- Created by: abbie0107
- Created on: 11-03-20 11:48
Classification of Schizophrenia
Schizophrenia is a serious mental disorder siffered by about 1% of the world population. The symptoms of schizophrenia can interfere with everyday tasks so many sufferers end up homeless or hospitalised.
The two major systems for the classification of mental disorder are the International Classification of Disease edition 10 (ICD-10) and the Diagnostic and Statistical Manual edition 5 (DSM-5).
The DSM-5 system only requires one of the positive symptoms - delusions, hallucinations or speech disorganisation - must be present for diagnosis whereas two or more negative symptoms are sufficient under ICD.
ICD-10 recognises a range of subtypes of schizophrenia and the DSM also used to do this but this has been dropped in the DSM-5.
Positive symptoms of schizophrenia are additional experiences beyond those of ordinary existence. They include hallucinations and delusions.
Hallucinations: unusual sensory experiences. Some are related to events in the environment but others have no relationship to the environment. Voices that are heard either talking to or commenting on the sufferer, often criticising them. The sufferer may see distorted facial expressions or occasionally people or animals that are not there.
Delusions: irrational beliefs. Common delusions involve being an important historical, political or religious figure, such as Jesus. They also commonly involve being persecuted, perhaps by government or aliens. Another class of delusions concerns the body. They believe that a part of them is under external control - it makes sense to them but is bizarre to others. Some delusions can lead to aggression.
catatonic behaviour - includes the inability or motivation to initiate a task, or to complete it once it is started, which leads to difficulties in daily living and can result in decreased interest in personal hygiene. Catatonic behaviours are characterised by a reduced reaction to the immediate environment
Negative symptoms of schizophrenia involve the loss of usual abilites and experiences. Examples include avolition and speech poverty.
Avolition: finding it difficult to begin or keep up with goal-directed activity i.e. actions performed in order to achieve a result. Sufferers of schizophrenia often have sharply reduced motivation to carry out a range of activities. Andreason (1982) indentified three indentifying signs of avolition; poor hygiene and grooming, lack of persistence in work or education and lack of energy.
Speech Poverty (Alogia): changes in patterns of speech. The ICD-10 recognises speech poverty as a negative symptom. The emphasis is on reduction in the amount and quality of speech in schizophrenia. This is accompanied by a delay in sufferer's verbal responses during conversation. The DSM places its emphasis on speech disorganisation in which speech becomes incoherent or the speaker changes topic mid-sentence. This is classified in DSM-5 as a positive symptom.
· Reliability: an important measure of reliability is inter-rater reliability - the extent to which different assessors agree on their assessments. Elie Cheniaux et al (2009) has two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. One psychiatrist diagnosed 26 with schizophrenia according to DSM and 44 according to ICD and the other diagnosing 13 according to the DSM and 24 according to ICD. This shows poor reliability.
· Validity: there are a number of validity issues to consider. We can see that schizophrenia is much more likely to be diagnosed using ICD than DSM. This suggests that schizophrenia is either over-diagnosed in ICD or under-diagnosed in DSM. This is poor validity.
· Co-Morbidity: morbidity refers to a medical condition or how common it is. Co-morbidity is the phenomenon that two or more conditions. If conditions occur together a lot then it calls into question the validity of their diagnosis and classification because they might actually be a single condition. In terms of classification, if very severe depression looks a lot like schizophrenia and vice versa. This is a weakness of diagnosis and classification. A meta-analysis by Swets et al 2014 found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant obsessive compulsive symptoms. Effects of this the patients tend to receive a lower standard of medical care which in turn adversely affects the prognosis for patients with schizophrenia.
- Symptom Overlap: there is a considerable overlap between the symptoms of schizophrenia and other conditions. This again calls into question the validity of both the classifcation and diagnosis of schizophrenia. Under ICD a patient may be diagnosed with schziophrenia but DSM may be diagnosed with bipolar disorder.
• Gender bias in diagnosis: The tendency for diagnostic criteria to be applied differently to males and females. If women are under-diagnosed then this suggests that the validity of the diagnosis of schizophrenia is poor, because the procedures for diagnosis work well only on patients of one gender. Broverman et al 1970 found that clinicians in the US equated mentally healthy adult behaviour with mentally healthy male behaviour as a result there was a tendency for women to be perceived as less mentally healthy.
• Cultural bias in diagnosis: African Americans and English people of Afro-Caribbean origin are several times more likely than white people to be diagnosed with schizophrenia. Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. Sixty-nine per cent of the US psychiatrists diagnosed schizophrenia but only 2 per cent of the British ones gave the same diagnosis.This suggests that the validity of the diagnosis is poor because either it is confounded by cultural beliefs and behaviours in patients, or by a racist distrust of black patients on the part of mental health practitioners.
No one gene is thought to be responsible for this disorder - it is more likely that different combinations of genes make individuals more vulnerable.
Schizophrenia runs in families: it has been noted that schizophrenia runs in families. This is quite weak evidence in itself for a genetic link as families share the majority of their genes and environment. The more closely related you are to the person with schizophrenia the more likely you are to have schizophrenia. Kendler et al found that the first degree relatives of those with schizophrenia were 18 times more at risk of developing the disorder. Gottesman (1991) found that identical twins have 48% chance of both of them developing schziophrenia if they have the genes and fraternal twins have a 17% chance.
Twin studies offer a unique opportunity for researchers to investigate the relative contribution of genetic and environmental influences. If MZ genetically identical twins are more concordant (similar) than DZ - who share only 50% of their genes, then this suggests that the greater similarity is due to genetic factors. Joseph (2004) conducted a meta-analysis of schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins. More recent methodologically sound studies where the researchers do not know whether the twin they are assessing is MZ or DZ have tended to report a lower concordance rate for MZ twins.
Adoption studies Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are use the most methodologically sound study. Tienari et al (2000) in Finland, Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just 4 (2%) of the 197 control adoptees. The investigators concluded that these findings showed that the gender Ability to schizophrenia had been decisively confirmed.
family similarities evaluation Research has shown that schizophrenia appears to run in families, supporting the argument for a genetic basis for the disorder. However, many researchers now accept that the fact that schizophrenia appears to run in families may be more to do with common rearing patterns or other factors that have nothing to do with heredity. For example, research on expressed emotion has shown that the negative emotional climate in some families may lead to stress beyond an individual's coping mechanisms, thus triggering a schizophrenic episode. Research has shown that only 50% of children where both parents have schizophrenia develop the disorder you would expect a 100% concordance rate if solely genetic reasons for developing the disorder which suggests other factors affect the developing of Schizophrenia.
Twins study evaluation The higher concordance rate in MZ twins may be due to the fact that MZ twins tend t be treated more similary than DZ twins so nurture may explain the concordance rates rather than nature. MZ twins are treated more similarly, encounter more similar environments and experience mote identity confusion (ie frequently being treated as the twins rather than as two distinct individuals) than DZ twins. As a result there is reason to believe that the differences in concordance rates between MZ and DZ twins reflect nothing more than the environmental differences that distinguish the two types of twin. The fact that the concordance rates are not 100% means that Schizophrenia cannot be a wholly genetic disorder.
Adoption studies evaluation A central assumption of adoption studies is that adoptees are not selectively placed. There is an assumption that the adoptive parents do not know about the schizophrenic background. Joseph (2004) claims that this is unlikely to have been the case, particularly in the early studies. In countries like Denmark and the US potential adoptive parents would have been informed of the genetic background of children prior to selection for adoption. Because the adoptive parents evidently received information about the child's biological parents, one might wonder who would adopt such a child
The dopamine hypothesis claims that an excess of the neurotransmitter dopamine in central areas of the brain (Brocas responsible for speech). Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions that are the characteristic positive symptoms of schizophrenia. Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. Drugs that increase dopaminergic activity Amphetamine is a dopamine agonist, ie. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter. exposure to amphetamines can develop the characteristics of a schizophrenic episode. This generally disappears with abstinence from the drug. A02: post-mortem examinations have shown an increase of dopamine in parts of the brain (Seeman 1987) found increases in dopamine receptor density of between 60-110% compared to controls.
More recent research revised the dopamine hypothesis Davis and Kahn (1991) proposed that the positive symptoms are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway. The negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway). Evidence Neural imaging. Patel et al. (2010), using PET scans to assess dopamine levels in schizophrenic and normal individuals, found lowers levels of dopamine in the dorsolateral prefrontal cortex of schizophrenia patients compared to their normal controls. Animal studies. Wang and Deutch (2008) induced dopamine depletion in the prefrontal cortex in rats. This resulted in cognitive impairment (e.g, memory deficits) that the researchers were reverse using olänzapine, an atypical antipsychotic drug thought to have beneficial effects on negative symptoms in humans.
Neural correlates are measurements of the structure or function of the brain that correlate with an experience. Both positive and negative symptoms have neural correlates.
Neural correlates of negative symptoms: motivation involves the anticipation of a rewards and certain regions of the brain. The ventral striatum are believed to be particularly involved in anticipation and abnormalities may be involved in the development of avolition. Juckel et al (2006) measured activity levels in the vental striatum in schizophrenia and found lower levels of activity than those observed in controls. They observed a negative correlation between activity levels in the ventral striatu, and the severtiy of overall negative symptoms.
Neural correlates of positive symptoms: Allen et al (2007) scanned the brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as theirs or others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group. Reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.
Mixed evidence for the dopamine hypothesis: dopamine agonists that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers (Curran et al, 2004). Antipsychotic drugs reduce the dopamine activity and both kinds of drug study suggest an important role for dopamine in schizophrenia. Some genes identified show that not only dopamine is important in the development of schizophrenia. (can be used as strength or weakness)
Correlation-Causation problem: most of the studies leave a lot of questions unanswered such as does the unusual activity in a region of the brain cause the symptom? The existence of neural correlates in schizophrenia therefore tells us relatively little in itself.
Noll (2009) argues that antipsychotic drugs do not alleviate hallucinations and delusions in about one-third of people experiencing these symptoms. Blocking the D2 receptors of these individuals has little or no effect on their symptoms. This suggests that dopamine isn’t the sole cause of positive symptoms, other neurotransmitter systems acting independently of the dopaminergic system, may also produce the positive symptoms.
This links to a major criticism of this study as, whilst the evidence for version three may come from living brains, much of the evidence for version two has come from animal lesion or post mortem studies which means that it has been indirectly collated. Furthermore, we are not necessarily able to generalise their findings to humans as we cannot assume that dead or animal brains will react to
biologically reductionist as it over simplifies the biology involved in the transmission of dopamine, and does not take individual differences such as patients’ genetics and hormones, and their respective effects, into consideration. Moreover, it assumes that all schizophrenics’ receptors work with the same degree of sensitivity, which is simply not a generalisation we can make.
There are a range of psychological explanations for schizophrenia and some of these have focused particularly on the family and it's role in making individuals particularly vulnerable to schizophrenia
The Schizophrenogenic Mother: Freida Fromm-Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from patients about their childhoods. Fromm-Reichmann noted that many of her patients spoke of a particular type of parent, the schizophrenogenic (schizophrenia-causing) mother. The schizophrenogenic mother is cold, rejecting and controlling and creates a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions and eventually schizophrenia.
Double-Bind Theory: Gregory Bateson et al (1972) agreed that family climate is important in the development of schizophrenia but emphasised the role of communication style within the family. The developing child finds themselves trapped where they fear they are doing the wrong thing, but receive mixed messages and feel unable to comment on the unfairness of the situation. When they get it wrong, they are punished and this leaves them with an understanding of the world as confusing and dangerous. Bateson was clear that this was neither the main type of communication in the family, nor the only factor in developing schizophrenia.
Evidence: Berger (1965) found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics did. However, this evidence may not be reliable as patients recall may be affected by their schizophrenia partially due to auditory hallucinations and thee inability to reality test.
Due to the inconsistent data is presents a causality problem this explanation as it isn't clear whether the dysfunctional family causes schizophrenia or whether the schizophrenia causes the dysfunctional family. This therefore suggests there is a problem with cause and effect. (weakness)
This explanation can be regarded as being environmentally reductionist as it doesn't consider other factors such as biology that may also have an influence on the development of schizophrenia. Kendler et al found that the first degree relatives of those with schizophrenia were 18 times more at risk of developing the disorder.
This explanation can be viewed as being unethical as it pins a blame on the family as being a cause of an individuals schizophrenia which can cause family members to feel guilty leading to higher level of expressed emotion that could increases the symptoms of those suffering with Schizophrenia . (weakness)
Expressed Emotion is the level of emotion, particularly negative emotions, expressed towards a patient by their carers. It contains several elements:
- Verbal criticism of the patient, occasionally accompanied by violence.
- Hostility towards the patient, including anger and rejection.
- Emotional over-involvement in the life of the patient, including needless self-sacrifice.
Kuipers et al (1983) found that high EE relatives talk more and listen less. High levels of EE are most likely to influence relapse rates. A patient returning to a family with high EE is about four times more likely to relapse than a patient whose family is low in EE. This suggests that people with schizophrenia have a lower tolerance for intense environmental stimuli. High EE leads to stress beyond their already impaired coping mechanisms, thus triggering a schizophrenic episode.
Family relationships: The importance of family relationships in the development of schizophrenia can be seen in an adoption study by Tienari et al. (1994), In this study those adopted children who had schizophrenic biological parents were more likely to become ill themselves than those children with non-schizophrenic biological parents. However, this difference only emerged in situations where the adopted family was rated as disturbed. Genetic vulnerability alone was not sufficient the illness only manifested itself under appropriate environmental conditions.
Individual differences in vulnerability to EE: Not all patients who live in high EE families relapse, and not all patients who live in low EE homes avoid relapse. Research has found individual differences in stress response to high EE-like behaviours. Altorfer et al found that 1/4 of the patients they studied showed no physiological responses to stressful comments from relatives. Not all patients are equally vulnerable to high levels of expressed emotion within the family environment. In cases where high EE behaviours are not perceived as being negative or stressful, they can do well regardless of how the family environment is objectively rated.
A02: The explanation of family dysfunction as a cause of schizophrenia has helped to develop therapies such as family therapy in order to help to treat the disorder . This explanation therefore has practical application.
COGNITIVE EXPLANATIONS: of schizophrenia emphasise the role of dysfunctional thought processing
Cognitive explanations of delusions: During the formation of delusions, the patient's interpretations of their experiences are controlled by inadequate information processing. A critical characteristic of delusional thinking is how individual perceives themselves as the central component in events (egocentric bias) and so jumps to conclusions about external events. This is manifested in patient's tendency to relate irrelevant events to themselves and arrive at false conclusions. Delusions in schizophrenia are resistant to reality testing. They are considered to have 'impaired insight’, an inability to recognise cognitive distortions and substitute more realistic explanations for events.
Cognitive explanations of hallucinations: Hallucinating individuals have increased sensitivity to their auditory stimuli (hypervigilance) and so have a higher expectancy for the occurrence of a voice than normal individuals. Aleman (2001) suggests that hallucination-prone individuals find it difficult to distinguish between imagery and sensory-based perception. For these individuals, the inner representation of an idea (e.g. What other people think of me) can override the actual sensory stimulus and produce an auditory image that is every bit as real. Hallucinating patients with schizophrenia are significantly more likely to wrongly attribute the source of a self-generated auditory experience to an external source than are non-hallucinatory patients with schizophrenia (Baker and Morrison, 1998). errors are not corrected by disconfirming evidence because Patients with schizophrenia do not go through the same processes of reality testing (such as checking external sources) that others would do