web viewcbt looks at not curing schizophrenia but teaching the patient how to change their thoughts...
TRANSCRIPT
SCHIZOPHRENIA;
Symptoms
Biological explanations & Evaluations
Cognitive explanations Evaluations
Similarities and Differences
Treatments
Symptoms
There are two types of symptoms when looking at schizophrenia; positive symptoms and negative symptoms.
Positive symptoms refer to an excess in behaviour, i.e. things that are present in the patient (but shouldnt be). Examples of positive symptoms are:
Hallucinations, where the patient hears or sees things that do not exist such as voices commenting on their behaviour
Delusions, such as delusions of control, where the patient thinks their actions are being controlled by outside forces
Thought insertion, where the patient thinks that the thoughts in their heads are put there by someone else
Thought withdrawal, where the patient thinks outside forces are removing their thoughts from their mind
Thought broadcasting, where the patient believes their thoughts are being broadcasted to others
Negative symptoms refer to behaviour that is missing. For example:
Poverty of speech, where the patient uses as few words as possible
Social withdrawal, where the patient no longer interacts with family and friends
The flattening affect, where the patient has a lack of expression in their voice and does not show emotions on their face
Five different types of schizophrenia:
Catatonic
Paranoid
Disorganised
Residual
Undifferentiated
Different symptoms present in different types of schizophrenia.
Biological explanations;
GENETIC FACTORS:
This explanation considers the role of genes in schizophrenia. Some psychologists think that a combination of genes could be responsible for schizophrenia. This is because schizophrenia does seem to run in families, suggesting a genetic link. It is thought that the presence of certain genes means some people may have a more vulnerable predisposition to schizophrenia, meaning something in the environment may trigger the onset. Family and twin studies are used to study the genetic influence on schizophrenia.
Studies to support this: Gottesman (1991)
Gottesman and Shields (1991) reviewed the evidence from 41 European studies that had identified a genetic link in schizophrenic patients. He found 1% of the general population had schizophrenia. However you were more likely to get it if you were close to someone genetically, who had schizophrenia. They identified a 48% concordance rate for MZ twins and a 15% for DZ twins. This study demonstrates the genetic link within schizophrenia but also highlights the role of the environment as if it was purely down to genetics; you would expect MZ twins who share 100% the same DNA, to both have schizophrenia if one did.
Evaluation of genetic factors as an explanation
Strengths
Family and twin studies evidence (such as Gottesman) give support for a genetic component as concordance rates go up in direct relationship to the degree of relatedness. For example, when one MZ twin has schizophrenia the incidence of the disorder occurring in the second twin is nearly 50% compared to only 15% in DZ twins.
Heston, who controlled environmental influences by comparing adopted children whose natural mothers had schizophrenia, with adopted children whose natural mothers did not, found that of the children with schizophrenia mothers, 10% went onto develop the disorder. None of the children from the comparative group did so. This supports genetic factors as it highlights how the disorder must have been genetically passed down as the children werent in the same environment as the schizophrenic mother.
Weaknesses
The large numbers of genes linked to schizophrenia are unlikely to all be associated with the disorder and it has been suggested that it may be a type of genetic mutation rather than a specific locus.
Gottesman and Shields study does act as supportive evidence but also highlights there has to be an environmental element, thus supporting the nurture side of the nature/nurture debate.
BIOCHEMICAL FACTORS:
The Dopamine hypothesis states that the brain of schizophrenic patients produces more dopamine than normal brains. This explanation arises from MRI and PET scans showing an excess of dopamine at the synapses of schizophrenia patients. It would explain why hallucinations occur as the brain is too active.
Strengths
Lindstroem et al used a PET scan to investigate the uptake of IDOPA which is used to make dopamine. Ppts were 10 schizophrenics who werent being treated for schizophrenia and 10 normal people. They found the IDOPA was used more quickly in schizophrenics, suggesting that they make more dopamine.
Homovanillic acid is a waste product of dopamine. Donnally et al. looked at the homovanillic acid that passed out of schizophrenics and non-schizophrenics, finding that schizophrenics produced more. This suggests that they also produce more dopamine, demonstrating the link between the neurotransmitter and the disorder.
Weaknesses
As excess dopamine is only measured after onset it could be effect not cause
Depatie and Lal found that apomorphine, a drug that increases the effect of dopamine, did not create schizophrenia symptoms in their participants. If an excess of dopamine was responsible for schizophrenia, then you would expect symptoms to occur when an excess of dopamine is inflicted.
Cognitive Explanation
The cognitive approach would see schizophrenia caused by a problem with processing information. Hemsley (1993) suggested schizophrenics cannot distinguish between information that is already stored and new incoming information. As a result, schizophrenics are subjected to sensory overload and do not know which aspects of a situation to attend to and which to ignore. The role of biological factors is acknowledged in this explanation it says that the condition has always existed, but is worsened by those around them
Studies that support the cognitive explanation:
Frith & Done;
(A) To see if cognitive functioning differed for non-schizophrenics compared with schizophrenics, focusing on their negative symptoms.
(P) They gave schizophrenics and non-schizophrenics a design fluency task.(R) Those with negative symptoms had more difficulty in creating their own responses.(C) This implies that their cognitions were different they had more trouble thinking of their own words.
A weakness with this study is that it only focuses on the symptoms of schizophrenia; they do not study what causes the problems with processing information.
Strengths
Focuses on the current cognitions
Plenty of research into the idea Frith and Done focused on negative symptoms of schizophrenia to see if cognitive function was different from those who did not have schizophrenia. Demonstrates how their cognitions were different, i.e. schizophrenics had more difficulty thinking of their own words.
Empowers the individual to change Ethical
Weaknesses
Ignores the environmental influences unlike Social approach
Unscientific
Blaming the individual can make the disorder worse - SFP
Is thinking irrational?
Which is the cause? Which is the effect? A lot of studies, i.e. Frith and Done focus on the symptoms of schizophrenia, not what causes the problems with information processing initially, therefore is this an explanation for schizophrenia.
Treating schizophrenia
Much like there are different approaches to explaining schizophrenia, there are different approaches in treating it. The approaches that look at treating schizophrenia are:
Cognitive - CBT
Social Care in the community
Biological Drug therapy
The Cognitive approach to treating schizophrenia:Cognitive behavioral therapy (CBT) is based on the idea that most unwanted thinking patterns, and emotional and behavioral reactions are learnt over a long period of time. It focuses on our present behavior and thoughts, rather than how these occurred. CBT looks at not curing schizophrenia but teaching the patient how to change their thoughts and live relatively normally. The aims are achieved though questioning and challenging the present thoughts. The steps are:
First engaging and establishing trust with their patient
Helping the patient to identify their behaviour as dysfunctional and what their delusions are
To challenge those delusions by looking at evidence
To help the patient to begin to test the reality of the evidence
Most people will require between eight to 20 sessions of CBT over the space of six to 12 months. CBT sessions usually last for about an hour.
Evidence;
Sensky cognitive treatment (A) To compare CBT with non-specific befriending interventions for patients with schizophrenia (P) There was a randomized controlled design, with ppts allocated to 1 of 2 groups:- CBT group- Non-specific befriending groupThere were 90 patients, aged 16-60 years. Both interventions were delivered by 2 experienced nurses who received regular supervision. Patients were assessed by blind raters at:- base line- after treatment- and at a 9 month follow up evaluation
They were assessed on measures including the Comprehensive Psychiatric Rating Scale, the Scale for Assessment of Negative Symptoms, plus a depression rating scale. Patients continued to receive routine care throughout the study. The patients received a mean of 19 individual treatment sessions over 9 months. Both interventions resulted in significant reductions in positive and negative symptoms and depression. After treatmen