This section focuses on the importance of the name "Etiotropic Trauma Management," explaining why it is and should be distinguished from its competitors. The distinguishment is not just semantics.
Other than ETM, all models used in the treatment and management of psychological trauma are nosotropically-based. "Nosotropic" refers to the method through which disease or psychological problems are approached from the perspective of the problem's symptoms. Like the etiology of psychological trauma, symptoms are produced with psychological and biological variants.
Biological symptoms are manifested by a trauma induced biological sequelae. It means that trauma initiated biological events create other and related events that then because of their relatedness act to sustain themselves, culminating in psychological symptoms that are adjudged by standard psychological appraisal processes as thought and behavioral abnormalities.
The biology of symptoms is explained in this About/ Comparison - Contrast section, and in the About/ Theory section. Examples of psychological symptoms are numerous and have been provided in detail in About/ Theory and Clinical/ Reversing Long-term Trauma Etiology/ Phase Three and in other books on the subject (About/ Bibliography).
When an approach to the treatment of psychological trauma is symptom focused, the psychologically (and nosotropically) trained helping agent discovers that something is wrong by observing thoughts and behaviors that, because of their differences from the norm, have become problems. The problem is that the person is not thinking and behaving properly; the client/patient is acting outside of the norm and should be assisted in correcting the apparent abnormality.
The biologically-oriented (and nosotropically trained) helping person/agent will concentrate on the biological symptoms/sequelae, using pharmacological additives to arrest the biological symptoms. Sometimes, the affected person acting alone tries to correct the apparently abnormal thoughts and behaviors (symptoms) through the use of psychological self-help measures.
Regardless of the specific method, the nosotropically-focused corrective process is supposed to continue until the biological and psychological abnormalities (symptoms) are controlled, or they no longer exist.
Comparing the two approaches, etiotropic and nosotropic, we use a continuum (figure 1) where we grade the models by their degree of causal-or symptom-focus. We have shown in this book (tutorial) that ETM, because of its unequivocal focus on etiology, deserves representation alone at the left or "etiotropic" end of that continuum. The other purist, behaviorism, the model that doesn't recognize any issues unless they are manifested by behavior (symptoms), should obviously hold down the other end of the continuum.
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In between these two approaches are psychodynamic models, which we grade toward the etiotropic side of the continuum, and the cognitive-behavioral model. It is assigned to the nosotropic side.
Because the cognitive-behavioral model identifies and corrects thoughts and behaviors (symptoms) as its first emphasis, albeit it also provides for some attempts to reconcile etiological issues, it should obviously be placed toward the right of center on the continuum.
The psychodynamic model's placement only to the left of center as opposed to its representing the entire etiological spectrum, however, is not so understandable, as psychodynamic models like client centered, some grief resolution and analytical-interpretive therapies have heretofore represented the etiotropic base of therapies. They are known for their searches through internal dynamics and those searches contrast dramatically with the behavioralism-based remedies where no such ventures are allowed (by tenet).
In fact these "contrasts" have caused intraprofessional (mental health) disputes about the efficacy of the competing models for most of this century. And the conflicts have resulted in assiduous efforts to distinguish one from the other.
Given the obvious differences between the ETM approach and the cognitive-behavioral and behavioral models, the question that should be asked and answered for purposes of distinguishment and clarification is: "What is the not-so-obvious difference between the psychodynamic and Etiotropic Trauma Management approaches that results in the assignment (in figure 2) of the former to the nosotropic component of the continuum and the latter exclusively to the etiotropic end, the outcome being a continuum that is almost all nosotropic, with the ETM providing the only exception?
The answer to this important question can be found by examining what I think are the pertinent tenets of psychotherapy, the name given to a host of helping approaches having functions and purposes other than the treatment of psychological trauma, but nonetheless that still serve as the predominant clinical model used by psychodynamic-oriented therapists to address trauma. In this approach, the address of etiologically-oriented issues like values, beliefs, feelings, loss, etc., issues that are also addressed in the ETM model, are simultaneously keyed to the identification of symptoms; albeit, the symptom identification is not usually a focus at the beginning of psychotherapy's application, but it does always become the focus by the end. The eventual intent of the therapy is to assists the individual to either control symptomatic thoughts and behaviors or abandon them because they no longer, post treatment, serve their original purposes.
Thus, the psychodynamic model has as good a reason to be placed on the nosotropic side of the continuum as on the other; we place it on the left of center because its beginning address of internal dynamics is so completely different from behaviorism. Although the application of ETM also results in symptom abatement, the ETM model accomplishes this feat not only without intending to bring about such an ending, but it also emphatically precludes the identification and focusing upon symptoms with the intent to bring about their change.
As discussed in About/ Theory/ Reversing Psychological Etiology, the rationale underpinning this distinguishing injunction is that such symptom focusing or keying paradoxically interferes with efforts to reverse the etiology. This interference is sustained to the degree that at some point in the application of the remedy the following will begin to occur:
for every element of cognitive intent-to-change-a-symptom that is introduced, there is a corresponding reduction in the psychological management system's ability to reconcile/reverse an element of the trauma-induced contradictions to the values, beliefs, images and realities comprising existential identity.
The circle is closed completely, that is, the paradox is sealed into a repetitive cycle, when the unreconciled trauma-induced contradictions to existential identity continue to foster additional symptoms (Figure 3).
The biological sections of this book also attempt to show that this apparently predominantly psychological process has the basis or initiation of its paradoxical roots in the trauma victim's neurology -- the physiology of the brain adapting to psychological trauma.
ETM's (TRT's) theoretical solution for this predicament, the solution being to preclude symptom change efforts while addressing the etiology, allows ETM to get, or to reverse, all of the etiology as opposed to getting or reversing only portions of it: the expectation when applying the nosotropically-influenced psychodynamic approach.
Hence, this special solution that is provided, in theory, by ETM, which solution is a function of TRT's structure and a solution that is not available through the application of psychotherapy, not only provides the principal difference between the ETM method and psychodynamic models, but also the difference between ETM and most other mental health methods taken together, and to especially emphasize the differences between ETM and the behavioral approach and its cognitive-behavioral counterpart, that respectively, make no and little pretense of addressing the trauma's etiology.
ETM's solution, that is, precluding symptom reduction efforts so that the etiology can be more fully addressed, is about 70% a function of stopping the predominant symptom-focused models from interfering with the etiology-reversal process. The other 30% involves shared identification and reconstitution of existential identity.
When we attempted to initiate this reversal by shutting down symptom change efforts, then, an obvious philosophical and methodological confrontation (therapy is not presented in a vacuum) between the competing models ensued. We were trying to prevent symptom address and ensure etiology-reversal and the competing (at least those therapies on the right of the continuum) models were trying to do the opposite, ensure symptom address and deny the need for etiology-reversal.
In the beginning (1979 - 1984), we tried to reconcile this confrontation by applying our models within the milieu of nosotropic concepts. We applied TRT in conjunction with nosotropic concepts and guidelines. After all, they were the predominant clinical/ management models that were controlling the mental health treatment process at the time (see About/ Development/ all chapters.
This attempt at compliance with the status quo failed, however, because the symptom-focused elements that were built into the status quo concepts and guidelines kept the repetitive cycle (described in figure 3) between symptom address and etiology-reversal constant, preventing us from achieving the results that we otherwise expected. The clinical mixtures produced the proverbial 1 step forward and 2 steps backward effect.
After substantial literature reviews of the subject, we concluded that the differences were insurmountable. We slowly gave up trying make the other methods work, but not before delineating additional and apparently even more concrete nosostropic deficiencies. The delineations follow.
Nosotropic deficiencies stem from several interrelated problems. Moreover, they are immutable within the context of the nosotropic management approach.
Generally, the problems result from inherent difficulties with symptoms' presentations. The difficulties produce treatment/management confusion, chaos, and idealogical/ methodological failure.
The first problem with the symptom-focused model is unreliability. That is, psychological symptoms tend to come and go; they change or disappear for long periods, even years or decades.
During the disappearances, there may be nothing to observe or evaluate, which infers that there is no problem, and in the case of psychological trauma and its neurobiological underpinings is often a false and sometimes a prospectively dangerous inference or assumption. Trauma left unaddressed, but defended stoically with intense control measures, can give the appearance that the prospective damage is overcome.
Although behavioral symptoms are not manifested, during this time the combinations of alterations to neuronal structures and functionings can lead to the depletion of neurotransmitters like serotonin, failures (desensitization) of other neurotransmitter receptor systems like the noradrenergic system, changes in neuroenzymic activities like the production of monoamine oxidase, and alterations to many other neural systems required to maintain psychological homeostasis (these neurological terms are explained in detail in the biological sections of the site; it is not necessary to understand the terms now other than to realize that the brain's functionings and its cellular structures are changing while behavioral symptoms may not necessarily be presenting).
This unseen but nonetheless formidable neural action then serves as a time clock that is ticking, but which ticking is not always accompanied by measurable behavioral symptoms, toward the eventual production of the combinations that result in extreme thought/behavioral consequences. They are symptoms that can become problems in and of themselves and that are very measurable, but almost and sometimes too late. For example, depression/disillusionment/despair, obsession, compulsion, aggression, violence and suicide attempts are psychological trauma symptoms that occur almost too late for remedy. And if suicide were considered a symptom of unresolved trauma, then that symptom's address would be too late.
The second problem results from indistinguishability. Psychological symptoms for a host of mental health problems, which can include the retention in memory of the experience of psychological trauma, are similar to the point of being indistinguishable.
This fact sets into motion a potpourri of conflicts over which underlying disorder or presenting symptom is the true problem; which, either symptom or disorder, is the cause of the other? One result of this complication, produced by symptom similarities, is the inevitable diagnostic conflict stemming from different professional perceptions, trainings, and assessment methods; conflict is caused by the various interpretations of the meanings of the like symptoms.
To take an example, of which there are many, assessment and treatment strategy problems routinely result from similarities that exist between symptoms of post-traumatic stress disorder and chemical dependency. On the one hand, and as the literature shows conclusively, the professional trained in post-traumatic stress will tend to view the current untoward behaviors as manifestations of the repressed psychological trauma, including the unequivocal view that the drug abuse is a mask of that trauma. The chemical dependency expert, on the other hand, will argue for the behaviors, including the drug abuse, to be interpreted as consequences of the disease or multifactorial biological and psychological processes comprising the complex syndromes of alcoholism or drug addition.
The third problem stems from negative synergism -- derision. Symptom presentation inconsistencies and similarities, to include those obvious conflicts emanating out of philosophical-and training-based competitions, produce a negative synergism to mental health care that becomes another and greater issue with which to contend. The conflicts resulting from interpretive differences over similarities produce a collision dynamic to attempts to solve problems stemming from or related to psychological trauma. Problem definition, stratagems, implementation procedures and remedies are precluded by the confusion resulting from the symptoms' similarities, presentation inconsistencies and the ideological and methodological derision from contributing to solutions as otherwise is hoped for by the mental health system and the public that uses it.
The results are the creations of huge mental health care compartments that operate within the parameters of the nosotropic approach, but at the same time in completely different clinical worlds from each other, and with hardly any recognition that the unreconcilable competition and subsequent derision even exists. These different worlds need not even be separated by more than a wall divider within a single treatment facility.
Eventually, this nosotropically-caused denominational approach to mental health care becomes primarily a problem with credibility -- multiple paradigms that are usually supported by their own research and that contrast sharply with the other denominations result in questions of logic for the system as a whole. The credibility question goes to the remedial system itself, and the people doing the questioning are the people, clients and patients, who must use it.
These issues of problems and credibility with the primary system, the nosotropic management model, have culminated in and eventually constituted what we consider to be a perpetually self-defeating approach to psychological trauma management. Because ETM focuses only on the etiology of trauma and not upon the measurement, evaluation, or changing of symptoms, the problems represented in the nosotropic model are not represented in ETM. It has good reason, then, to be distinguished from its nosotropic counterpart and competitor.
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