The Psychobiology of Hysteria
Hysteria is often regarded as the archetypal psychodynamic illness. Freud carried out much of his early work on hysteria, and many psychiatrists continue to use a psychodynamic model to understand hysterical phenomena. Although analytic concepts such as symbolism and identification make the psychopathology ofmany individual cases more comprehensible, the fields of experimental psychology, genetics, and cerebral pathology also contribute greatly to our understanding of the condition. It should be noted that "hysteria" does not appear in recent diagnostic nomenclature. Instead, DSM-IV describes and artificially separates 2 groups of conditions, the somatoform and the dissociative disorders, which have a great deal in common. Because of the large overlap between them, it seems appropriate to continue to use "hysteria" as an umbrella term for these 2 groups ofdisorders. Hysterical syndromes are common in general hospital psychiatric practice. In a series of 1752 consecutive psychiatric consultations in a general hospital, I found that hysteria (all subgroups) was diagnosed in 156 of 1127 women (13.8%) and in 58 of 625 men (9.3%) (Mai 1982).
Epidemiologic surveys have shown that these conditions are also prevalent in the community. Woodruffand others (1971) estimated that Briquet's syndrome (somatization disorder) had a prevalence of2% in the general female population, and the NIMH Epidemiological Catchment Area Study found a cross-sectional prevalence of 4% for somatization syndromes (Swartz and others 1991).
Learning theory presupposes that behavior which is rewarded is reinforced and that which is not rewarded is inhibited. It is difficult to demonstrate scientifically that somatization may be learned, although it is reasonable to infer that a child may acquire and develop such behavior by observing a sick parent or sibling. The term "illness behavior" is sometimes used to describe the somatizing patient.
This phrase was introduced by Mechanic (1972) to describe the behavior displayed by individuals in reaction to their perception ofsymptoms and health problems. The success of behavior therapy in the treatment of these disorders also suggests that maladaptive learning may have an important role to play in their etiology. Both Murphy (1982) and Goldberg and others (1989) have successfully applied behavior therapy principles to the treatment of these conditions; they are also a central component ofmy own approach (Mai 1995), particularly in chronic syndromes. Similar principles likely contribute to symptom formation in dissociative disorders.
Familial and genetic factors are of undoubted relevance in hysteria. An increased prevalence of hysteria has been found in the 1st-degree relatives of patients with hysteria. Briquet (1859), Mai and Merskey (1980), and Arkonac and Guze (1963) found that male relatives of patients with Briquet's syndrome have an increased prevalence of antisocial personality and alcoholism and that female relatives ofmales in prison have a high prevalence of Briquet's syndrome. These studies, however, were not designed to disentangle the respective influence of social and genetic factors in this condition.
A few studies have focused more specifically on the genetic transmission of susceptibility to hysterical disorders. In a study comparing concordance in monozygotic and dizygotic twins, Torgersen (1986) found 29% concordance in the former and 10% in the latter. The author conceded, however, that similarity of childhood experience may have influenced these rates. In an extensive familial study, Ljungberg (1957) concluded that hereditary factors of a polygenic kind play a significant role in the development of hysteria, but this conclusion was not confirmed in a subsequent analysis ofhis data (Shields 1982). Similar negative conclusions were found in a study comparing concordance of hysteria in monozygotic and dizygotic twins (Slater 1961). After reviewing this report, Shields (1982) concluded that there is some evidence supporting the role of genetic factors in hysterical personality, but little for other hysterical syndromes. Cloninger and others (1984) drew a similar conclusion with reference to functional somatic symptoms. Although it did not deal specifically with hysteria, their conclusion is supported by a more recent study by Muhs and Schepank (1995), who compared "neurosis" concordance rates in 21 monozygotic and 29 dizygotic twins. These authors found that heredity factors were more important in personality disorders than in more transient neurotic states and that environmental factors exercised some protective influence.
The relationship between hysteria and cerebral pathology is ofgreat interest. Merskey and Buhrich (1975) found that a high proportion ofpatients with hysteria had cerebral pathology, in particular epilepsy and multiple sclerosis, but this has not been confirmed in a nonneurological population (Roy 1979). It has also been proposed, on a priori theoretical grounds, that hysteria is a dysfunction ofmemory and attention associated with inhibition of afferent stimulation (Ludwig 1972) and that there is bifrontal cerebral impairment, particularly in the nondominant hemisphere (Flor- Henry and others 1981). Although practical evidence in favor of these theoretical constructs is as yet lacking, it should be remembered that conversion symptoms and organic cerebral disease are not mutually exclusive phenomena. Not only may they occur together, but cerebral pathology may itself promote the development of somatization.
The study ofhysterical syndromes has been bedeviled for centuries by semantic confusion, clinical prejudice, and patient defensiveness. Because of their clinical complexity, these syndromes present a major challenge to the treating physician, and they may be poorly managed on this account. The physicians most interested in the management ofpatients with these conditions (the liaison psychiatrists) often do not see them because of the reluctance of consultants to refer such patients or of the patient to see a psychiatrist. Furthermore, the referral is sometimes carried out in a threatening manner, thus reinforcing patient belief systems that reject possible psychogenic factors. By contrast, the physicians who do see the patients (particularly neurologists and general internists) have little interest in treatment once organic disease has been ruled out. Education both ofphysicians and of the public is necessary to minimize these impediments to effective management of the somatizing patient.
Fortunately, there is light at the end of the proverbial tunnel. Although the areas ofgenetics and cerebral pathology in relation to hysteria have developed little over the last decade, excellent recent publications on the phenomenology ofhysteria (Merskey 1995) and on the treatment offunctional somatic symptoms (Mayou and others 1995) have contributed much to our understanding ofthese conditions, and their continued investigation is now on a firm scientific foundation. Further research into the epidemiology, psychopathology, genetics, and management ofthese conditions would not only be of great theoretical interest but would also help reduce the huge burden that they place on the health care system (Demers 1995).
Arkonac 0, Guze S. 1963. A family study ofhysteria. N Engl J Med 268:239-42.
Briquet P. 1859. Traite de l'hystdrie. Paris: Bailliere. Cloninger C, Sigvardson S, Von Knorring A, and others. 1984. Adoption study ofsomatoform disorders. Arch Gen Psychiatry 41:863-71.
Demers M. 1995. Frequent users of ambulatory health care in Quebec: the case ofdoctor shoppers. Can Med Assoc J 153:37-42.
Flor-Henry P, Fromm-Anch D, and others. 1981. A neuropsychosocial study of the stable syndrome of hysteria. Biol Psychiatry 16:601-26.
Goldberg D, Gask L, O'Dowd T. 1989. The treatment of somatization: teaching techniques of reattribution. J Psychosom Res 33:689-95.
Ljungberg L. 1957. Hysteria: a clinical prognostic and genetic study. Acta Psychiatry Neurol Scand 32(112 Suppl). Ludwig A. 1972. Hysteria: a neurological theory. Arch Gen Psychiatry 27:771-7.
Mai F. 1995. "Hysteria" in clinical neurology. Can J Neurol Sci 22:101-10.
Mai FM. 1982. Briquet's syndrome (hysteria) and the physician. Can Med Assoc J 127:99-100.
Mai FM, Merskey H. 1980. Briquet's treatise on hysteria. Arch Gen Psychiatry 37:1401-5.
Mayou R, Bass C, Sharpe M. 1995. Treatment of functional somatic symptoms. Oxford: Oxford University Press.
Mechanic D. 1972. The concept of illness behavior. J Chron Dis 15:189-94.
Merskey H. 1995. The analysis of hysteria. London: The Royal College of Psychiatrists Academic Series.
Merskey H, Buhrich N. 1975. Hysteria and organic brain disease. Br J Med Psychol 48:359-66.
Muhs A, Schepank H. 1995. The influence of hereditary factors in psychogenic disorders. Psychopathology 28:177-84.
Murphy G. 1982. The clinical management of hysteria. JAMA 247:2559-64.
Roy A. 1979. Hysteria: a case note study. Can J Psychiatry 24:157-60.
Shields J. 1982. Generoca; studies ofhysterical disorders. In: Roy A, editor. Hysteria. New York: J Wiley. p 41-56.
Slater E. 1961. The thirty-fifth Maudsley lecture: hysteria 311. J Ment Sci 107:359-81.
Swartz M, Landerman R, George LK, Blazer D, Escobar J. 1991. Somatization disorder. In: Robins L, Regier D, editors. Psychiatric disorders in America. New York: Free Press. p 220-57.
Torgersen S. 1986. Genetics of somatoform disorders. Arch Gen Psychiatry 43:502-5.
Woodruff R, Clayton P, Guze S. 1971. Studies of diagnosis outcome and prevalence. JAMA 215:425-8.
rating: 4.88 from 8 votes | updated on: 30 Apr 2007 | views: 5394 |