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Psychological Approach to Schizophrenia Disorder

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Schizophrenia is a chronic and severe neuropsychiatric disorder which produces a disruption of patients’ lives at different functional levels, such as neurochemical, neurophysiological, neuroanatomical, emotional, cognitive and even social.[1] Schizophrenia has a profound effect on both the individuals affected and society. In most cases, it is manifested as a result of the interaction of both genetic and psychological factors, as well as certain environmental conditions.[2] Patients with a diagnosis of schizophrenia die 12-15 years before the average population.[3] This causes more loss of lives than most cancers and physical illnesses. This essay will discuss how the two psychological approaches, biological and cognitive, explain the aetiology and treatment strategies which are in place to prevent the condition.

The first plausible biological theory is the dopamine hypothesis. A dopaminergic imbalance in the brain is thought to give rise to the symptoms of schizophrenia, which are characterized into positive, negative and cognitive. It was initially thought that there was too much dopamine in the brain of patients with schizophrenia.[4] This belief was based on observations which suggested that positive symptoms were associated with hyperstimulation of D2 receptors in the striatum. Benzel et al[5] stated that 3 genes: COMT, DRD4, AKT1; are associated with excess dopamine in specific D2 receptors, leading to acute episodes and positive symptoms, which include delusions and hallucinations. The study provides evidence that genetic information among these loci may increase susceptibility to schizophrenia. Gottesman[6] found an association between schizophrenia and genetic similarity. Identical twins have the highest risk, they are 48% more likely to develop schizophrenia, and the risk of non-identical twins lies between 10-15%. This does not insinuate causation but merely suggests that the disorder tends to run in families.

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Another biological explanation is the viral infection theory. Many epidemiological studies have indicated that viral infections may play a role in many cases of schizophrenia.[7] Nucleic acids were extracted from defined regions of cases and controls and analysed by four methods. These methods helped identify DNA and RNA species present in the brains of individuals with schizophrenia, but absent in lower concentrations in samples from control individuals. These studies resulted in the identification of viral-associated sequences, which may be associated with disease pathogenesis. Up to 10–20% of schizophrenia cases may be caused by infectious aetiologies.[8] Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. The specific mechanisms of bacterial infections and brain disorder are unclear, although, recent findings suggest that the maternal inflammatory response may be associated with foetal brain injury.

Furthermore, pregnancy, delivery and neonatal complications can lead to schizophrenia. Weinberg[9] found that symptoms which occur very frequently in schizophrenia can be linked to damage while the brain is developing in the womb. Symptoms can also be linked to the mother developing flu whilst pregnant, implying people born in winter after an influenza epidemic, are more susceptible to developing schizophrenia. Studies[10, 11] have also found that signs of asphyxia at birth are associated with an increased risk of schizophrenia in adults. Patients with schizophrenia have an excess of obstetric complications in their early developmental histories, and such complications are associated with a younger age at onset of their disease. Huttunen’s study[12] suggested that maternal stress during pregnancy, especially during the second trimester, consequently can affect the temperament of the child and increase the risk of psychiatric and behavioural disorders including schizophrenia.

The cognitive model generally regards schizophrenia as a thought disorder. It has two aspects, the first[13] seeks to derive the variety of abnormalities of behaviour and experience, which characterises the disorder in terms of an alteration in the way stored material influences the processing of information. In this endeavour, it’s varying usages and modes of operation require considerable clarification. It does, however, seek to address the subtler experimental, perceptual and cognitive phenomena which may be present. The second aspect of the model concerns the possible neural bases of the cognitive dysfunction. The view of schizophrenia here is resulting from a disturbance at one or more points in neural circuits, which result in contextually appropriate stored material influencing stimulus processing.

Hemsley study[14] suggested that people diagnosed with schizophrenia cannot filter information, therefore, they address too much irrelevant information. Hence overwhelming their capacity to understand and make sense of the information obtained, consequently causing them to interpret the world differently. Thus, hallucinations were internal thoughts not recognised by the schizophrenic and were interpreted as their external reality. Frith[13] supported Hemsley[14] stating the basic cognitive dysfunction could potentially be difficulties developed with the self-monitoring of intentions and actions, leading to individuals own intentions not being recognised. Frith’s model[13] explained the onset and maintenance of the positive symptoms of schizophrenia. He also further expressed that irregular neural pathways were created between the hippocampus and the prefrontal cortex which originated from the faulty filtering. This resulted in the disruption of dopamine levels.

Drury et al [15] proposed that schizophrenics experience difficulties interpreting the beliefs and intentions of others, adding weight to Frith’s theory that schizophrenics suffer deficiency in meta-representation. Essentially, there could be alternative interpretations of Drury et al study[15] because the poor performance of schizophrenics may be due to information processing overload in dealing with the complex nature of the task. This suggests that schizophrenia is not due to problems with meta-representation, as Frith indicated, but due to difficulty filtering information and attending relevant information, as suggested by Hemsley[14]. Meyer-Lindenberg et al study[16] agrees with Frith’s model[13] as it also implies a link between faulty processing and high dopamine levels. This makes the cognitive approach appear promising, as it links the biological and clinical aspects of the disorder. Both studies[13,14] found that basic cognitive disturbances resulted in the cause of schizophrenia symptoms. But, this is the explanation for the symptoms of schizophrenia but not the aetiology of schizophrenia itself. Therefore, the cognitive theory alone cannot explain the disorder. In addition, the cognitive approach is limited because it can only provide an explanation for the positive symptoms, it offers no explanation for negative symptoms, for example, affective flattening. It also assumes that cognitive dysfunction is the cause of schizophrenia when there is a possibility that schizophrenia causes cognitive dysfunction.

Schizophrenia requires support which is more comprehensive, intensive and continuous than most chronic medical conditions. Schizophrenic patients require a foundation of treatment that includes both pharmacological and psychosocial treatment approaches.

Somatic treatment of schizophrenia through earlier attempts met with some success, but the introduction of chlorpromazine into clinical practice in the mid-1950s was the beginning of modern treatment.[17] Drug treatment is effective in managing acute psychosis, reducing the risk of relapse and allows the patient to function more effectively and appropriately. Additionally, they are also successful at treating hallucinations and delusions. However, they may not be as beneficial with other symptoms, such as reduced motivation and emotional expressiveness. The development of new antipsychotic drugs in the 1990s had been influenced by the dopamine hypothesis. The newer antipsychotics, apart from clozapine, seemed to be as effective in treating positive symptoms as traditional antipsychotics, but have fewer and less severe side effects.[18] Clozapine is more effective than traditional antipsychotics and is only offered to patients who have not responded to other antipsychotic drugs. Antipsychotic drugs reduce dopamine activity and improve the severity of symptoms which suggests that the dopamine hypothesis is valid.

Two forms of Cognitive behavioural therapy (CBT) are progressively being used in attempt to treat people with a diagnosis of schizophrenia.[19] Stress management is the first form, it involves working with individuals to help them cope with the stress associated with psychotic experiences. A detailed evaluation is carried out which consists of the problems and experiences an individual is having, their triggers and consequences, and developing strategies to help cope with them. Cognitive techniques, such as distraction from intrusive thoughts and using relaxation techniques, is an example of a procedure used. This approach has proven successful in preventing or delaying schizophrenia moving into a first episode.[20,21] The second, known as belief modification, involves attempts to change the nature of delusional beliefs the individual may hold.[19] It involves the use of verbal challenge and behavioural hypothesis testing. The verbal challenge encourages the individual to view a delusional belief as just one of several possibilities, they are not told the belief is wrong but is asked to consider an alternative view provided by the therapist. A similar process is used to challenge hallucinations, focusing on the patient’s beliefs about their power, identity and purpose. Behavioural hypothesis testing involves challenging any thoughts in a more direct, behavioural way. The number of studies to evaluate this type of intervention is relatively small. Jones et al[22] concluded from his four randomized trials, that these interventions reduced both the frequency and the impact of hallucinations. While they had a limited impact on the measures in delusional beliefs, they reduced the amount of distress associated with them. In comprehension, those taught ways of challenging their delusional beliefs or hallucinations were half as likely to relapse.

The biological and cognitive approaches do not explain the cause and complexity of schizophrenia in a clear and distinct manner, a combination of approaches is needed. The cognitive and biological approach are linked and so you cannot consider one explanation without considering the other. But, this also makes the theories appropriate and consistent due to them being so connected. Drug treatment is effective at managing many of the symptoms. Antipsychotic drugs, being the most common, improve the severity of the symptoms by reducing dopamine activity. Thus, supporting the dopamine hypothesis of the biological approach. CBT has been found to have a significant effect in reducing both positive and negative symptoms. Therefore, the cognitive approach has great potential to be valid, treatments based on cognitive assumptions are effective in improving schizophrenia symptoms.    

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