CENTER ON BEHAVIORAL MEDICINE
Psychogenic: Related Paper
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Current Research on Psychogenic
Psychogenic symptoms, regardless of whether they progress into diagnosable illnesses or psychosomatic diseases, are expressed through the body, involve the autonomous nervous system and provide a pathway of response to situations of endogenous or exogenous emotional disturbance (Kirmayer, Groleau, Looper, & Dao, 2004). Psychogenic symptoms are generally short-lived phenomena, transitory in nature, bordering on pathology, traceable to an event-stimulus, have an emotional content causally and chronologically connected to the precipitating event, and most often cease with the cessation of the stimulus. In many cases, an intrapsychic processing of the event is patently lacking and the participation of the individual’s personality is limited (Merskey, 2004). Typical examples of psychogenic symptoms are those connected with the fright-fear reaction (fright is the unexpected sensory perception of threat, fear is the understanding of the impending or just escaped danger) which may cause tachycardia, hyperventilation, hypertension, cold sweat, tremor, fainting, flushing or pallor of the face and other reactions (Blodgett, 1985). These physical reactions are generally immediate and short lived but can also be delayed or ex post and last for a considerable time. In psychoanalytic theory, psychogenic symptoms have an etiology rooted in emotional conflict: it is the intrapsychic processing of a situation-stimulus that is the cause of physical manifestations. The symptom is a complex defense mechanism rich in psychological meaning (McCabe, 2000).
The change of paradigm to a biopsychosocial model that has taken place in modern medicine is important in considering that among the most assiduous, and often most disappointed visitors to outpatient clinics or to the family doctor are individuals who complain of signs and symptoms that have no apparent physiological foundation. Frustrating for the doctors and for the patients themselves, the difficult and at times impossible diagnosis and treatment of psychogenic symptoms put a quantitatively important burden on the healthcare system. A group of researchers of the Department of Public Health and Policy in London, England reports that twenty percent of first-time medical visits in seven medical specialties are motivated by symptoms that do not find explanation or resolution within the traditional biomedical approach and that they put to the test, sometimes for years, the diagnostic and relational resources of the doctor and other caregivers (Nimnuan, Hotopf, & Wessely, 2001).
With a biopsychosocial lens, it is possible to differentiate between diseases for which biological factors, such as toxic agents, infections, traumas or genetic factors have a preponderant causative role and diseases for which the psychosocial factors, under the guise of emotions and conflicts, real or perceived, are the determinant ones (Kirmayer et al., 2004). In this light, the indivisible nature of the individual is kept firmly in focus and pathological symptoms or phenomena are investigated in a complementary and contemporaneous way from a psychological and physiological point of view.
Historically, psychogenic symptoms have been recognized as physiological responses to stressors whose function is to attenuate or regulate anxiety since the early decades of the Twentieth century. Although controversial, Reich’s energy model (Best, 1999; Mann & Hoffman, 1992), clearly derived from Freud’s dynamic theory (Freud, 1996), was based on the assumption that all biopsychological processes follow a pattern of charging and discharging of energy, whereby a mechanical load is converted to an electric charge, which is followed by a discharge and a consequent mechanical relaxation. When this psychodynamic progress is impeded the organism lives in a state of continuous charge; if this condition becomes chronic, it morphs into a powerful structure of defense. In this perspective, physiological and psychological disorders can both be traced to the existence of the defense mechanisms through which the chronic overload may be expressed (Best, 1999; Efron, 1997).
According to an early interpretative model first developed by Bikov (1933; Bikov, 1939), psychogenic pathology was considered a maladaptive associative tie between a stimulus and the reaction mechanisms coordinated by our most advanced cerebral structures, chiefly the prefrontal cortex. Negative interactions at the cortical level were postulated to determine a pathological response in the organism. Advancing the hypothesis of existential analysts according to whom the psyche determines the modality with which the body exists in the world, Boss (2000) believes that pathology expresses either the only modality with which the body opens up and relates to the world, or the excluded modalities, those that cannot be safely expressed and thus are manifested pathologically. From this point of view, the parts of the body attacked by the disease symbolize those relationships with the world that have been pathologically interrupted or exasperated. What determines the illness, according to this view, is therefore not an interaction between mind and body, but it is an alteration of the relationship between the subject and the world. From within a Gestalt theory, von Weizsächer (1950) thought that for a full understanding of pathological phenomena it is necessary to differentiate between causative events in the life of an individual that are perceived as physical changes, from those that expressed by thoughts, dreams, fantasies, and finally from those that translate in relationships and interactions with the others.
Among the researchers and theorists that focused more on biological aspects of pathology, Cannon (1914) introduced the idea that psychogenic symptoms may be due to stress. The adopted behavior could be of "attack" or "escape" according to Cannon (1933; Cannon, 1936), or of "adaptation" according to a later development of the theory by Selye (1973). When the efforts of the subject fail because the level of anxiety exceeds the individual’s ability to respond, the lowering of the immune defenses of the organism creates vulnerability to disease (Selye, Goldberger, & Breznitz, 1993). Alexander (1941) spoke of this condition as “specificity of conflict". He maintained that just like laughter is the response to joy and crying is to pain, hypertension is the response to anger and fear, gastric secretions to hunger, asthma to an unconscious and repressed impulse to scream, and so forth. Alexander’s work marks the birth of this symbolic language of the body’s organs. In 1954, Alexander expanded on prior research and contributed greatly to our understanding of the specificity of psychosomatic diseases, classifying them in a coherent system that instituted a parallelism between specific intrapsychic conflicts (in psychoanalytic terms) and psychological disturbances. According to Alexander, psychosomatic diseases and their symptoms derive from an altered distribution of the energy provided by the nervous system when it induces the "fight" or “flight” response in real or perceived danger situations (Alexander, 1944). Therefore, in situations of chronic anger, aggression, or hostility, the noradrenergic sympathetic system is subjected to the pressure of repressed emotions, such as aggressiveness and competitiveness, and remains in a state of semi-permanent noradrenergic excitation. In his pioneering research, Alexander maintained that emotional conflict states were involved in the etiology of several psychosomatic illnesses through the mediation of central nervous system (CNS). According to his views, the two components of the CNS, the sympathetic and the parasympathetic, play a role in the course of various diseases, as for example the parasympathetic in peptic ulcers and the sympathetic in essential hypertension (Alexander, 1950, 1954).
Subsequent studies, particularly those carried out in the last twenty years, have made it clear that it is not only the nervous system that is affected by emotional reactions, but also the endocrine system (Carlson, 2005; Rubin, 2003; Sonino & Fava, 1998). Virtually all hormones (ACTH, cortisol, GH, prolactin, LH, testosterone and other gender-related hormones) react to emotional stimulation, while neuropeptides are now considered as the most likely points of contact between the brain and the rest of the organism, i.e. between mind and body (Ayd, 1991; Chrousos, 1985; Dallman, Akana, Strack, Hanson, Sebastian, Chrousos, McCarty, Pacák, Cizza, & Sternberg, 1995; Maes, Claes, Vandewoude, & Schotte, 1992).
The hypothalamic-pituitary-adrenal axis, through the CRF (Corticotrophin Release Factor), the adrenocorticotropic hormone (ACTH) and cortisol, is emerging as the most important in the response by the individual to stressful agents, whether physical or psychological (Crane, Ebner, & Day, 2003; Ginsberg, 2005; Gutman, Owens, Skelton, Thrivikraman, & Nemeroff, 2003; Volpi, Rabadan-Diehl, & Aguilera, 2004). CRF and ACTH also mediate important functions of the CNS. The CRF has numerous behavioral influences, as does the ACTH. In many experiments cortisol and ACTH are elevated by stress but they can be reduced with a relaxation treatment that includes biofeedback (Dallman et al., 1995). The hypothalamic-pituitary-gonadal axis is equally important; one of its most remarkable psychogenic effects is the so-called reversible dwarfism in institutionalized children who are deprived of affection, where the delay in growth is secondary to lower levels of GH, which is secreted again in the right quantities as a result of affective contact (Pelleymounter, Joppa, Ling, & Foster, 2002). LH and testosterone secretions in males increase as a result of visual stimuli of explicit sexuality, while they are reduced as a result of stress situations where the subject perceives a threat to one’s self (Morgentaler, 1999). The hypothalamic-pituitary-prolactin axis is not only involved in breast-feeding, but it is also activated in situations of stress. Disorders of the menstrual cycle that have a psychogenic basis may be mediated by anomalous stress-induced elevations of prolactin (Campino, Torres, Ampuero, & González, 1999; Roy-Byrne, Rubinow, Hoban, & Grover, 1987; Torner & Neumann, 2002; Yuen, 1986).
Another area of intense research and that completes the picture of connections between psychological and biological nature of human life is the study of neuropeptides, or peptides that are active in association with neural tissue. As of 2006, over 40 neuropeptides have been identified (Brain & Cox, 2006). Present in the brain and in peripheral organs, many neuropeptides (as for example CRF, endogenous opioid peptides such as endorphins and encephalin, LH-RH, gastrointestinal TRH, peptides, Y-neuropeptides, and immunomodulatory peptides) are important regulators of nervous and metabolic functions (Williams, Cai, Elliott, & Harrold, 2004). All neuropeptides appear to be extremely sensitive to emotional stimuli and situations of stress and represent a very important tool in mediating mind-body interactions either in inducing or in reducing the effects of a psychogenic process, as for example in the etiology of eating disorders (Jimerson & Wolfe, 2004; Wilding, 2002).
The list of psychogenic symptoms that may progress into full-blown pathologies is very long. Among the most important are the psychogenic loss of appetite or exaggerated hunger that may lead to the eating disorders anorexia, bulimia and obesity (Dowson, 2004; Jimerson & Wolfe, 2004; Myers & Smith, 1985; Wilding, 2002); symptoms affecting the gastrointestinal system that may lead the development of colitis, ulcers, chronic gastritis, gastric acidosis, pyloric stenosis, irritable or spastic colon, stypsis, nausea and vomit, and psychogenic diarrhea (Anonymous, 1992; Mookerjee & Mukhopadhyay, 1998; Yoneda, Watanobe, & Terano, 2001); symptoms affecting the respiratory system as for example psychogenic cough, bronchial asthma attacks, hyperventilation, dyspnea, and the hiccups (Ayd, 1991); symptoms that affect the cardiovascular system such as arrhythmias, coronary disease (angina pectoris, myocardial infarction), essential hypertension, and migraines (Pert, 2002); symptoms that appear on the skin, i.e. psoriasis, flushing and redness, acne, dermatitis, pruritus, hives, hair loss, dry skin, profuse perspiration (Calikuu, Yucel, Polat, & Baykal, 2002); symptoms that affect the musculoskeletal system such as tension headaches, muscular cramps, wryneck, fibromyalgia, arthritis, back pain; symptoms that first appear in the genitourinary system, for example menstrual pains, difficulty in urination, enuresis, impotence (DiBartolo & Barlow, 1996; McCabe, 2000; Riley & Riley, 2000; Wylie, 1997); symptoms manifested in the endocrine system such as hypopituitarism, hyper- or hypothyroidism, hypoglycemia, diabetes mellitus (Björntorp, Holm, & Rosmond, 1999; Jonsdottir, 2000).
In conclusion, it can be stated that psychogenic symptoms are those that make use of our most archaic defense mechanisms, by expressing and releasing emotional discomfort through physical manifestations in the body. These symptoms may reveal the anxiety, the suffering, and the existence of emotions that are much too painful to be acknowledged and openly experienced. They are pathways for the discharge of otherwise uncontainable emotional energy. They are a creative adaptation to pain, especially when the individual lacks metaphorical or symbolic modes of expression or lacks the awareness of the real causes underneath his or her psychological distress. This type of patient may be well connected with reality, but possessing a worldview that is rich in facts and concreteness while poor in emotions and expression of affect. These are individuals who have difficulty in managing feelings of anger, fear, disappointment, displeasure, or dissatisfaction. All their defensive efforts are directed to circumscribing, negating or pushing away unacceptable affective content, even at the cost of destroying their body.
Alexander, F. (1941). Clinical versus experimental approach in psychosomatics. Psychosomatic Medicine, 3, 330-336.
Alexander, F. (1944). Fundamental concepts of psychosomatic research: Psychogenesis, conversion, specificity. Archives of Neurology & Psychiatry (Chicago), 51, 208-210.
Alexander, F. (1950). Psychosomatic medicine: Its principles and applications: W. W. Norton & Co, Inc.
Alexander, F. (1954). The psychosomatic approach in medical therapy. Acta Psychotherapeutica, Psychosomatica et Orthopaedagogica, 2, 284-300.
Anonymous. (1992). Psychogenic vomiting--a disorder of gastrointestinal motility? The Lancet, p. 279.
Ayd, J. F. J. (1991). Stress, neuropeptides, and systemic disease. JAMA: Journal of the American Medical Association, 266(2), 280.
Baxter, C. L., & White, W. D. (2003). Psychogenic coma: A case report. International Journal of Psychiatry in Medicine, 33(3), 317-322.
Best, A. R. (1999). The holistic healing resource of erotic energy: From Wilhelm Reich's orgone energy to modern interdisciplinary theories. Univ Microfilms International.
Bhatia, M. S., Chandra, R., & Vaid, L. (2002). Psychogenic cough: A profile of 32 cases. International Journal of Psychiatry in Medicine, 32(4), 353-360.
Bikov, K. M. (1933). Functional connection of the brain cortex with the internal organs. Fiziologicheskii Zhurnal SSSR, 16, 93-110.
Bikov, K. M. (1939). The cerebral cortex and its relation to the internal organs. Arkhiv Biologicheskikh Nauk, 54, 3-21.
Björntorp, P., Holm, G., & Rosmond, R. (1999). Hypothalamic arousal, insulin resistance and type 2 diabetes mellitus. Diabetic Medicine, 16(5), 373-383.
Blodgett, N. (1985). Stage fright. ABA Journal, 71(10), 26.
Boss, M. (2000). Recent considerations in daseinsanalysis. Humanistic Psychologist, 28(1), 210-230.
Brain, S. D., & Cox, H. M. (2006). Neuropeptides and their receptors: Innovative science providing novel therapeutic targets. British Journal of Pharmacology, 147, S202-S211.
Breseta, M. A. (1938). Tics in childhood. Archives of Pediatrics, 55, 703-712.
Calikuu, C., Yucel, B., Polat, A., & Baykal, C. (2002). Expression of anger and alexithymia in patients with psychogenic excoriation: A preliminary report. International Journal of Psychiatry in Medicine, 32(4), 345.
Campino, C., Torres, C., Ampuero, S., & González, G. B. (1999). Bioactivity of prolactin isoforms: Lactation and recovery of menses in nursing women. Human Reproduction, 14(4), 898-905.
Cannon, W. B. (1914). The interrelations of emotions as suggested by recent physiological researches. American Journal of Psychology, 25(2), 256-282.
Cannon, W. B. (1933). Chemical mediators of autonomic nerve impulses. Science, 78, 43-48.
Cannon, W. B. (1936). Gray's objective theory of emotion. Psychological Review, 43, 100-106.
Carlson, L. E. (2005). Introduction to psychoneuroimmunology. Canadian Psychology, 46(1), 53-55.
Chrousos, G. P. (1985). Corticotrophin releasing factor: Basic studies and clinical applications. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 9(4), 349-359.
Crane, J. W., Ebner, K., & Day, T. A. (2003). Medial prefrontal cortex suppression of the hypothalamic–pituitary–adrenal axis response to a physical stressor, systemic delivery of interleukin-1ß. European Journal of Neuroscience, 17(7), 1473-1481.
Dallman, M. F., Akana, S. F., Strack, A. M., Hanson, E. S., Sebastian, R. J., et al. (1995).
The neural network that regulates energy balance is responsive to glucocorticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. In Stress: Basic mechanisms and clinical implications. (pp. 730-742): New York Academy of Sciences.
DiBartolo, P. M., & Barlow, D. H. (1996). Perfectionism, marital satisfaction, and contributing factors to sexual dysfunction in men with erectile disorder and their spouses. Archives of Sexual Behavior, 25(6), 581.
Dowson, J. (2004). Associations of the severity of depressive disorders in women with psychogenic low weight. Journal of Affective Disorders, 78(3), 279-284.
Efron, A. (1997). Life energy reading: Wilhelm Reich and literature. Paunch, 67-68.
Freud, S. (1953). Fragment of an analysis of a case of hysteria. London: Hogarth.
Freud, S. (1996). Zwangsvortellungen und Phobien: Ihr psychischer Mechanismus und ihre Aetiologie. Jahrbuch der Psychoanalyse, 37, 196-205.
Ginsberg, A. B. (2005). Negative feedback of the hypothalamic-pituitary-adrenal axis: Glucocorticoid modulation of stress-induced gene expression in the paraventricular nucleus and pituitary gland. University Microfilms International.
Grumet, G. W. (1987). Psychogenic coughing: A review and case report. Comprehensive Psychiatry, 28, 28-34.
Gutman, D. A., Owens, M. J., Skelton, K. H., Thrivikraman, K. V., & Nemeroff, C. B. (2003). The corticotropin-releasing factor-sub-1 receptor antagonist R121919 attenuates the behavioral and endocrine responses to stress. Journal of Pharmacology and Experimental Therapeutics, 304(2), 874-880.
Jimerson, D. C., & Wolfe, B. E. (2004). Neuropeptides in eating disorders. CNS Spectrums, 9(7), 516-522.
Jonsdottir, I. (2000). Neuropeptides and their interaction with exercise and immune function. Immunology & Cell Biology, 78(5), 562-570.
Kardos, P. (2000). Proposals for a rationale and for rational diagnosis of coughs. Pneumologie, 54, 110-115.
Kirmayer, L. J., Groleau, D., Looper, K. J., & Dao, M. D. (2004). Explaining medically unexplained symptoms. Canadian Journal of Psychiatry, 49(10), 663.
Maes, M., Claes, M., Vandewoude, M., & Schotte, C. (1992). Adrenocorticotropin hormone, ß-endorphin and cortisol responses to oCRF in melancholic patients. Psychological Medicine, 22(2), 317-329.
Mann, W. E., & Hoffman, E. (1992). The legacy of Wilhelm Reich: Many contemporary holistic approaches to mind-body healing have their roots in the pioneering theories of this controversial psychiatrist. Yoga Journal (106), 30.
McCabe, D. (2000). Evaluation of a cognitive behavior therapy program for people with sexual dysfunction [Research summary]. The Canadian Journal of Human Sexuality, 9(3), 213.
Merskey, H. (2004). Somatization, hysteria, or incompletely explained symptoms? Canadian Journal of Psychiatry, pp. 649-651.
Mookerjee, G., &
Mukhopadhyay, A. (1998).
Patterns of stress states and motivation of upper and lower
disorder patients. Psychological Studies, 43(3), 80-84.
Myers, K. M., & Smith, M. S. (1985). Psychogenic polydipsia in a patient with anorexia nervosa. Journal of Adolescent Health Care, 6(5), 404-406.
Nimnuan, C., Hotopf, M., & Wessely, S. (2001). Medically unexplained symptoms: An epidemiological study in seven specialities. Journal of Psychosomatic Research 51(1), 361-367.
Pelleymounter, M. A., Joppa, M., Ling, N., & Foster, A. C. (2002). Pharmacological evidence supporting a role for central corticotropin-releasing factor-sub-2 receptors in behavioral, but not endocrine, response to environmental stress. Journal of Pharmacology and Experimental Therapeutics, 302(1), 145-152.
Pert, C. B. (2002). The wisdom of the receptors: Neuropeptides, the emotions, and body-mind. Advances in Mind-Body Medicine, 18(1), 30.
Riley, A., & Riley, E. (2000). Controlled studies on women presenting with sexual drive disorder: Endocrine status. Journal of Sex & Marital Therapy, 26(3), 269-283.
Roy-Byrne, P. P., Rubinow, D. R., Hoban, M. C., & Grover, G. N. (1987). TSH and prolactin responses to TRH in patients with premenstrual syndrome. American Journal of Psychiatry, 144(4), 480-484.
Rubin, R. T. (2003). Psychoneuroendocrinology: The scientific basis of clinical practice. American Journal of Psychiatry, 160(11), 2073.
Selye, H. (1973). The evolution of the stress concept. American Scientist, Vol. 61(6), 692-699.
Selye, H., Goldberger, L., & Breznitz, S. (1993). History of the stress concept. In Handbook of stress: Theoretical and clinical aspects (2nd ed.). (pp. 7-17): Free Press.
Sonino, N., & Fava, G. A. (1998). Psychological aspects of endocrine disease. Clinical Endocrinology, 49, 1-7.
Torner, L., & Neumann, I. D. (2002). The brain prolactin system: Involvement in stress response adaptations in lactation. Stress: The International Journal on the Biology of Stress, 5(4), 249-257.
Volpi, S., Rabadan-Diehl, C., & Aguilera, G. (2004). Vasopressinergic regulation of the hypothalamic pituitary adrenal axis and stress adaptation. Stress: The International Journal on the Biology of Stress, 7(2), 75-83.
von Weizsächer, V. (1950). Funktionswandel und Gestaltkreis. Deutsche Zeitschrift für Nervenheilkunde, 164, 43-53.
Weinberg, E. G. (1980). Honking: Psychogenic cough tic in children. South African Medicine Journal, 57, 198-200.
Wilding, J. P. H. (2002). Neuropeptides and appetite control. Diabetic Medicine, 19(8), 619-627.
Williams, G., Cai, X. J., Elliott, J. C., & Harrold, J. A. (2004). Anabolic neuropeptides. Physiology & Behavior, 81(2), 211-222.
Wylie, K. R. (1997). Treatment outcome of brief couple therapy in psychogenic male erectile disorder. Archives of Sexual Behavior, 26(5), 527.
Yoneda, M., Watanobe, H., & Terano, A. (2001). Central regulation of hepatic function by neuropeptides. Journal of Gastroenterology, 36(6), 361.
Yuen, B. H. (1986).
in breast milk and plasma of women with hyperprolactinemia,
and menstrual dysfunction. International Journal of Fertility, 31(1),