Schizophrenia Is a Family of Severe Psychotic Research Paper

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Schizophrenia is a family of severe psychotic disorders that affect the person, their family, and society as a whole. While the disorder has been described clinically for over a century, the cause of schizophrenia is not well understood. Different theories have been postulated as to the cause of schizophrenia that stirred the age-old nature vs. nurture debate. When the evidence is viewed from a holistic perspective it becomes clear that schizophrenia must result from a combination of innate and environmental factors. Such theories, integrating both biological and environmental factors, have been proposed. By taking a broader view of the cause of schizophrenia we can not only better understand it, but learn how to more effectively treat it.

Schizophrenia is a catastrophic illness that may appear in adolescence but more often is apparent by early adulthood. It is actually a class of severe mental disorders as opposed to one specific disorder. All of the schizophrenic disorders consist of distortions or reality (American Psychiatric Association, 2000). The proposed etiology of the schizophrenic disorders has been a topic of interest in psychology and psychiatry for many years and has ranged from poor parenting to an infection incurred by the mother during pregnancy to an innate imbalance of neurotransmitters. All of these speculative singular casual models of this disorder have been empirically demonstrated not to fully explain the cause schizophrenia. It has become clear that schizophrenia has multiple causes and is best explained in terms of a diathesis stress model or the predisposition model of schizophrenia (Feldman, 2008).

Although severe psychotic symptoms/disorders have been recognized by physicians and have been described in literature for centuries, the classification of psychotic disorders into specific syndromes such as manic-depressive illness (bipolar disorder) or schizophrenia really occurred only approximately one hundred years ago. Schizophrenia was initially defined in the late nineteenth century by Emil Kraepelin working with a team of psychiatrists, which also included Alois Alzheimer, the discoverer of Alzheimer's disease. Because the symptoms of schizophrenia will often produce severe incapacity in the person suffering from it, Kraepelin originally named the disorder as "dementia praecox." Dementia praecox was originally distinguished as a separate disorder from dementia because it occurred in relatively young people rather than elderly people. Kraepelin also distinguished it from manic-depressive illness (his other class of mental disorders) based on how long symptoms persisted. Dementia praecox was more persistent, whereas manic-depressive disorder was sporadic in nature and manic depressive patients sometimes improved on their own. Years after Kraepelin's definition of dementia praecox, Eugene Bleuler suggested that the disorder be renamed to schizophrenia, which means "fragmented (or split) mind." This definition led to some popular confusion with schizophrenia and multiple personality disorder (now termed dissociative identity disorder), but the two are separate disorders. Schizophrenia does not involve multiple personalities, whereas dissociative identity disorder does (American Psychiatric Association, 2000).

As mentioned above, schizophrenia is characterized by a mixture of signs and symptoms, no one of which is necessarily present in a single case, and therefore is a family of disorders. In this sense, it differs from many other psychiatric disorders, which are typically defined by a single prominent feature. For example depression is characterized by dysphoric mood, mania is characterized by elevated mood, and panic disorder is characterized by the presence of panic attacks. The absence of a single defining or identifying feature for schizophrenia has sometimes made this disorder difficult for people to understand.

One of Kraepelin's early notions was to delineate so-called "functional psychoses" from "organic psychoses." The organic psychoses included disorders like the different dementias and epilepsy, disorders of which Kraepelin was aware of the specific brain pathology involved and that led to their presentation. However, the brains of affective patients and schizophrenia patients looked normal in post-mortem examinations (prior to the advent of neuro-imaging techniques post-mortem analysis was the only method to learn human neuroanatomy). For this reason Kraepelin termed affective disorders and schizophrenia "functional psychoses" implying there was no gross pathology found in the brains of these patients. However, modern neuroimaging has found evidence of an organic basis for some affective and schizophrenic disorders so the term "functional" depression or "functional" psychosis is not often used to describe them any longer.

When schizophrenia was viewed as a functional disorder many advocated that the concept of schizophrenia was unreliable and not a real disorder, but instead was a sociological phenomenon (people with schizophrenia were really normal people driven insane by the world). One of the early observations was that schizophrenia tends to run in families. An early interpretation of these observations was that schizophrenia was a reaction to a macabre family environment. For example, Fromm-Reichmann (1948) identified the schizophrenogenic mother who alienated the child and induced psychosis by being cold and distant. The mother's behaviors consisted of rejecting, being impervious to the feelings of others, having rigid and strict morals concerning sex, and a fear of intimacy with others. These behaviors isolated and affected the young child resulting in the psychotic behavior of schizophrenics. Other purely environmental causes were proposed. Bateson, Jackson, Haley, and Weakland (1956) proposed the double-bind hypothesis that schizophrenia results from a reaction to intolerable stress within the family. In this model conflicting commands are placed by the authority figures in the family in such a way that it becomes impossible for the child to satisfy one command without breaking another, eventually resulting in distortions of reality. Wynne, Ryckoff, Day, and Hirsch (1958) discovered that disturbed families of schizophrenics maintained a facade of familial harmony along with a denial of problems, labeled pseudomutuality. Bowen (1960) noted that schizophrenic patients often improved in hospital but deteriorated when returned to their families, supporting the double-blind and other familial hypotheses. Research by Brown, Bone, Palison, and Wing J.K. (1966) demonstrated that the quality of the family environment into which discharged schizophrenic patients returned is predictive of their return to hospital. This finding has been replicated several times and Brown introduced the term "expressed emotion" (EE) to describe the level of criticism, hostility, and emotional dependency connected to the patient. Patients from low-EE homes were about one-sixth as likely for relapse as those from high-EE homes. Norton (1982) noted that communication difficulties in families predicted the later onset of schizophrenia, but this finding was not specific as there was a similar association with later onset of manic patterns of behavior. Tienari (1991) found that the adopted children of schizophrenic mothers demonstrate greater psychopathology if they are raised in a disturbed family than controls raised in a similarly disturbed family.

The findings that schizophrenia runs in families, or that certain family environments were associated with greater relapses, does not necessarily mean that family environments cause schizophrenia as these relationships are correlational or associational in nature. However, they do suggest a significant environmental contribution to schizophrenia. In addition, family and twin studies have indicated a strong genetic link to schizophrenia. The hypothesis of a purely genetic theory would suggest that schizophrenia is due to a physical disorder of the brain, genetic in origin, and caused by a gene or by various genes in combination. Gottesman (1991) and Sarason & Sarason (1996) suggest that 48% of monozygotic twins, whose twin is schizophrenic, will develop it themselves compared to 17% of dizygotic twins. Similar concordance rates for schizophrenia have been expressed by other studies and schizophrenia has one of the strongest genetic associative relationships of any mental disorder (Feldman, 2008; Picchioni & Murray, 2007). Other powerful evidence for a biological cause comes from the efficacy of antipsychotic drugs in the treatment of schizophrenia and recent advances in biological research have demonstrated differences in the brains of people with schizophrenia compared to normals (Feld, man, 2008; Picchioni & Murray, 2007). An innate lack of the neurotransmitter dopamine in the brains of schizophrenics has been implicated as a causal factor in the expression of schizophrenia, and later research as also implicated reduced levels of serotonin and perhaps norepinephrine are present in the brains of these individuals (Picchioni & Murray, 2007).

If we consider all the evidence, we cannot fully discount environmental contributions to schizophrenia. In addition, we cannot rule out a biological contribution to this family of disorders as well. For example, if schizophrenia were a purely genetic or a biologically-based disorder then the concordance rate in monozygotic twins would be closer to 1.0 as in purely genetic disorders like Huntington's disease. Likewise, if it were a disorder with a purely environmental cause then adoption studies of monozygotic twins would not produce similar concordance rates for adopted twins that go to different homes and twins reared in the birth home. In addition, we now understand that the effects of genes on behavior are often dependent on environmental cues (Lewontin, Rose, & Kamin, 1985). Therefore, I believe that the current models of schizophrenia need to consider both the environment and biological contributions.

The stress vulnerability model was first proposed by Zubin and Spring (1977). This model suggested that an individual has unique biological, psychological, and social factors that all can influence their…[continue]

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