Kringlen also published more extensive case records for his monozygotic twins than any other researcher had done (pp. 7-8)."
The information gained by these studies was significant. One, in particular, conducted by William Pollin and his colleagues set out to disprove the biological or genetic factors, and to establish the basis for.".. psychodynamic, interpersonal phenomena that might have some significant etiologic role with respect to schizophrenia (Torrey, p. 9)." What Pollin and his colleagues found, instead, was that there were significant physiological conditions in the twins examined who had schizophrenia (p. 9).
The most significant findings were a history of lower birth weight and more obstetric complications in the affected twins in discordant pairs, and more neurological abnormalities in the affected twins (Pollin & Stabenau, 1968; Mosher et al., 1971). The findings, said these researchers, suggested that "the intrauterine experience of one twin, relative to the co-twin, tends to be unfavorable or deficient, leading to a relative physiological incompetence and immaturity at birth and in the neonatal period." Shifting from biological observations to psychological theorizing, the researchers theorizing "The twins studied by Pollin and colleagues were investigated more thoroughly than those in any other previous schizophrenia twin study. The researchers then interpreted their findings as follows: "These [biological] differences may induce attitudes and relationship patterns in the family which accentuate dependency and ego identity problems, and retard self-differentiation in the less favored twin" (Pollin & Stabenau, 1968). It should be noted that Pollin et al. published virtually no data to support their psychological interpretation, despite extensive and intensive analyses of the families. Such an interpretation, which appears absurd in the context of 1990s schizophrenia research, was representative of much 1960s theorizing about this disease (Torrey, p. 9)."
This should, for most people, establish the physiological nature of schizophrenia. The fact that Pollin, et al., did not publish their conclusions as to the psychological premise for the disease should also support that their own study, intended to eliminate the physiological basis for the disease, only further substantiated it. There is every reason to expect this to resolve the question of psychological vs. physiological nature of the disease, so that progress towards developing a means by which to improve treatment and initiate preventative measures to mitigate the numbers of cases of schizophrenia; but it has not. The debate as to the physiological nature of the disease vs. The psychological nature of it continues, regardless of the data.
John G. Csernansky (2002) look at symptoms of schizophrenia, specifically "symptom clusters (p. 29)." Most studies do support the onset of the disease in adolescence (p. 29).
In the late 1930s Kurt Schneider established a pragmatic system for the assessment of schizophrenic symptoms. He defined "first-rank" symptoms as those that maximized diagnostic specificity, including audible thoughts; voices arguing, discussing, or commenting; influenced thought (i.e., thought withdrawal, thought broadcasting); and delusional perception. Perplexity, depressive or euphoric mood changes, and emotional impoverishment were viewed as second-rank symptoms. Schneider's reliance on clinically relevant and readily recognized symptoms was a strength of his system and a factor in his influence on the development of diagnostic criteria. Interestingly, some recent work suggests that Schneiderian first-rank symptoms may not be useful in differentiating schizophrenia from other psychotic disorders (Csernansky, p. 31)."
These symptom clusters, Trower and Harrop aruge, is indicative of an "incubating" phenomenon, and that 51% of all news cases of schizophrenia were reported to be between ages 15 and 25 (Harrop and Trower, p. 33). However, the same study revealed that 82.5% were between 15 and 35 years of age (p. 33). First symptom manifestation was 86%, and those manifestations were within the past 12 months of the study period (p. 33). Harrop and Trower argue this means that the majority of those individuals suffering from schizophrenia do not manifest their first symptoms in adolescence (p. 33). They argue, too, that this means that the disease is not path-physiological, but is psychological in nature.
The disruption in association is certainly reason to suspect that schizophrenia is psychological in nature (Weinter, Irving, 1997, 27). However, when we consider the existing evidence that has surfaced only in this century with the advent of the magnetic resonance imagery (MRI) scan (Fuller, p. 103). The scan images the body focus in sections, and disease progress can be witnessed by the physicians in ways that it was never previously seen. What the MRI show in patients suffering schizophrenia, is that the disease does create changes in the brain that are visible on the MRIs (p. 103).
The most commonly observed abnormality is mild to moderate dilatation of the lateral and third ventricles, now shown to occur in schizophrenia in over 100 controlled studies (Hyde et al., 1991). These studies have established that the dilatation is not an effect of medication taken by patients, for it was seen in the pneumoencephalography studies before such medication was available and it is seen in studies of newly diagnosed patients before they have taken any medication. The studies also suggest that the ventricular dilatation is static, present at the onset of the schizophrenia and not progressing further. In addition, mild to moderate ventricular dilatation is also found in some patients with brain tumors, stroke, multiple sclerosis, Alzheimer's disease, and bipolar disorder, as well as occasionally being present in normal individuals with no known brain pathology; thus it is a nonspecific finding (Fuller, p. 103)."
There are other changes that can be seen on the MRIs too. The hippocampus, where critical limbic functions are processed, is impacted (p. 103). This is a finding that has been extensively reported by researchers (p. 103). There have been other changes in the brain reported by various research groups that would suggest that the disease is patho-physiological in nature.
Thomas Lee (1991) says that the Human Genome Project has reported that there are genetic components of schizophrenia (p. 267). It is, however, a relatively new study, and an area that requires much more thorough study both for the causes, the treatment, and, perhaps eventually, the preventative measures. There remains, however an overwhelming amount of information and evidence to support the contention that schizophrenia is patho-physiological disease. This is not to suggest that there is no need for mental health interventions and treatment, because the manifestations of the disease is agreeably a psychological one, and one that warrants care and treatment. There remains hope though that the future holds promise of identifying the genetic patterns and identifiers of those people who will become afflicted with the disease.
Csernansky, J.G. (Ed.). (2002). Schizophrenia: A New Guide for Clinicians. New York: Marcel Dekker. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=109107379 http://www.questiaschool.com/PM.qst?a=o&d=113408413
Harrop, C., & Trower, P. (2003). Why Does Schizophrenia Develop at Late Adolescence? A Cognitive-Developmental Approach to Psychosis. Hoboken, NJ: Wiley. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=113408491 http://www.questiaschool.com/PM.qst?a=o&d=111909680
Heinrichs, R.W. (2001). In Search of Madness: Schizophrenia and Neuroscience. New York: Oxford University Press. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=111909680 http://www.questiaschool.com/PM.qst?a=o&d=85769272
Lee, T.F. (1991). The Human Genome Project Cracking the Genetic Code of Life. New York: Plenum Press. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=85769274 http://www.questiaschool.com/PM.qst?a=o&d=108472776
Read, J., Mosher, L.R., & Bentall, R.P. (Eds.). (2004). Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. New York: Brunner-Routledge. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=108472778 http://www.questiaschool.com/PM.qst?a=o&d=5000780969
Spear, L.P. (2002). The Adolescent Brain and the College Drinker: Biological Basis of Propensity to Use and Misuse Alcohol. Journal of Studies on Alcohol, 63(2), 71+. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=5000780969 http://www.questiaschool.com/PM.qst?a=o&d=6984618
Torrey, E.F. (1994). Schizophrenia and Manic-Depressive Disorder the Biological Roots of Mental Illness as Revealed by the Landmark Study of Identical Twins. New York: Basic Books. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=6984618 http://www.questiaschool.com/PM.qst?a=o&d=35617977
Weiner, I.B. (1997). Psychodiagnosis in Schizophrenia. Mahwah, NJ: Lawrence Erlbaum Associates. Retrieved December 22, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=35617977
Researchers Chris Harrop and Peter Trower (2003) would argue that schizophrenia is not a biological disease. However