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What is Schizophrenia?
Schizophrenia= a type of psychosis, a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality
Most common psychotic disorder
Affects about 1% of the population
Men are more likely to have schizophrenia than women
Hallucinations and delusions are most commonly reported by people with the disorder
Diagnosis of Schizophrenia
Diagnosis of any mental health condition are made using the Diagnostic and Statistical manual of Psychiatric Disorders (DSM)
Classifying Schizophrenia from DSM-V:
A: Two (or more) of the following each present for a significant portion of time during a 1 month period (or less is successfully treated). At least one of these must be 1, 2 or 3;
Delusions
Hallucinations
Disorganised speech (e.g. frequent derailment or incoherence)
Grossly disorganised or catatonic behaviour
Negative symptoms (i.e. diminished emotional expressions)
Symptoms of Schizophrenia
Delusions (false beliefs) – bizarre beliefs that seem real to the person with schizophrenia, but they are not real. Sometimes these delusions can be paranoid (i.e. persecutory) in nature. Delusions may also involve inflated beliefs about the person’s power and importance. There may also be delusions of reference where it is believed that events in the environment are directly related to them e.g. special messages being relayed via TV.
Speech poverty – lessening of speech fluency and productivity, reflecting slow or blocked thoughts. May produce fewer words in a test of verbal fluency (e.g. name as many animals as you can in one minute) due to a difficulty in spontaneously producing the words. May also be reflected in less complex syntax e.g. fewer clauses, shorter utterances (associated with long illness and early onset of illness).
Hallucinations (false perceptions) – bizarre, unreal perceptions of the environment that are usually auditory (hearing voices) but may also be visual (seeing lights, objects or faces), olfactory (smelling things) or tactile (e.g. feeling that bugs are crawling on or under the skin). Many schizophrenics report hearing a voice or voices telling them to do something (ie hurt themselves or others) or commenting on their behaviour.
Avolition – the reduction of, or inability to initiate and persist in, goal-directed behaviour (e.g. sitting in the house for hours every day, doing nothing). Avolition is distinct from poor social function or disinterest, but is often confused with this.
Positive vs Negative Symptoms of Schizophrenia
DSM-V: One positive symptom must be present
ICD-11: Two or more negative symptoms are sufficient for diagnosis
Reliability in Schizohrenia diagnosis
Reliability= The consistency of a measuring tool (e.g. The DSM) or other tests used in diagnosis. A test/tool must be valid for it to be reliable
Test-Retest Reliability
Doctors must be able to reach the same conclusions about a patient at two different points in time. The DSM and other tests must enable this to occur, so a patient isn’t ‘labelled’ with a diagnosis which then changes or is re-diagnosed as another condition later on.
Inter-Rater Reliability
The extent to which different assessors agree on their assessments.
Doctors must reach the same conclusions about a patient’s diagnosis. The DSM and other tools must enable inter-rater reliability. Eg. Doctors should be able to consult the DSM about a patient, independently from each other and achieve the same diagnosis.
Cheniaux et al (2009) study
Two psychiatrists asked to independently diagnose 100 patients using both DSM and ICD criteria. One psychiatrist diagnosed 26 with schizophrenia according to the DSM and 44 according to the ICD. The other diagnosed 13 with schizophrenia according to DSM and 24 according to ICD. This research suggests the inter-rater reliability of classification systems is poor because we would expect the same number of diagnoses made irrespective of criteria used
AO3 EVALUATION: Reliability in Schizophrenia
Cultural differences in diagnosis- Research suggests there is a significant variation between countries when it comes to diagnosing schizophrenia i.e. culture has an influence on the diagnostic process. Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed schizophrenia but only 2% of the British ones did.
Research support- Roseham (1973) investigated how situational factors affect a diagnosis of Schizophrenia. 8 pseudo-patients went to 12 different hospitals in the US and reported hearing voices. Once admitted, they stopped simulating symptoms. All pseudo-patients admitted with a diagnosis of Sz, one admitted with manic-depression. Normal behaviour was interpreted as symptoms of the disorder. Pseudo-patients were kept in for periods ranging from 7-52 days, the average stay was 19 days. All pseudo-patients discharged as “in remission”. 35 real patients detected sanity. This demonstrated the unreliability of diagnostic tools
Validity in Schizophrenia Diagnosis
Validity= The correctness, accuracy and meaningfulness of a diagnosis- do different classification systems arrive at the same diagnosis of the same patient?
This means it must represent something real and be distinct from other disorders.
The DSM must enable a valid diagnosis to be made, by ensuring it measures what it claims to measure (symptoms of a disorder, schizophrenia) which is different to other mental health conditions and enables psychiatrists to recognise symptoms & provide treatment.
AO3 EVALUATION: Validity in Schizophrenia Diagnosis
Gender Bias- Occurs when accuracy of a diagnosis is dependent on the gender of an individual. This may occur due to gender-biased diagnostic criteria, or clinicians basing their judgements on stereotypical beliefs held about gender. Broverman et al. (1970) found the clinicians in the US equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour therefore women tended to be seen as less mentally healthy.
Symptom Overlap- Many of the symptoms of schizophrenia are also found in other disorders such as depression and bipolar disorder. Read (2004) states that most people with schizophrenia have sufficient symptoms of other disorders that they could also receive at least one other diagnosis.
Comorbidity- Refers to the extent that two or more conditions co-occur. Schizophrenia often occurs alongside substance abuse, anxiety and depression. If conditions occur together a lot of the time, then this calls into question the validity of their diagnosis and classification (may actually be a single condition). Buckley et al. (2009) estimated that co-morbid depression occurs in 50% of patients, and 47% also have a lifetime diagnosis of co-morbid substance abuse. Swets et al. (2014)carried out a meta-analysis and found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant OCD obsessive-compulsive symptoms.
Biological explanations of Schizophrenia
Biological explanations of schizophrenia suggest that individuals are biologically determined to develop schizophrenia based on genes and neurotransmitters
What are the biological explanations of Schizophrenia?
Genetics
The Dopamine Hypothesis
Neural Correlates
Biological explanations of Schizophrenia: Genetics
Heredity (genetics) is one possible cause of schizophrenia. Schizophrenia tends to run in families and the risk of an individual developing schizophrenia is higher for those with biological relatives with schizophrenia than those without. It is thought that different combinations of genes make a person more vulnerable to schizophrenia.
Schizophrenia is thought to be polygenic – this means that its development is not determined by a single gene but a few (maybe as many as 108 genes).
Each individual gene confers a small increased risk of SZ (it is polygenic).
Other research has identified different candidate genes implicated in the development of Sz. This suggests the disorder is aetiologically heterogeneous - different combinations of genes can lead to the condition.
Genes associated with the increased risk included those coding for the functioning of a number of neurotransmitters including dopamine
Family Studies
Family Studies have confirmed that risk of schizophrenia increases in line with genetic similarity to a relative with the disorder. In Gottesman’s (1991) large-scale family study. He concluded that Sz is more common in the biological relatives of a Schizophrenic individual and the closer the degree of genetic relatedness, the greater the risk. For example, someone with an aunty with schizophrenia has a 2% chance of developing it, increasing to 9% if the individual is a sibling and 48% if they are an identical twin.
This shows that genes do play an important factor, however if genes were the only cause of schizophrenia then the percentages surely should be 100%,
The theory could be seen as deterministic; just because we are ‘predisposed’ by our genes cannot mean we necessarily get the disorder schizophrenia.
Twin Studies
If Monozygotic (MZ) twins are more concordant than Dizygotic (DZ) twins, then this suggests that the greater similarity is due to genetics.
Joseph (2004) points out that MZ twins are treated much more similarly, encounter more similar environments and experience more ‘identity confusion’ (frequently being treated as ‘the twins’ rather than as individuals) than DZ twins.
Adoption Studies
Are a way of truly separating the influence of genetics and environment, by investigating individuals who are genetically related by reared apart.
Tienari et al. (2000) found that of 164 adoptees whose biological mothers had been diagnosed with Schizophrenia, 6.7% also received a diagnosis, compared to just 2% of the 197 control adoptees (born to non-schizophrenic mothers).
Adoption Study (Heston, 1966)- Followed up on 47 children whose mothers were hospitalised with schizophrenia in Oregon, USA. The children were placed with family or into foster homes within 72 hours of their birth. Heston found that 16.6% of the children were diagnosed with schizophrenia. Heston also looked at 50 control children, none of whom developed schizophrenia. The children of schizophrenic mothers were also more likely to be diagnosed as mentally retarded or psychopathic. They were also involved more frequently in criminal activities.
AO3 EVALUATION: Genetics as an explanation of schizophrenia
Environmental factors- One limitation of the genetic explanation is that there is clear evidence to show that environmental factors also increase the risk of developing schizophrenia. These factors include both biological and psychological influences. Biological risk factors include birth complications (Morgan et al 2017) and smoking THC-rich cannabis in teenage years. Psychological risk factors can include childhood trauma which leaves people more vulnerable to adult mental health problems in general but there is now evidence for a particular link with schizophrenia. In one study by Nina Markved at al (2017), 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues. This means that genetic factors alone cannot provide a complete explanation for schizophrenia
Twin Studies
Twin studies seem to indicate that there is a strong genetic component to the disorder
Twin studies demonstrate that there may be a predisposition to develop schizophrenia, however, the fact that both twins do not always develop schizophrenia means that environmental factors must also play a part
The fact that the concordance rate for twins is not 100% means that schizophrenia cannot be accounted for by genetics alone
Sample sizes of such twin studies is always going to be very small so therefore it is difficult to generalise to the general population
Biological explanations of Schizophrenia: The Dopamine Hypothesis
The Dopamine Hypothesis claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia.
The Role of Dopamine
Dopamine is a neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure
Messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions.
Schizophrenics are said to have too many 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 (it stimulates nerve cells containing dopamine, causing the synapse to be flooded with dopamine).
Drugs that decrease dopaminergic activity: there are many different antipsychotic drugs but what they all have in common is that they block the activity of dopamine, thus eliminating symptoms such as hallucinations and delusions
Hyperdopaminergia
The original dopamine hypothesis focused on the role of high levels of dopamine (hyperdopaminergia) in the subcortex (central areas of the brain).
For example, an excess of dopamine receptors in Broca’s area may be associated with speech poverty and/or auditory hallucinations.
Hypodopaminergia
More recent versions of the dopamine hypothesis focus on abnormal dopamine systems (hypodopaminergic) in the cortex.
Goldman-Rakic et al. (2004) concluded that low levels of dopamine in the prefrontal cortex are implicated in the negative symptoms of Sz.
It may be that both hyper and hypo dopaminergia are correct. It could be that high levels in some parts of the brain are linked to positive symptoms and low levels in other parts of the brain are linked to negative symptoms.
The dopamine hypothesis has been revised by Davis and Kahn (1991), who proposed that the positive symptoms are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.
AO3 EVALUATION: The Dopamine Hypothesis
Research support- Research support comes from the development of drug therapies that specifically target dopamine. The effectiveness of these drugs demonstrate that dopamine is implicated in schizophrenia. Curran et al. (2004) - dopamine agonists (e.g. amphetamines) increased levels of DA and can induce Sz-like symptoms in non-sufferers
Individual differences- This explanation does not consider individual differences It can be considered biologically reductionist as it only explains schizophrenia by focusing on the role of one neurotransmitter.
Biological explanations of Schizophrenia: Neural Correlates
Neural correlates changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour or mental disorder.
Neural correlates are measurements of the structure or function of the brain that occur in conjunction with an experience, in this case schizophrenia.
There is growing evidence that schizophrenia is down to structural abnormalities in the brain.
Brain scanning techniques have made it possible to investigate living brain images.
Both positive and negative symptoms have correlates.
Neural Correlates- Ventricular Space
Weinberger and Wyatt (1982) found that the ventricles in the brains of schizophrenic patients were, on average, twice as large as those of normal subjects.
Suddath et al. (1990) found that in 15 pairs of twins, the schizophrenic twin was easily identified by visual inspection of the ventricles in 12 of the pairs.
Keshavan et al. (2008) found evidence for alterations in the brain’s structure and suggested that these alterations could be related to the genetic predisposition to the disorder. The alterations include a loss of grey matter in certain areas of the brain.
Neural Correlates- Avolition and Ventral Staritum
Neural correlates are patterns of structure or function in the brain that occur alongside specific experiences, e.g. Sz.
These patterns of structure or function may be implicated in origins of positive and negative symptoms.
Motivation involves anticipation of a reward. The ventral striatum is believed to be involved in this anticipation. Juckel at al. (2006) measured activity levels in the ventral striatum and a control group. They found lower levels of activity in this area in the brains of schizophrenic individuals.
Neural Correlates- Hallucinations and superior temporal gyrus
Allen et al (2007) using brain scanning techniques for schizophrenic patients suffering from auditory hallucinations and compared them to a control group.
During this procedure, the participants identified pre recorded speech as theirs or others.
The research found lower activation levels in the superior temporal gyrus and anterior cingulate gyrus in the hallucination group. They also made more errors.
We can conclude that reduced activity in these two areas is a neural correlate of auditory hallucination.
Neural Correlates- active flattening and Amygdala
The amygdala is responsible for our basic feelings such as lust, fear and hunger.
Research suggests that a small amygdala in schizophrenic individuals can be linked to affective flattening (a loss of emotion)
Neural Correlates- Disorganised thoughts/Delusions and the Prefrontal Cortex
The prefrontal cortex enables us to think logically and organise our thoughts
Research suggests that in schizophrenic individuals, there is a lower level of activity in the prefrontal cortex. This can help to explain positive symptoms such as delusions and disorganised thoughts
AO3 EVALUATION: Neural Correlates
Empirical Evidence- There is objective, scientific evidence to support the theory that neural correlates are implicated in the development of schizophrenia. MRIs have made it possible to investigate living brain images which is an advance on merely having to rely on post mortems.
Correlational Evidence- Findings of the research are inconsistent and it is biologically reductionist. There are also issues of causality. Cause and effect can not be established with brain abnormalities, it is still uncertain whether structural abnormalities/reduced functioning predispose to schizophrenia, or whether the onset of the clinical symptoms causes these changes.
An alternative hypothesis: the diathesis-stress model - this suggests that there may be a disposition to schizophrenia but it only develops if there is an environmental stressor
Drug therapy treatments for Schizophrenia
The most common treatment for Sz is drug therapy which seeks to target the biological causes of Sz - dopamine.
Antipsychotics can be taken as a short-term or long-term solution for Schizophrenic individuals.
Antipsychotics can also be taken alongside other forms of therapy.
They can be divided into typical (traditional) or atypical (second-generation drugs)
These drugs are not cures but only aim to minimise the symptoms of the disorder
Typical Antipsychotic drugs
Dopamine antagonist:
Typical drugs work by reducing the effects of dopamine and therefore reducing the positive symptoms of schizophrenia (hallucinations and delusions).
They are dopamine antagonists (they bind to, but do not stimulate, dopamine receptors; especially the D2 receptors).
For example, Chlorpromazine is a dopamine antagonist
Block of Dopamine receptors:
In order to be effective, Kapur et al. (2000) estimate that between 60% and 75% of D2 receptors in the mesolimbic pathway must be blocked.
Block dopamine receptors in the synapses, and can also have a sedation effect.
Unfortunately, however, for this to happen a similar number of D2 receptors in other areas of the brain must also be blocked, leading to undesirable side-effects.
Atypical Anitpsychotic drugs
Target Dopamine and Serotonin:
Second generation e.g. clozapine.
Compared to typical antipsychotics, atypical antipsychotics have a lower risk of side effects, have a beneficial effect on negative symptoms and cognitive impairment, and are suitable for treatment-resistant patients.
Target dopamine and serotonin.
Reduces depression and anxiety as well as improving cognitive functioning.
Atypical antipsychotics work by blocking D2 receptors, but unlike typical antipsychotics, they rapidly dissociate to allow normal dopamine transmission; this is what leads to less side effects.
Furthermore, whereas typical antipsychotics bind only to D2 receptors, atypical antipsychotics have a stronger affinity for serotonin receptors and a lower affinity for D2 receptors.
Atypical receptors have proven to reduce the symptoms of schizophrenia and have only claimed to reduce the effects of negative symptoms, but there is not clear evidence for this yet
Side effects of the drug Chlorpromazine
Side effects of Clozapine
AO3 EVALUATION: Drug therapies for treating Schizophrenia
Research support- Thornley et al. (2003) - compared Chlorpromazine to a placebo group. Results showed that Chlorpromazine was associated with better functioning and reduction of symptom severity (1121 ppts analysed). Relapse rate was also lower when Chlorpromazine was taken (512 ppts analysed). Gilbert et al. (1995) - 53% of patients relapsed within 10 months of stopping medication, compared to 16% who continued taking it.
Positive implications for the economy- Drug therapies are relatively cheap to manufacture and work more quickly than psychological therapies. This enables individuals to manage their symptoms more quickly and live “normal” lives. This means they can hold down a job, pay their taxes and contribute to the economy.
Over-reliance on the dopamine hypothesis- Antipsychotics work on the assumption that dopamine levels are too high (they block dopamine receptors). However, in parts of the brain, dopamine levels are too low.
Side effects can range from mild to fatal- Neuroleptic malignant syndrome (NMS) is a side effect of typical drugs. NMS can cause fever, muscular rigidity and an altered mental state. Agranulocytosis is a side effect of atypical drugs. This symptom affects the white blood cells in the body which are needed to fight infection
Chemical cosh argument- It is widely believed that antipsychotic drugs are used in hospital situations to calm and control the patient, rather than to benefit them. Short-term use is recommended to calm patients by the National Institute for Health and Clinical Excellence (NICE). Some researchers argue that this is human rights abuse (Moncrieff, 2013). As a result of the calming effects antipsychotics can have on patients, some researchers question the validity of research demonstrating them to be effective. Healy (2012) suggests it is easy to show “positive effects” in patients who have been calmed as a result of these drugs
Nature vs Nurture debate- Drug therapies only target dopamine as a cause of schizophrenia. Drug therapies only focus on the nature side of this debate and ignores the role of nurture in the development of schizophrenia. Research also suggests that schizophrenia can occur due to family dysfunction, childhood trauma, migration, etc. Arguably, an interactionist approach is best when considering forms of treatment for schizophrenia
