Schizophrenia

Schizophrenia
-Shannon Sumrall, M.A., M.Ed., LPC, NCC

The diagnosis of schizophrenia is controversial, often misused, and often socially damaging to patients. In our contemporary culture schizophrenia is considered a severe mental disorder that is characterized by a wide range of symptoms. The cause of schizophrenia is not known, as scientists are not even sure if it is one disorder or several with different causes, although there are many theories and a great deal of research into possibilities. Cross-cultural research has identified the diagnosis worldwide across human populations. The two main prevailing views of the diagnosis of schizophrenia are the medical disease model, which is currently the most popular, that sees schizophrenia as a biological disorder of the brain and the other view that sees schizophrenia as a transitory emotional disorder with an environmental cause. The current understanding of schizophrenia is well explained in the following: "No specific gene has yet been found; no biochemical defect has been proven responsible; and no specific stressful event seems sufficient, by itself, to produce schizophrenia" (BBC News b, 2002). The American Psychiatric Association's (APA) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) defines schizophrenia as follows: "Schizophrenia is a disorder that lasts for at least 6 months and includes at least one month of active-phase symptoms (i.e. two [or more] of the following: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms)" (APA, 2000, p. 298). The negative symptoms include affective flattening, alogia, and avolition. The related but distinct disorders of schizophreniform and schizoaffective disorders are also explained. The DSM-IV-TR also draws distinctions between positive and negative symptoms. Paranoid, disorganized, and catatonic are subtypes of schizophrenia which are defined by the DSM-IV-TR. The DSM-IV further elaborates that "No single symptom is pathognomonic of Schizophrenia;" (p. 299).

Schizophrenia is believed to be widespread with worldwide lifetime prevalence rates estimated to be at 0.2 % to 1.5% of the general population, meaning approximately 1% of the population develop schizophrenia during their lives, with men and women being equally affected (Jablensky, 1995). The disruptions of this diagnosis can cause considerable problems with the social, emotional, and economic realms of life. Rupp & Keith (1993) estimated that schizophrenia medical costs in the United States had been between $16 and $19 billion for 1990 alone, accounting for 2.5% of the total health care expenditures the U.S. that year.

There has been a substantial effort from those that support the medical disease model to demonstrate that schizophrenia has a biological origin. These include family, twin, adoptee, offspring of twins, and linkage and association studies supporting a genetic predisposition (Gottesman & Shields, 1972; Sherman et al., 1997), studies showing structural brain abnormalities (Chua & McKenna, 1995; Andreasen, 1997), and studies implicating biochemical problems in the brain, such as in the functioning of the dopamine neurotransmitter in schizophrenia (Davis, Kahn, Ko, & Davidson, 1991; Carlsson, 1995; Maas et al. 1997). The conclusions to be drawn from the medical disease model and the research pointing to genetic defects, brain defects, and biochemical defects is that schizophrenia is an organic and incurable disease due to brain lesion or inborn metabolic defects (Modrow, 1995).

Critics of the genetic predisposition studies point out that if schizophrenia is caused by a genetic defect then the concordance rate in identical twins should be 100% and not the 46% identified by Gottesman and Sheilds and that this 46% is actually a discordance in need of explanation (Modrow, 1995). Another genetic fact is that children of schizophrenics that are raised by a schizophrenic parent, with environmental and genetic factors working in similar directions, have only one chance in five of developing schizophrenia (Karon, 1995). Structural brain abnormality studies that demonstrate defects in schizophrenics have also been criticized and refuted by various other studies that demonstrate no difference between schizophrenics and normal controls (Weinbeger, Wagner, & Wyatt, 1983; Yates, Jacoby and Andreasen 1987; Smith, Baumgartner & Calderon, 1987). It has been argued that role of biochemical changes in the brain are not a cause of schizophrenia, but rather an effect of the condition; and the increase of dopamine receptors in the brains of chronic schizophrenics is a reaction to prolonged stress from their condition since dopamine is a stress hormone (Modrow, 1995).

The long term prognosis, gained from studies that have followed schizophrenic patients for more than 25 years, is that approximately 35% fully recover and another 35% function independently and are self supporting with some possibility of residual symptoms (Bertram, 1995). A long-term follow up study of profoundly disabled schizophrenics twenty to twenty-five years after their hospital release, with an average of 16 years of schizophrenic symptoms and an average total disability of 10 years, found that 68% of these subjects were free of schizophrenic symptoms and 45 % were free of all psychiatric symptoms (Harding, 1984; Harding, et al., 1987). Three major long term studies have also found that about 25% of schizophrenic patients ultimately made a full recovery (Bleuler, 1972; Ciompi & Muller, 1976; Huber, Gross, & Schuttler, 1975).

The prevalence of schizophrenia across cultures at a constant rate has been shown from the results of a series of studies performed by the World Health Organization (WHO), that began with the International Pilot Study of Schizophrenia in the 1960s (WHO, 1979). WHO studies have included thousands of patients in 20 separate research centers in 17 countries (Tanaka-Matsumi & Draguns, 1997). These studies included the following cities: Aarhus (Denmark), Agra (India), Cali (Columbia), Ibadan (Nigeria), Taipei (Taiwan), Prague (Czechoslovakia), London (United Kingdom), Moscow (Soviet Union), and Washington, D. C. (Jablensky, 1987). The WHO studies have produced two major findings showing comparable rates of schizophrenia around the world, but very different courses for the diagnosis (Siegert, 2001). Schizophrenic patients from the Third World displayed a significant difference in the course and outcome of their illnesses (as shown via a two-year follow-up), displaying a remarkable tendency to recover more quickly and completely from their illness (Sass, 1997). The first finding has not been controversial while the second has produced controversy with several diverse explanations. Siegert (2001) explains this from the point of the existence of specific domains of cognition that are universal and that by examining the typical cognitive difficulties, with the relevant cognitive domains in mind, and with an understanding of the likely evolutionary function of these cognitive modules we could be lead to a clearer understanding of the cognitive basis of schizophrenia. Modularity, evolution, and culture could be integrated in this model to develop cross-cultural models of disturbed cognition in schizophrenia (Siegert, 2001). Another explanation is that the Third World settings researched by the WHO studies were all in developing cultures, where the forces of Westernization, industrialization, and modernization were powerful influences on the environment (Sass, 1997). Contrasted to the developing Third World societies is research with hunter-gatherer, tribal, and preliterate cultures, that have had limited contact with technologically advanced societies, which seems to indicate that they rarely experience schizophrenia (Torrey, 1980; Warner, 1985).

Many psychiatrists, and others who care for the mentally ill, are often trained from schizophrenia textbooks written at the turn of the last century by such notables as Kraepelin and Bleuler whose books state flatly that improvement and recovery are not to be expected; and the American Psychiatric Association's newest Diagnostic and Statistical Manual also repeats this old pessimism (Harding, 2002). The belief that schizophrenic disorders have an irrevocably progressive and deteriorating course with a malignant final result, will inevitably color the treatment goals (Perris, 1989). This can be seen in the fact that the most commonly used therapy in treating schizophrenics is the administration of neuroleptic drugs, which are known to cause severe and often irreversible brain damage, which is justified on the basis that schizophrenia is a biochemical imbalance in the brain (Modrow, 1995). These are the same drugs that are known as pharmaceutical lobotomies or chemical straightjackets which have been used in controlling the mentally retarded, animals, Soviet political dissidents, rebellious children, and prisoners (Modrow, 1995). If at least one-third of the patients can fully recover and two-thirds socially recover it seems a serious matter to produce brain damage; and there is also evidence that regardless of short-term benefits, long-term medication may have the consequence of precluding a full recovery (Karon, 1995). Another problem is that by insisting that the cause of schizophrenia is totally biological it becomes virtually impossible for patients to achieve psychological insight into their situation and they are left to view aspects of themselves as meaningless and inscrutable conditions of disease (Modrow, 1995).

Economics has been a determining factor in pushing the current biological model of schizophrenia. Medical school psychiatric departments rely on research grants which are far more numerous in biological psychiatry and so this has resulted in the psychiatric faculties being primarily biological psychiatrists who teach what they know (Karon, 1995). Competition from psychologists, psychiatric nurses, clinical social workers, and numerous counselors in conjunction with the development of nonmedical psychotherapies (such as reality therapy, encounter therapy, gestalt therapy, existential therapy, client-centered therapy, behavior modification, family therapy, transactional analysis, and rolfing) in the 60's and 70's had taken many clients away from psychiatry and drove the field into a massive propaganda campaign to convince the public that all mental disorders (including schizophrenia) were of a biological origin and should only be treated by medical doctors (Modrow, 1995). The American Psychiatric Association commissioned a study that suggested that reasonable psychiatrists will not practice psychotherapy as they will not make more than $100,000 a year, where three times that amount can be made by evaluating and medicating (Karon, 1995).

Recognizing a qualitative difference between organic psychoses and functional disorders such as schizophrenia is important as organic psychoses always result in a marked deterioration in mental abilities, while schizophrenia is known to leave the mental facilities intact (Hyde, T. M., Nawroz, S., Goldberg, T.E., et al., 1994). Some schizophrenics have demonstrated amazing intellectual abilities even while extraordinarily psychotic (Modrow, 1995). A recent popular culture example of such intellectual ability was presented in the movie A Beautiful Mind, about the Nobel Prize-winning mathematician and schizophrenic John F. Nash Jr., which resulted in a response of several articles questioning the medical model of incurable schizophrenia (BBC News a, 2002; Barry, 2002; Harding, 2002). Reading case studies of schizophrenics it is easy to see a comparison with their experiences and the very similar experiences that are defined by others to be mystical or religious phenomena. C. J. Jung phrased it well: "Let the dreamer walk about and act as though he were awake and we have at once the clinical picture of dementia praecox [schizophrenia]" (Arieti, 1974).

References

I overcame schizophrenia, BBC News a. Retrieved March 26, 2002, from http://news.bbc.co.uk/hi/english/health/newsid_1820000/1820728.stm

Schizophrenia: The facts, BBC News b. Retrieved March 26, 2002, from http://news.bbc.co.uk/hi/english/health/medical_notes/newsid_1079000/1079451.stm

American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Association.

Andreasen, N. C. (1997). Linking mind and brain in the study of mental illnesses: A project for a scientific psychopathology. Science, 275, 1586-1593.

Arieti, S. (1974). Interpretation of Schizophrenia (2nd ed.). New York: Basic Books.

Barry E. (2002). Group stirs debate over schizophrenia, Boston Globe Online. Retrieved March 26, 2002, from http://www.boston.com/dailyglobe2/062/metro/Group_stirs_debate_over_schizophrenia+.shtml

Bleuler, M. (1972). Die schizophrenen Geistesstorungen im Lichte langjahriger Kranken-und Familiengeschichten. Stuttgart: Thieme.

Carlsson, A. (1995). The dopamine theory revisited. In S. R. Hirsch and D. R. Weinberger (Eds.), Schizophrenia (pp. 379-400). Oxford, England: Blackwell Science, Ltd.

Chua, S. E. & McKenna, P. J. (1995). Schizophrenia–a brain disease: A critical review of structural and functional cerebral abnormality in the disorder. British Journal of Psychiatry, 166, 563-582.

Ciompi, L., & Muller, C. H. (1976). Lebensweg und Alter der Schizophrenen. Eine katamnestische Langzeitstudie bis ins Senium. Berlin, Heidelberg, New York: Springer.

Davis, K. L., Kahn, R. S., Ko, G., & Davidson, M. (1991). Dopamine and schizophrenia: A review and reconceptualization. American Journal of Psychiatry, 148, 1474-1486.

Gottesman, I., & Shields, J. (1972). Schizophrenia and genetics: A twin study vantage point. New York: Academic Press.

Harding, C. M. (1984). Long-term Functioning of Subjects Rediagnosed as Meeting the DSM III Criteria for Schizophrenia. (Doctoral Dissertation). Burlington, University of Vermont.

Harding, C. M., Brooks, G. W., Ashikaga, T., Strauss, J. S., et al (1987). The Vermont Longitudinal Study of Persons with Severe Mental Illness, II: Long-Term Outcome of Subjects Who Retrospectively Met DSM-III Criteria for Schizophrenia. American Journal of Psychiatry, 144(6), 727-735.

Harding, C.M. (2002). Beautiful Minds Can Be Recovered, New York Times. Retrieved March 26, 2002, from http://www.successfulschizophrenia.com/articles/bmreview.html

Hyde T. M. , Nawroz S., Goldberg T. E. , Bigelow L. B. , Strong D., Ostrem J. L., Weinberger D. R., Kleinman J. E. (1994). Is there cognitive decline in schizophrenia? A cross-sectional study. British Journal of Psychiatry, 164, 494-500.

Huber, G., Gross, G. & Schuttler, R. (1975). A long-term follow-up study of schizophrenia: Psychiatric course of illness and prognosis. Acta Psychiatrica Scandinavica, 52, 49-57.

Jablensky, A. (1987). Multicultural studies and the nature of schizophrenia: A review. Journal of the Royal Society of Medicine, 80, 162-167.

Jablensky, A. (1995). Schizophrenia: The epidemiological horizon. In S. R. Hirsch and D. R. Weinberger (Eds.), Schizophrenia (pp. 206-252). Oxford, England: Blackwell Science, Ltd.

Rupp, A., & Keith, S. J. (1993). The costs of schizophrenia: Assessing the burden. Psychiatric Clinics of North America, 16, 413-423.

Karon, B. P. (1995). Foreword: In search of truth. In J. Modrow, How to become a schizophrenic: the case against biological psychiatry (pp. xi-xiv). Everett, Washington: Apollyon Press.

Maas, J. W., Bowden, C. L., Miller, A. L., Javors, M. A., Funderburg, L. G., Berman, N., & Weintraub, S. T. (1997). Schizophrenia, psychosis, and cerebral spinal fluid homovanillic acid concentrations. Schizophrenia Bulletin, 23, 147-154.

Modrow, J. (1995). How to become a schizophrenic: the case against biological psychiatry. Everett, Washington: Apollyon Press.

Perris, C. (1989). Cognitive Therapy with Schizophrenic Patients. New York: Guilford Press.

Sass, L. A. (1997). The consciousness machine: Self and subjectivity and schizophrenia and modern culture. In U. Neisser & D. A. Jopling (Eds.), The conceptual self in context: Culture, experience, self-understanding (pp.203-230). Cambridge: Cambridge University Press.

Sherman, S. L., DeFries, J. C., Gottesman, I. I., Loehhlin, J. C., Meyer, J. M., Pelias, M. Z., Rice, J., & Waldman, I. (1997). Recent developments in human behavioral genetics: Past accomplishments and future directions. American Journal of Human Genetics, 60, 1265-1275.

Siegert, R. J. (2001). Culture, cognition, and schizophrenia. In J. F. Schumaker & T. Ward (Eds.), Cultural Cognition and Psychopathology (pp. 171-189). Westport, Connecticut: Praeger.

Smith, R. C. Baumgartner, R., & Calderon, M. (1987). Magnetic Resonance Imaging Studies of the Brains of Schizophrenic Patients. Psychiatry Research, 20, 33-46.

Tanaka-Matsumi, J., & Draguns, J. G. (1997). Culture and psychopathology. In J. W. Berry, M. H. Segall, & C. Kagitcibasi, (Eds.), Handbook of cross-cultural psychology (pp. 449-491). Allyn & Bacon.

Torrey, E. F. (1980). Schizophrenia and civilization. New York: Aronson. Warner, R. (1985). Recovery from schizophrenia. London: Routledge & Kegan-Paul.

Weinberger, D. R., Wagner, R. R. & Wyatt, J. (1983). Neuropathological Studies of Schizophrenia. Schizophrenia Bulletin, 9, 193-212.

World Health Organization. (1979). Schizophrenia: An international follow-up study. Geneva, Switzerland: Author.

Yates, W. R., Jacoby, C. G., and Andreasen, N. C. (1987). Cerebellar Atrophy in Schizophrenia and Affective Disorder. American Journal of Psychiatry, 144, 465-467.