| FAQ | Staff
| Links | Contact
-Shannon Sumrall, M.A., M.Ed., LPC, NCC
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).
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
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).
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).
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,
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).
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,
I overcame schizophrenia,
BBC News a. Retrieved March 26, 2002, from http://news.bbc.co.uk/hi/english/health/newsid_1820000/1820728.stm
The facts, BBC News b. Retrieved March 26, 2002, from http://news.bbc.co.uk/hi/english/health/medical_notes/newsid_1079000/1079451.stm
Association (2000). Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition, Text Revision. Washington, DC: American Psychiatric Association.
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.
(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.
& 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
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.
(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.
(1987). Multicultural studies and the nature of schizophrenia: A review. Journal
of the Royal Society of Medicine, 80, 162-167.
(1995). Schizophrenia: The epidemiological horizon. In S. R. Hirsch and D.
R. Weinberger (Eds.), Schizophrenia (pp. 206-252). Oxford, England: Blackwell
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:
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
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:
Smith, R. C.
Baumgartner, R., & Calderon, M. (1987). Magnetic Resonance Imaging Studies
of the Brains of Schizophrenic Patients. Psychiatry Research, 20, 33-46.
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.
R., Wagner, R. R. & Wyatt, J. (1983). Neuropathological Studies of Schizophrenia.
Schizophrenia Bulletin, 9, 193-212.
Organization. (1979). Schizophrenia: An international follow-up study. Geneva,
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.
| FAQ | Staff
| Links | Contact
information on this site is educational in context and is not to be used to
diagnose, treat or cure any disease. Please consult your licensed health care
practitioner before using this or any healthcare or medical information.