The Condition of Schizophrenia - Essay Example

259274 The Condition of Schizophrenia Searching for the precursors to schizophrenia is like searching through the ashes of a burned home looking for the clues as to the single tiny light on the Christmas tree that ignited it, starting the fire that burned the house down. Schizophrenia is a pathophysiological condition, which remains largely a dark secret to the individual suffering the disease, the family and friends who try to accept and understand it, and to the medical community providing the support in treatment and care to the patients diagnosed with the disease. Often times an individual’s history has no sign of trauma, or other events that mental health workers often look for when trying to understand a patient’s condition in order to design a treatment plan that addresses that condition (Hienrichs, R. Walter, 2001, p. 4). Where does the therapist look, then, to understand the pathophysiological condition? R. Walter Heinrichs (2001) writes that schizophrenia is a disease of ideas, emotions, ultimate privacy, and the annihilation of privacy (p. 21). “It is an illness where everyday meanings gather gently, insistently, into fantastic convictions, or rage abruptly into storms of secret logic no mind can understand. It is an illness of extreme imagination and the collapse of imagination; of power and prejudice, ambition, and apathy (p. 21).” Heinrichs describe the condition in such poetic and elegant terms that it almost erases the horror of what is later described, or the terror that grips the mind of the patient in the throngs of mental anguish and torment as they are convinced that their bodies have been invaded by parasites that control their thoughts and actions (p. 21). Schizophrenia is disease, the origins of which must be pieced together, and often is elusive as to exactly what experiences or events in life might trigger the condition. The Path of Schizophrenia In some circles, experts continue to debate whether or not schizophrenia is a biological disease, or a psychological problem. The many aspects of psychosis that manifest in patients diagnosed with schizophrenia would suggest that it is a biological problem (Harrop, Chris and Trower, Peter, 2003, p. 13). Research on schizophrenia has led to three recurring conclusions about the disease: 1. Stress is involved in the onset and relapse 2. Dopamine-based medications can be therapeutically useful 3. The condition most often manifests itself in late adolescence (Harrop and Trower, p. 33). It is the dopamine based medication to which patients respond in a positive way that is the basis for the argument that schizophrenia is a biological condition, not a psychological one. Condition three is actually a swing factor, and it could go in support of either argument, for or against the biological argument for the disease. Therefore, the argument that it is a biological condition must rule out, or mitigate conclusion three in order to substantiate the biological basis as the condition. The easiest way, of course, to prove that the disease is biological in nature would be to find a link between the disease and the genetic code. Dr. Fuller Torrey, M.D. (1994), examined the biological roots for schizophrenia. Torrey cites the study of twins in arriving at conclusions as to the biological basis for the disease (1994). At the end of the 19th century, Torrey writes, twins became the tool for scientific research to understand genetics in relationship to disease (p. 3). The need to better understand genetically hereditary diseases like diabetes, Alzheimers, and some forms of cancer has made the research involving twins less objectionable today. It has served to expedite the understanding of genetics and human genome projects towards success in ways that could not have been accomplished but for the participation of twins in the studies. Obviously, unlike those conducted in Nazi Germany, today’s participants are willing ones, with a personal or social interest in contributing to studies that lead to the eradication of diseases. “Benjamin Rush, the father of American psychiatry, was among the first to recognize the psychiatric research potential of twins. Commenting in 1812 on a pair of identical twins both of whom had suicided, Rush observed the "hereditary sameness of organization of the nerves, brain and blood ves sels on which . . . the predisposition to madness dwells" (Price, 1978) (Torrey, pp. 5-6).” Working in a German psychiatric clinic, Hans Luxenburger began his studies of twins and schizophrenia in 1920 (Torrey, p. 6). Luxenburger found that 58% of identical twins studied had higher concordance for schizophrenia than did fraternal twins, which manifested zero percent (Torrey, p. 6). Franz Kallman conducted studies in 1935 using twins to study schizophrenia (p. 6). His studies were interrupted by Hitler’s Third Reich, and, because his father was Jewish, Kallman was forced to leave Germany, and he immigrated to America, where, in New York City, he continued his research using twins and records from a New York psychiatric hospital (p. 6). Kallman’s studies supported Luxenburger’s research, finding that the number of identical twins with schizophrenic episodes was greater than that of fraternal twins (p. 6). “In many of the pairs in which only one twin had developed schizophrenia, Kallmann noted that the twins were young and so there was still time for the second twin to develop the disease. He therefore corrected for this age factor and reported concordance rates of 86% for identical twins and only 15% for fraternal twins. According to Kallmann, such figures proved that schizophrenia is caused by a recessive gene. Since no other twin researcher has reported concordance rates close to those of Kallmanns, the methodology of his research has been the subject of spirited debate among both detractors (Lewontin et al., 1984, pp. 207-213) and defenders (Shields et al., 1967) (Torrey, p. 6).” Kallmann’s studies have been challenged, because of issues with the methodology (p. 6). Four other earlier studies that relied upon hospital records alone were also challenged. Subsequent studies, however, have been done on twins with schizophrenia (p. 7). Many of the studies conducted were thorough, using modern technology to ensure no challenges could be raised. The twins studied were examined by the researcher personally, and blood tests were taken to prove the identical relationship, and the twins were fingerprinted (p. 7). “Between 1963 and 1973 three Scandinavian schizophrenia twin studies were carried out and were, in terms of sampling methodology, the best studies ever conducted, using national twin registries, which were maintained in Scandinavian countries for every twin born in each country. Such registries could be compared with psychiatric records to identify virtually every twin who had ever been treated psychiatrically. Pekka Tienari ( 1963, 1975) worked in Finland, Einar Kringlen ( 1967) in Norway, and Margit Fischer ( 1973) in Denmark. Kringlen interviewed all his twins and followed them for many years. Tienari also interviewed most of his twins, but one third of Fischers twins had died prior to her study so she had to rely on hospital records and family histories to establish a diagnosis. 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 versus 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 versus the psychological nature of it continues, regardless of the data. Debate 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. Schneiders 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). This, however, would be adamantly debated by other experts and researchers as inconclusive, and that this data is unsubstantiated. They might also allege that there are numerous problems with making these conclusions based on the methodology being employed. What all this information suggests, is that there is not enough understanding about schizophrenia to make sound conclusions at this time. There is a need for more and much more extensive research on schizophrenia. References Csernansky, J. G. (Ed.). (2002). Schizophrenia: A New Guide for Clinicians. New York: Marcel Dekker. Retrieved December 19, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=109107379 Harrop, C., & Trower, P. (2003). Why Does Schizophrenia Develop at Late Adolescence? A Cognitive-Developmental Approach to Psychosis. Hoboken, NJ: Wiley. Retrieved December 19, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=113408491 Heinrichs, R. W. (2001). In Search of Madness: Schizophrenia and Neuroscience. New York: Oxford University Press. Retrieved December 19, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=111909680 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 19, 2008, from Questia database: http://www.questia.com/PM.qst?a=o&d=6984618 Read More