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89. Новые исследования психосоматического понятия специфичности. Г. Поллок (89. Recent Studies of the Psychosomatic Specificity Concept. George H. Pollock)

Chicago Institute for Psychoanalysis; Northwestern University Medical School, USA

In recent years various clinical studies, observations and other investigations have given support to the psychosomatic specificity hypothesis, which was developed in Chicago over the past forty years. In this paper I will briefly report on more current research ralated to this hypothesis.

In 1970, Pilot and I discussed a case of identical twin brothers, one of whom developed a symptomatic duodenal ulcer, while the other was symptom free and radiologically negative. Utilizing our specificity prediction methodology, our Chicago research group was able to correctly predict which twin was ill and which one was symptom free, as well as the diagnosis of the disease in the sick twin. We found a great similarity in the brothers psychological pattern in terms of drive quality and quantity, basic intrapsychic conflicts and defense structures. Since we assumed an identical biological predisposition, the pertinent differences between the twins seemed to cluster around the psychological "onset situation". By this is meant external and internal factors likely to mobilize specific basic conflicts with concomitant affective disruption and physiologic sequelae. Our group was able to "predict" the set of circumstances which could lead to the development of an ulcer in the previously illness-free twin. When life circumstances changed in the direction of the so-called predicted onset situation, the second twin developed an acute duodenal ulcer. As this life situation was reversed, the patient once again became symptom and sign "free". Such an "experiment in nature" provided by life offered us the opportunity to explore the predictive and explanatory power of the psychosomatic specificity hypothesis and to utilize another methodology to test this hypothesis. The study of identical twins allows us to hold constant the X factor and thus reduce the variables studied.

As our explanatory and predictive formulations become more precise, we believe it may be possible to identify "high risk" individuals, and so provide leads to the development of preventative, or prophylactic, interventions in such "loaded" premorbid situations.

To turn to other research: Silvan Tomkins (1962) demonstrated that what can be identified by observation as affective behavior in infants consists, primarily, of the patterned activity of the facial muscles. There seem to be specific associations between particular facial muscles and particular emotions. The activation and selection of the combinations of muscular groups involved is seemingly involuntary and sub-cortically governed. It was Darwin (1872) who attempted to demonstrate that the expression of emotions in man was related to similar expressions in animals. These expressions, evolved from lower forms, undoubtedly had survival value, and it is suggested that they were "selected for" their adaptive value in the evolution of man. More current socio-biological research will undoubtedly attempt to study the impact of such inherited capacities on group adaptation and communication. It was Tomkins (1962), focusing on the facial musculatures of man, who distinguished the following eight basic affective modalities and their main facial characteristics:

(1) Surprise-startle: eyebrows up, eyes blink.

(2) Interest-excitement: eyebrows down, tracking behavior, attitude of looking and listening.

(3) Enjoyment-joy: smile, lips widened up and out, slow deep breathing.

(4) Distress-anguish: crying, arched eyebrows, corners of the mouth turned down, tears and rhythmic sobbing.

(5) Contempt-disgust: sneer, upper lip lifted.

(6) Anger-rage: frown, jaw clenched, face red.

(7) Fear-terror: eyes frozen open, pale, cold, sweaty, facial trembling with hair erect.

(8) Shame-humiliation: eyes cast down, head down.

Basch (1974) has noted, "these behavior patterns involve much more than the easily identifiable activity of the facial musculature. The observable facial expressions reflect an underlying more general muscular and glandular response of the body, including the general physiologic reactions mediated by the autonomic nervous system, which, in later life, are called 'feelings'. Indeed, we have here a series of inherited response patterns through which the organism is mobilized to respond to external or internal stimulation. Neurophysiology studies have corroborated that affective behavior is automatic (not voluntary) and under the direct control of the sub-cortical centers. In evolutionary terms, the old brain, not the new, controls this type of behavior". What one can infer here is the potential for tracing the pathways from emotion to facial muscles back to the central innervation centers and thus complete the neurophysiological loop.

The contributions of Darwin and Tomkins may be seen as directly connected with the work of Cannon, whose studies provide the basic matrix for our clinical psychosomatic specificity research. The specific emotional state produces specific facial and internal physiological reactions. While these specific reactions are not exclusively and invariably linked solely to the one antecedent affective state, none the less, the pattern that emerges is specific, phylo-genetically evolved, and at least initially of survival value. With changes externally in the psycho-social environment, the seemingly universal specific reactions still occur, but the linkage of stimulus field to response field is less obvious, less direct. Our clinical studies may illuminate and augment these promising leads.

Let me now return to clinical research: J. J. Groen, an outstanding Dutch investigator, in a lecture deliviered at Mt. Sinai Hospital in New York in 1950" reported on his research on "Emotional Factors in the Etiology of Internal Diseases". Groen asked two basic questions:

"1) Is there to be found in patients with a certain illness a common personality type, which is more or less specific for their disease, in the sense that it is different from the personality of normal individuals, and of patients with other diseases? Could it be that their personality structure had predisposed these patients to the development of their disease, under the stress of an unfavorable life situation?

2) Was there to be found in the life history of these patients a time relationship between the emotional conflicts which they had experienced and the inception of their disease, and evidence that an emotional conflict situation had come first, and the outbreak or recurrence of the disease second? If this proved to be true, then the possibility of an etiologic role of the emotional conflict, acting on a predisposed personality, could be envisaged. Alternatively, was it possible to trace any so-called 'spontaneous' curves in the course of the disease to an improvement in the patient's life situation?" (1951, p. 73).

The just reported twin study seemingly answers the last question positively but I wish to present Groen's results from his Amsterdam research before discussing his questions and their possible answer. Groen writes:

"A comparison of the psychiatric and psychological data, collected from the various groups of patients, with each other, and with similar data from 'normal' (healthy) persons revealed, that the patients suffering from some diseases showed a number of traits in their personality structure which distinguished them from other groups on the one hand, and from healthy subjects, on the other. It was not so much a difference in individual traits, but rather а соmbinatiоn of certain character traits that distinguished the patients with one disease from another" (1951, p. 79).

Groen found that the emotional difficulties experienced by the patients shortly before the illness appeared or became aggravated were similar to conflicts of patients suffering from the same disease, but these differed from those observed in patients with other diseases. "Internal conflict situations of a definite type, which had preceded the appearance of the disease, were clearly identified in cases of ulcerative colitis, peptic ulcer, and bronchial asthma. In pulmonary tuberculosis and rheumatoid arthritis the findings, though less definite, pointed in the same direction, while in essential hypertension chronic conflict situations also of a distinctive type were encountered. These findings were different from those in 'control' patients who suffered from Hodgkin's- disease, various forms of carcinoma, or leukemia" (1951, p. 79).

Groen summarizes his position on psychosomatic specificity as follows:

"Some individuals, with a certain character structure, seem to be predisposed by the nature of their personality structure to react to a difficult life situation, which threatens their security, not by adequate action, but by emotional conflict. The latter varies with the type of personality and the nature of the stress situation. If the conflict is not discharged by action or speech, it persists and can create a state of acute or chronic emotional tension, which seeks another outlet. In this way it may affect one or another of the organs in the vegetative sphere, in accord with the nature and degree of the tension induced" (1951, p. 80).

Groen found that psychosomatic observations made during the German occupation of the Netherlands in World War II (1940-1945) also supported the validity of the concept of psychosomatic specificity (1951, pp. 83-84). He writes movingly of his observations and one must admire him for his ability to collect data on psychosomatic responses to stress as well as study peptic ulcer, bronchial asthma, ulcerative colitis, migraine, hyperthyroidism, and hypertension while under direct personal threat.

We would answer Groen's questions somewhat differently today than we would have forty years ago. However we might find that many of his queries are still valid today, and clinical investigators should reinvest their interest and energy in studying these stress disorders.

At a future time, we hope to report in fuller detail on studies made at the Chicago Institute by Sackin and myself on childhood peptic ulcer. Briefly, our method allowed us to systematically obtain independent but concurrent data on the child who was ill, his mother, father and selective siblings. We obtained associative anamnestic data on all of our subjects and in some instances were fortunate in being able to follow individuals for a long period of time and in intensive fashion while they were in treatment with different therapists. By correlating these data we could obtain a picture of current individual and crucial familial interactions at conscious and unconscious levels. We did find a specificity in operation - this related to the child's, mother's and father's personality structure, onset and defensive operations of the child, his relationship with his mother and father, and the relationship between the parents themselves. In fact our data suggested that there might be an "ulcerogenic" mother, with a very specific personality organization of her own, but one which was so intertwined with that of her ill child that one might consider a pathological symbiosis at an intrapsychic level that continued from pregnancy onward. On the basis of this research we believe we can identify the "high risk vulnerable child" and our findings suggest the feasibility of preventive intervention in childhood psychosomatic disorders, even before onset of the actual disease.

My purpose in this essay has not been to rehabilitate the psychosomatic specificity hypothesis which I believe to be viable, but to present the historical development of the concept, consider its many dimensions, criticisms, supporting evidence, current research and possible further usefulness. We have and will continue to investigate the hypothesis using different research strategies, always mindful that an hypothesis is at best an approximation to truth.

In our clinical work, a preventive psychosomatic medicine seems more possible than we thought previously. In the light of recent experience, the specificity hypothesis must be considered a cornerstone of such an approach even though it emphasizes many different specificities, each interacting one with the other, with an eventual outcome reflected in a disease process. Mason, a physiologist, has recently written on specificity in the organization of neuroendocrine response profiles (1974).

Mason's research coming from another direction seemingly supports the general hypothesis of psychosomatic specificity. In his June 1975 paper, Mason questions and suggests a re-evaluation of the concept of the nonspecificity of pituitary-adrenal cortical response. He suggests that stress might "be defined in terms of providing a general rubric which encompasses the whole spectrum of interacting factors, stimulus, response, and the intervening processes such as appraisal of threat, coping styles or organization of psychological defenses, and the social milieu, which must all be viewed together in a dynamic perspective when evaluating stimulus-response relationships in any given individual in any given stressful situation" (1975). "Psychosocial stress" may be the terminological successor to "psychosomatic interrelationships". Whatever the label the concepts are old enough to have a history, and they are worthy of ongoing and future study.

Before closing I wish to briefly cite a recently reported prospective study begun nearly thirty years ago by Dr. Caroline B. Thomas at the Johns Hopkins University School of Medicine. Dr. Thomas and her colleagues found that psychobiological characteristics in youth could predict susceptibility to later adult pathology and disease-notably suicide, coronary occlusion, malignant tumor, mental illness and hypertension. Groups of medical students, who in later years developed one of these five disorders, had distinctive psychological and physical profiles while they were in medical school. The data on women "very much" followed trends in the male group. From our point of view these findings, along with those of Groen, Tomkins, and our own twin studies and research on childhood duodenal peptic ulcer, are additional evidences favoring the psychosomatic specificity hypothesis.


1. Basch, Michael F. (1974), The nature, control and communication of affect. [Unpublished manuscript].

2. Cannon, W. B. (1929), Bodily Changes in Pain, Hunger, Fear and Rage: An Account of Recent Researches into the Function of Emotional Excitement. (Second Edition, 1953). Boston: Charles T. Branford Company.

3. Cannon, W. B. (1939), The Wisdom of the Body. New York: W. W. Norton and Co. (revised edition).

4. Darwin, Charles (1872), The Expression of the Emotions in Man and Animals. New York: D. Appleton and Company (reprinted, Chicago: University of Chicago Press, 1965).

5. Groen. J. (1951), Emotional factors in the etiology of internal diseases. Journal of the Mount Sinai Hospital, 18: 71-89.

6. Herrington, B. S. (1975), Study links psychobiological traits to future pathology. Psychiatric News, 10/22:25-26, 32, November 19, 1975.

7. Mason, John W. (1974). Specificity in the organization of neuroendocrine response profiles. In: Frontiers in Neurology and Neuroscience Research, P. Seeman and G. M. Brown, editors. Toronto: University of Toronto Press, pp. 68-80.

8. Mason, John W. (1975), A historical view of the stress field. Journal of Human Stress, 1:22-35.

9. Pollock, George H. and Pilot, Martin L. (1970), Psychosomatic specificity hypothesis testing. Bulletin of the Menninger Clinic, 34:85-88.

10. Tomkins, Silvan S. (1962). Affect. Imagery, Consciousness. I. The Positive Affects. New York: Springer Publishing Ce., Inc.

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