Biopsychosocial Model for Schizophrenia (Term Paper Sample)

Biopsychosocial Model for Schizophrenia
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Biopsychosocial Model for Schizophrenia
Schizophrenia is defined as a brain disorder which affects an individual’s ability to perceive or look at the world and also process information. According to Tiwari et al (2010) the disease affects approximately 1% of the world's population where 7 of every 1000 adults in a population are affected. The current approach to schizophrenia is deeply absorbed into the bio psychosocial model. This was originally articulated by Dr. G. Engel in 1997 (Ader et al 2004). Before this model, people used the biomedical model. The biomedical model denied the emotional and social process of illness and emphasized more on the biological characteristics of disease (Engel, 2002). According to Ader et al (2004), The bio psychosocial model understands the patient's experience with disease in a multi-layered model, from the biomedical, psychological and social aspects of health. This paper promotes the biopsychosocial model as an important ingredient in understanding the relationship between the mental and physical mechanisms of schizophrenia. Brain localization, genetic association and environmental factors that trigger the onset of this disorder are discussed.
Brain Localization
Schizophrenia is essentially termed a disorder which occurs in brain's network connectivity (Fornito et al 2012). Research in the past decade terms schizophrenia as a disconnection syndrome where the brain’s networks irregularities result to disorganization in behavior and cognition. The link that connects psychopathic symptoms and brain connectivity emerged about a century ago. A scientist known as Wernicke acknowledged that schizophrenia was caused by abnormalities in the brain's association fibers. However, scientists have tested the neurobiological origins of this disorder using modern neuroimaging. With this in mind, scientists had found the potential of using technology for major advances in the study of schizophrenia.
According to a test done by scientists in 2010, results found people with schizophrenia disorder had less hub clustering, a lower regional strength, and increased diversity in connectivity. This accounted for a weakly integrated brain profile. When the findings were positively correlated with behavioral performance on verbal fluency trials, the investigation showed that there were in-group differences in functional connectivity. Participants who had schizophrenia had significantly reduced functional connectivity.
Genetic Factors
According to Tiwari et al. (2010) schizophrenias largest known risk factor is genetics. There has been genetic research on schizophrenia for over the last 20 years. These studies show high schizophrenia inheritability. With Modern technologies in molecular genetics, scientists have the ability to detect gene variation in most complex diseases such as Alzheimer's disease. This prompted the urgency to locate genetic loci in schizophrenia; hence researchers expanded their approach to this disorder. As a result, the genetic association studies on schizophrenia were formed and they came up with Schizophrenia Gene (SZGene) database catalogs. Regardless of this, detecting the genetic architecture has not been viable as gene-wide association studies inform the sobering complexity of schizophrenia, involving various genes, each with its own small effect.
Though it has been a major challenge to find the genetic basis for schizophrenia, research has consistently delivered loci observations, expression and function of genes associated with schizophrenia. Tiwari et al.,( 2010) notes that liability in schizophrenia is approximately 80% heritable. Genetic subjectivity to schizophrenia signifies the interplay between genetics and disease. Irregularities in brain structure and function are likely caused by susceptible genes. Opening and liberating the genetic complexities that produce and sustain the illness is an essential guidance in developing new and better treatments. Tiwari et al. (2010) notes that schizophrenias liability difference is largely genetic. This means that, genetics role in psychiatric disorders will continue to be a major focus for schizophrenia experts, not only now but even in the future.
Environmental Factors
Epidemiological research attempts to weave a framework for exogenous contributions to schizophrenia. Even as research on the latest "susceptibility" gene command attention, scientific evidence documents a positive correlation between environmental exposures and the occurrence of schizophrenia. Among exogenous factors that predispose to this disease, data places prenatal circumstances, exposure to infections, migration, and mental and physical abuse as key factors. The more recently identified hazards in the etiology of schizophrenia are cannabis use and urbanicity. In a meta-analysis of seven studies, Oh and Petronis (2008) found overwhelming evidence that links cannabis use to an increase in schizophrenia. Though the implications are not quite clear, research suggest neurochemical changes or self-medication behaviors to dull the presence of psychotic symptoms.
Following seminal studies in the 1900s, urban areas have been the center of sophisticated research on the geographical properties of schizophrenia. In their environmental study in 1939, Farris and Dunham reported the highest rates of schizophrenia were concentrated in overcrowded areas of cities. That these findings have been replicated in other studies (Krabbendam & van Os, 2005 and Oh & Petronis, 2008) highlights the need to elucidate the effect of urbanicity in the onset of schizophrenia and develop health resources for individuals residing in this environment. While the exact putative urban relationship may not be clear, the importance of this work lies in the fact that the rate of schizophrenia in urban areas is double that of rural areas. Another key concern for schizophrenia ecological research is the mechanism of gene-environment interaction. Considering the large number of people who live in urban areas, only a tiny proportion develop schizophrenia. Hence, urban living in schizophrenia etiology is contingent on some other effect (Krabbendam & van Os, 2005).
Biopsychosocial Representation
When Engel (2002) proposed the biopsychosocial model, he believed psychiatric medicine was in crisis. The categories of human distress were not properly addressed, illness was defined in terms of somatic properties and the traditional authority of physicians was not a logical philosophy for their helping role. While there are measures of success in the policies and strategies developed under the biomedical model, it lacks the fundamental social and subjective experience of illness (de Bilbao, 2011). Hence, the basis for a new medical model.
Adaptive and compensatory mechanisms are critical to understanding the origin and psychosocial presentation of schizophrenia. Thus, it is important the clinician gather a relevant and comprehensive history. Kotsiubinskii (2002) cautions the nature of biological adaptation in corresponding brain structures to loss of psychosocial integrity remains unclear. As the mind-body adapt to the loss of an intact system, essential functions compensate for defects. Within this adaptation and compensatory network, composite elements necessary to survival create a diathesis-stress dynamic that triggers the onset of pathological phenomena. As such, defects in mental associations lead to behaviors that arise from specific areas in the brain (Fornito et al.).
Whereas each person has a selection of psychological health resources, adaptations form the basis of the dealing with stressors. Vulnerability to psychological health creates a major risk to schizophrenia genesis. Under the influence of risks, such as predisposing factors (genetics, environment), precipitating factors, (drug abuse, macro-population), and perpetuating factors, (stressors, stigma) a primary assault to vulnerability exhaust psychological defenses. The disease disrupts cognition, language, thought, and emotion. Problems between correlation of the mind and the brain lead to distortions in emotions, mentation, and social functioning (Kotsiubinskii, 2002). Depression is a common comorbidity among others such as anxiety, suicide risk, low self-esteem, and feelings of hopelessness (Buckley, 2008).
Management of schizophrenia is not a simple linear trajectory but a discontinuous process with different stages of the disease and interactions with the environment (Buckley, 2008). Chronic psychopathology reflects the intensity of the mental damage (Kotsiubinskii, 2002). It is vital the person receives uninterrupted mental health services. Referrals to services such as psychosocial and cognitive therapy with individualized treatment to meet specific needs and frequent updates will maximize effectiveness. An assertive and proactive approach to help the person remain in treatment and live a sovereign life is the goal of treatment. Optimal treatment includes support from family, vocational services, and substance abuse treatment if needed. Psycho-education for family and patient is vital to empowerment in the treatment process. Medications are a bedrock of treatment, but only one facet says Buckley. A strong relationship between caregiver and patient is shown to exert a positive influence on the design of treatment for schizophrenia. Those requiring inpatient services need a multidisciplinary team to provide care 24 hours a day.
Conclusion
To coordinate the complex demands of day-to-day life, the human brain has developed mechanisms to manage the many sensory and motor data that represent goals or rules that guide behavior. Adequate engagement of multiple brain regions, genes, and environmental dynamics determine the ...