Biological and Cognitive Approaches for the Treatment of Schizophrenia

Critically evaluate how the biological and cognitive approaches within psychology explain the cause of and how they aim to treat Schizophrenia.

Schizophrenia is a severe mental disorder that affects a person’s perception of reality by affecting their comprehension of thoughts and emotions. [1] Schizophrenia has many symptoms that can be filtered out into 3 main categories; positive symptoms such as hallucinations, delusions and thought disorders that are not seen in healthy people, negative symptoms such as reduced expression of emotions, reduced feelings of pleasure in everyday life and a difficultly of beginning and sustaining tasks, and finally, cognitive symptoms such as difficulty focusing, difficulty with higher motor functions e.g. understanding information and making a rational decision based on it and a decreases in the ability in using their working memory. [1] Schizophrenia was first characterized in 1908 by the Swiss psychiatrist, Eugen Bleuler. [2] However, it is believed the mental disorder Dementia Praecox was the first medical formulization of schizophrenia which was described by Arnold Pick, a professor of psychiatry at the University of Charles in Prague around 1891. [2] Furthermore, studies show that 220,000 people in England and Wales have been diagnosed with schizophrenia, which in 2007 accounted for approximately 30% of the total expenditure on adult mental health and social care services.[3] Over the years there have been many different theoretical approaches within in psychology aimed to explain and in turn treat schizophrenia. More to the point, there are two main approaches being cognitive and biological that have dominated the field when it comes to explaining and treating this mental disorder. [4] In this essay I aim to critically evaluate how the two approaches above explain and aim to treat this devasting disorder of the mind.

The cognitive approach within psychology theorizes that behavior is based on the how the mind processors external stimuli [5]. In 1952, Jean Piaget defined a schema as “a cohesive, repeatable action sequence possessing component actions that are tightly interconnected and governed by a core meaning”. [6] Thus, meaning that the symptoms of schizophrenia are caused by a problem in the mental processes and recalling certain schemas. [7] In conjunction with this, symptoms of schizophrenia can include a  decrease in working memory and difficulty with higher motor function. [1] Confirming this, meta-analysis of studies by D. Dickinson, M.E. Ramsey and J. M. Gold illustrated that mental processing speed of patients was the largest single cognitive impairment in schizophrenia. [8] However, Knowles et al went on to disprove this by showing there were multiple moderating factors that affected the mental processing speed of the patients, including an antipsychotic medication that had been prescribed to the patients. [9]  This then opens the door to argue that this cannot be the case in schizophrenia as a patient can suffer from various symptoms that alter their perception of the environment, such as hallucinations. Therefore, the behavior they then portray is based on faulty information so we cannot assume that a patients mental thought processes are the cause of the behaviour and schizophrenia.

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There have been different methods aimed to treat schizophrenia within the cognitive approach, but whilst researching this topic it came to my attention that the most common way to treat schizophrenia was cognitive behavioural therapy (CBT). CBT helps manage patients’ problems by attempting to changing the way they think and behave via talking it through with a trained psychiatrist. [10] Furthermore, CBT was originally developed for depression by Dr. Aaron T. Beck around the 1960s at the university of Pennsylvania. [11] The aims of CBT as illustrated by Dr. A Beck encompassed the aspirations: developing a therapeutic relationship with the patient, developing a collaborative list of problems and deciding on a clear goal for therapy sessions. [12] Over the years CBT has been around there have been many studies carried out to determine if it is an effective way to treat schizophrenia. In May 1999 a study was carried out by G. Haddock with 21 inpatients experiencing a recent-onset acute schizophrenia episode, in his study he deduced that the recovery period of symptoms was decreased by 25-50%. [13]Furthermore, the time the patients spent in hospital was 50% of that of the control patients. [13] However, after further reviewal it showed that this study was limited as: it was not carried out by a blind and independent assessor, the CBT treatment consisted of several elements and the control treatment didn’t control for non-specific aspects of therapy. [13]Furthermore, meta-analysis of CBT compared with a non-cognitive therapy exhibited no significant differences, which begs the conclusion that CBT is effective as a treatment for schizophrenia.   However, it does not excel forms of therapy that are more perceptible and transparent. [14] So my evaluation of CBT used as a treatment would be that it is effective and does work, but no more or less than any other cognitive treatment. Thus, I would hypothesize that this is due to how schizophrenia does not have set symptoms and can affect one patient very differently to another. Therefore, the way a psychiatrist may treat one patient effective could render useless in the treatment of another patient.

The biological approach to schizophrenia is more complicated, many different studies have theorized different causes from subtle differences in the structure of the brain to altered levels of certain neurotransmission chemicals such as dopamine. [15] The most prominent biological cause of schizophrenia seems to be the dopamine hypothesis. The dopamine hypothesis was first proposed around the 1970s but there since has been two different versions of the dopamine hypothesis, the second in 1991 and with both technological and medical advances a third hypothesis is being developed. [16] The first emerged after the discovery of antipsychotic drugs and the studies of Carlsson and Lindqvit who observed that after administering the drug to animals an increase in metabolism of dopamine occurred. [16]The antipsychotic drugs seen to be effective to psychosis worked as they blocked the reuptake of dopamine and other chemicals I the brain, resulting in their dissipation. [17] It was then further studies showing that clinical effectiveness of the antipsychotic drugs was directly related to the affinity for dopamine receptors, it was this that reinforced the hypothesis. [18] However, this hypothesis didn’t make any links to other causes such as genetics and neurodevelopment. [16] Furthermore, the study’s where only confined to dopamine and no thought was given to any risk factors known for schizophrenia. [16] The second hypothesis arose in 1991 where most the focus turned on to the D2 receptors, after finding clozapine was an effective with patients that the typical antipsychotic drugs were non-functional. [19] Positron emission tomography studies then revealed a reduced cerebral blood flow to the frontal cortex. [16] Furthermore, damage observed of dopamine receptors in the prefrontal cortex results higher concentration of dopamine and D2 receptor density in the striatum, [20] whereas, application of dopamine agonists to prefrontal areas reduced dopamine metabolite levels. [21] This provided the structure to triangulate that schizophrenia is caused by frontal hypodopaminergia resulting in striatal hyperdopaminergia. [16] However, there are flaws in this hypothesis due to the methods the evidence was obtained such as; most  the evidence the hypothesis was based on was produced from testing on animals which have a similar anatomy to humans but not an identical anatomy and the hypothesis was also based on evidence that used predated technology which has since advanced. [16] Furthermore, the hypothesis was deficient in direct evidence that for elevated striatal dopaminergic function and had no direct evidence low concentration of dopamine in the frontal cortex. Leaving it unclear how the dopaminergic abnormalities where related to the symptoms of schizophrenia. [16] Another explanation to schizophrenia would be the serotonin hypothesis. This hypothesises the cause of schizophrenia to be serotonergic overdrive in the cerebral cortex, specifically in the anterior cingulate cortex and the dorsolateral frontal lobe. [22] However, the evidence for the hypothesis was based on how Lysergic acid diethylamide effects the serotonin receptors in the cerebral cortex, LSD much more prominent effect on the serotonin receptors than what occurs in the patients of schizophrenia. [23]

The number of different methods of treating schizophrenia biologically are not of any shortcomings. Antipsychotic drugs are the most popular treatment of all stages of schizophrenia, there are two main types of drugs: first generation antipsychotic (FGA) agents and in 2005 a new wave of drugs such as clozapine, where made available called the second-generation antipsychotic (SGA) agents. [24] During the period between 1960 to 1980 FGAs to characterize the drugs as effective or a placebo. [24] The exact mechanism of antipsychotic drugs is unknown, however the dopamine hypothesis suggests that FGAs are D2 receptor antagonists. [25] Thus, they reduce dopaminergic neurotransmission in the four dopamine pathways. [25] However, this does not account for the serotonin overdrive in the cerebral cortex. Furthermore, FDAs can cause negative side effects to the patients such as ‘tardive dyskinesia’. [26] Much similar to the FGAs, there isn’t a known mechanism to how SGAs work and they share the same suggestions on how they work using the dopamine hypothesis. [27] However, the serotonin hypothesis suggest that SGAs is a serotonin-2A receptor antagonist, which blocks the serotonin pathways. [27] However as with the case in FGAs the SGAs also cause negative side effects, in the Clinical Antipsychotic Trials of Intervention 1061 of the 1432 patients that took part in the study discontinued the treatment due to harsh and intolerable side effects. [28] So to conclude, I would say that antipsychotic drugs are effective at treating negative and positive symptoms of schizophrenia, however, they do not cure schizophrenia and in most cases the negative side affects of these agents leave the patient with no other choice but to discontinue the use of them.

In conclusion, I would suggest that you can’t explain the cause of schizophrenia using one psychological approach. Furthermore, to treat schizophrenia in the most effective way for the patient you must combine multiple approaches into the treatment plan.

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