as narcissistic and borderline personalities, as well as a host of schizophrenic and psychosomatic conditions, is the splitting or repressing of introjected aggressive impulses engendered by parental hostility, an intrapsychic mechanism requisite to countering the dangers these impulses pose to dependency security, should they achieve consciousness or behavioral expression.

It is unlikely that singular origins would be as ubiquitous as clinicians often posit them, but, even if they were, their ultimate psychological impact would differ substantially depending on the configuration of other concurrent or later influences to which individuals were exposed. "Identical" causal factors cannot be assumed to possess the same import, nor can their consequences be traced without reference to the larger context of each individual's life experiences.

To go one step further, there is good reason, as well as evidence, to believe that the significance of early troubled relationships may inhere less in their singularity or the depth of their impact than in the fact that they are precursors of what is likely to become a recurrent pattern of subsequent parental encounters. It may be sheer recapitulation and consequent cumulative learning that ultimately fashions and deeply embeds the entrained pattern of distinctive personality attributes we observe. Although early encounters and resolutions may serve as powerful forerunners, the presence of clinical symptoms may not take firm root in early childhood but may stem from repeated reinforcement.

Despite these arguments, the authors of this text share the commonly held view that, unit for unit, the earlier the experience, the likely greater its impact and durability. For example, the presymbolic and random nature of learning in the first few years often precludes subsequent duplication and, hence, "protects" what has been learned. But, we believe it is also true that singular etiologic experiences, such as "split introjects," are often only the earliest manifestation of a recurrent pattern of parent-child relationships. Early learnings may fail to change, therefore, not because they have jelled permanently but because the same slender band of experiences that helped form them initially continues and persists to influence them for years.

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