A Case Study on the Biopsychosocial Approache
In this assignment the writer will discuss how young people are susceptible to the severe and persistent mental illness of Schizophrenia. This mental illness is a debilitating brain disorder , with onset in late adolescence and early adulthood (DSM-IV-TR, 2000). To get a clearer perception of this illness the author will use a case study to illustrate how this disorder is understood. John is fifteen year old youth on his second admission to hospital.
John was diagnosed with early on-set of schizophrenia last year and has been tried on numerous medications. John suffered the loss of a close friend last year and his father states that “john has gone down hill rapidly since”. Johns mother was diagnosed with schizophrenia at the age of twenty five but she reports feeling abnormal at an earlier stages in her life. John reports his Quality of life to be non existent, and that he has no social skills or aspiration to complete college.
Johns attending hospital due to relapse of his symptoms and he is currently been tried on a new antipsychotic called clozapine which is a second generation antipsychotics used to treat both the negative and positive symptoms of schizophrenia, this will be further discussed in the assignment. When the disorder appears in adolescence this means more life years of disability particularly as the prognosis and outcome for early onset cases is often worse than for adult onset cases.
Specifically, adolescent onset predicts less independence, poorer educational achievement or access to further education, less likelihood of employment and poverty of social relationships in adult life (e. g. Hollis, 2000). Schizophrenia is often a lifelong illness linked with high rates of morbidity and disability for sufferers. Stanley et al (2007) describes Schizophrenia as a complex, debilitating brain disease impairing perception, cognition, volition, social communication, emotions, and causing delusional and hallucinatory experiences.
The exact cause of most schizophrenia is not known, but research suggests that a combination of factors, including heredity, biology, psychological trauma and environmental stress, may be involved. The writer will now discuss how these factors have contributed to john being diagnosis with this mental illness. Schizophrenia tends to run in families, which means the probability of developing schizophrenia may be passed on from parents to their children. Cannon et al (1998) has found that genetic factors play a significant role in the etiology of the disorder, with heritability estimated at approximately 83%.
As john’s family history is examined it becomes clear that genetics plays a major role in john been labelled with this severe and persisting mental illness. John’s mother was diagnosed with schizophrenia at the age of twenty-five buts reports experiencing abnormalities in her teenage years.
In the past the main way predicting that a child was at risk of developing schizophrenia was through genetics. It is now known, however, that such a sampling strategy would exclude the majority of persons who develop schizophrenia (Gottesman and Erlenmeyer-Kimling, 2001).
New studies are being carry out to detecting early symptoms in children, these studies are specifically designed to monitor any abnormalities in motor and language development, intellectual and cognitive impairment, disturbances in emotional and behavioural functioning, as well as social and interpersonal maladjustment (Bearden et al. , 2000; Cannon et al. , 2002; Done et al.
, 1994; Hans et al. , 2000; Jones et al. , 1994). The brains of people with schizophrenia look a little different from the brains of people without it, but the differences are small.
Which generates significant evidence supporting a neurodevelopmental basis for schizophrenia (Church et al.
, 2002; Lipska and Weinberger, 2002; Murray and Lewis, 1987; Remschmidt, 2002; Weinberger, 1995). Schizophrenia has been linked with special chemicals in the brain called neurotransmitters. Neurotransmitters help nerve cells in the brain communicate with each other. If these chemicals are out of balance or not working properly, messages may not make it through the brain correctly, leading to symptoms. Previous studies have recognised that schizophrenia is characterised by disruption of a network of connected regions (Lawrie, 2004).
Sometimes, the fluid-filled cavities at the center of the brain, called ventricles, are larger in people with schizophrenia. The “disconnection hypothesis” of schizophrenia is based mainly on studies that report disrupted functional connectivity between the prefrontal cortex and other brain regions (Friston and Frith, 1995; Lawrie et al. , 2002; Meyer-Lindenberg et al. , 2001; Kim et al. ,2003) and suggest a relationship between these deficits and both clinical and cognitive features of schizophrenia. Also, the overall gray matter volume is lower, and some areas of the brain have less or more metabolic activity than normal.
Research has highlighted a difference in neurological soft signs rates (NSS), which are delicate, noticeable signs of neurological impairment that cannot be generalised to a specific brain region (Mohr et al. , 2003). Patients suffering from schizophrenia have considerably higher rates of NSS than unaffected individuals (Bombin et al. , 2005; Compton et al. , 2007a, Gupta et al. , 1995; Heinrichs and Buchanan, 1998).
Among patients with schizophrenia, NSS are associated to greater cognitive and social impairment (Mohr et al. , 2003).
The stage of development, of the onset of schizophrenia may play a role in the degree and nature of brain alterations. As Johns is diagnosed with earlier-onset schizophrenia, it’s believed to have a more profound symptom severity and deficits in morphometric and biological measures compared to later-onset individuals (Thompson et al. , 2001).
It has also been argued that adult-onset schizophrenia is linked with more prominent deficits in the later maturing brain regions, such as the frontal and temporal lobes (Gogtay et al. , 2004; Mehler and Warnke, 2002).
This will greatly influence development functions such as speech and language, and cognitive and psychosocial abilities, which have not yet fully matured. It also stated by emedtv(2008) that through microscopically examining brain tissue of dead patients, show that changes occur with the characteristics of brain cells in people with schizophrenia. It is also believed that many of these changes occurred in the womb, because they are not accompanied by glial cells, which are always present when a brain injury occurs after birth.
Studies of environmental influences on schizophrenia indicate a number of prenatal complications increase the risk of schizophrenia.
A study done by Ellman et al (2007) investigates whether health-risk behaviours among schizophrenic pregnant women were associated with an increased incidence of obstetric complications. Obstetric complications have been defined as an error or mistake that has occurred during normal course of events and offspring development during pregnancy, labour-delivery, and the early neonatal period (McNeil, 1988).
Nilsson et al (2002) found that women diagnosed with schizophrenia before the birth of their babies were at especially heightened risk for obstetric complications and that smoking partially mediated these effects. This raises the question whether it could be t possible that it is the schizophrenic mother’s engagement in health-risk behaviours, rather than her genetic arrangement for the disorder, that is related to increased incidence of Obstetric complications. John’s mother used nicotine as a co-morbidity in combating aversive symptoms.
In support of this hypothesis, Smith et al (2002) suggests that nicotine has been reported to improve cognition, negative symptoms, and physiological abnormalities in schizophrenia patients. The genetic model alone does not fully explain domestic schizophrenia. What is more, different genotype-environmental interactions have been hypothesized to contribute to the incidence and development of schizophrenia. Current schizophrenia theories suggest no single cause of schizophrenia exists.
Instead, schizophrenia genetics leave some people susceptible to the illness, which is triggered by environmental factors (National Institute of Mental Health 2004).
Life stressors may also trigger schizophrenia in people whose genetics leave them susceptible to the illness. Ending relationships, leaving home, and other life stressors have been linked to schizophrenia onset in some cases. In Johns case notes it has been highlighted that the death of a close friend has had a major impact on progression and early on-set of this mental illness.
Through-out the last year john has tried five different antipsychotics with-out success, he is now to commence Clozapine to combat both positive (i. e.
hallucinations, delusions, racing thoughts), negative (i. e. apathy, lack of emotion, poor or nonexistent social functioning)symptoms. Clozapine remains the only medication that has shown consistent superiority over other antipsychotics in the management of patients who fail to benefit adequately from standard treatment (Kane 2006).
Most experts recommend that at least 2 antipsychotics should be tried before going on to clozapine.
It is widely agreed that six week trial period be monitored before completely committing to this drug. It is also recognised that most psychiatrist are reluctant to start young adults on clozapine due to the severe side affects but Kane(2006) argues that many clients who might benefit from clozapine are not given a trial , and even among those who are, it is often far later in the illness course than is appropriate. Conclusion
With the knowledge provided in this paper it is clear that genetic factors play a major role in the etiology of schizophrenia. But with further research the writer has come to the conclusion that the genetic model alone contribute to the occurrence and development of schizophrenia. Many other factors can influence the response of the schizophrenia genetics.
In this case study it was the death of a close friend which triggered the response. The author also argues that clozapine should be more widely used especially in early on-set cases.
