Schizophrenia

Schizophrenia- A severe mental illness where contact with reality and insight are impaired, an example of psychosis. More commonly diagnosed in men than women.

Classifacation of SZ- 2 major systems for classifacation of the mental disorder:

• World health organisation's International Classifacation of Disease edition 10 (ICD-10)
• American Psychatric Association's Diagnostic and Statistical Manual edition 5 (DSM-V

Positive symptoms- Atypical symptoms experienced in addition to normal experiences.

• Hallucinations
• Delusions

Negative symptoms- Atypical experiences that represent the loss of a usual experience such as clear thinking or 'normal' levels of motivation.

• Avolation
• Speech poverty

Reliability- Cheniaux (2009) had two psychiatrists independently diagnose 100 patients using both DSM and ICD criteria. Inter-rater reliability was poor, with one psychiatrist diagnosing 26 with SZ according to DSM and 44 according to ICD, and the other diagnosing 13 according to DSM and 24 according to ICD. This poor reliability is a weakness of diagnosis of schizophrenia.

Validity- One standard way to assess validity of a diagnosis is criterion validity. Looking at figures from Cheniaux (2009) we can see that schizophrenia is much more likely to be diagnosed using ICD than DSM, which suggests that schizophrenia is either over-diagnosed with ICD or under-diagnosed with DSM.

Co-morbidity- If conditions occur together a lot of the time then this calls into question the validity of their diagnosis and classification because they might actually be a single condition. Buckley (2009) concluded that around half of patients with a diagnosis of SZ also have a diagnosis of depression or substance abuse. This poses a challenge for both classification and diagnosis. If half of patients were all diagnosed with depression, maybe we are just bad at telling the difference between 2 conditions.

Sympton overlap- Both SZ and bipolar have the same positive and negative symptoms. Questions validity and whether SZ and bipolar are actually the same condition.

Genetic basis: Has been noted for many years SZ runs in families. This is weak evidence for genetics as most family members also share the same environment. However, there have been systematic investigations of the extent to which greater genetic similarity between family members is associated with the likelihood of both developing SZ.

Candidate genes- Individual genes are believed to be associated with risk of inheritence. Because a number of genes each appear to confer a small increased risk of SZ it appears that SZ is polygenic. Because different studies have identified different candidate genes it also appears that SZ is aetiologically heterogenerous. Ripke (2014) carried out a study combining previous data from genome-wide studied of SZ. The genetic make-up of 37,000 patients was compared to 113,000 controls: 108 seperate genetic variations were associated with risk of SZ. Genes associated with increased risk included those coding for the functioning of a number of neurotransmitters including dopamine.

Neurotransmitters- The brain's chemical messengers appear to work differently in the brain of a patient with SZ. In particular, dopamine is thought to be widely involved. Dopamine is important in the functioning of several brain systems that may be implicated in the symptoms of SZ. 

Hyperdopaminergia in subcortex- Original version of the dopamine hypothesis focused on the possibly role of high levels or activity of dopamie in the subcortex. An excess of dopamine receptors in Broca's area may be associated with poverty of speech and hallucinations. 

Hypodopaminergia in the cortex- Recent versions of the dopamine hypothesis have focused on instead of abnormal dopamine systems in the brain's cortex. Goldman-Rakic (2004) have identified a role for low levels of dopamine in the prefrontal cortex in the negative symptoms of SZ. 

It may be that both hyper and hypodopaminergia are correct explanations- both high and low levels of dopamine in different brain regions are involved in SZ. 

Neural correlates- Patterns of structure or activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience. 

Neural correlates of negative symptoms- Avolation involves the loss of motivation. Motivation involves the anticipation of a reward, amd certain regions of the brain such as the ventral straitum are believed to be particularly involved in this anticipation. Juckel (2006) have measured activity levels in the ventral straitum in SZ and found lower levels of activity than those observed in controls. Moreover, they observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms. Thus activity in the ventral straitum is a neural correlate of negative symptoms of SZ. 

Neural correlates of positive symptoms- Allen (2007) scaned brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified pre-hallucinations and compared to a control group whilst they identified pre-recorded speech as theirs to others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group, who also made more errors than the control. We can thus say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.

- Role of psychological environment is important but unclear: The evidence supporting the role of biolgical factors in schizophrenia is overwhelming. However, there is also evidence to suggest an important role for environmental factors, including psychological ones such as family functioning during childhood. After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%.

+ Role of mutation: SZ can take place in the absence of family history of the disorder. One explanation for this is mutation in parental DNA, for example, in paternal sperm cells. This can be caused by radiation, poison or viral infection. Evidence for the role of mutation comes from a study showing a positive correlation between paternal age and risk of SZ, increasing from around 0.7 with fathers under 25 to over 2% in fathers over 50. (Brown 2002). 

- Correlation-causation problem: Number of different neural correlates of SZ symptoms, including both positive and negative symptoms. Although soem studies are useful in flagging up particular brain systems that may not be working normally, this kind of evidence leaves some questions unanswered such as does the unusual activity in a region of the brain cause the symptom? 

Schizophrenogenic mother- Fromm-Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on the accounts she heard from her patients about their childhood. She noted that many of her patients spoke of the mother being cold, rejecting and controlling, and tends to create a family climate characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions, and ultimately schizophrenia. 

Double-bind theory- Bateson (1972) agreed that family climate is important in the development of schizophrenia but emphasised the role of communication style within a family. The developing child regularly finds themselves trapped in situatons where they fear doing the wrong thing, but recieve mixed messages about what this is, and feel unable to comment on the unfairness of this situation of seek clarification. When they 'get it wrong' the child is punished by withdrawal of love. This leaves them with an understanding of the world aas confusing and dangerous, and this is reflected in symptoms like disorganised thinking and paranoid delusions. 

Expressed emotion- the level of emotion expressed towards a patient by their carers. Contains several elements:

• Verbal criticism of the patient, occasionally accompanied by violence.
• Hositlity towards the patient, including anger and rejection.
• Emotional over-involvement in the life of the patient, including needless self-sacrifice.

These high levels of expressed emotion in carers directed towards the patient are a serious source of stress for the patient. This is primarily an explanation for relapse in patients with SZ. However, it has also been suggested that it may be a source of stress that can trigger the onset of schizophrenia in a person who is already vulnerable due to their genetic-makeup. 

A cognitive explanation for any phenomenon is one which focuses on the role of mental processes. Schizophrenia is associated with several types of abnormal information processing, and these can provide possible explanations for schizophrenia as a whole. SZ is characterised by disruption to normal thought processing. We can see this in many of its symptoms. We have already seen that reduced processing in the ventral striatim is associated with negative symptoms, whilst reduced processing of info in the temporal and cingulate gyri are associated with hallucinations. This lower than usual level of information processing suggests that cognition is likely to be impaired. Frith (1992) idenitifed two kinds of dysfunctional thought processing that could underlie some symptoms:

• Metarepresentation is the cognitive ability to reflect on thoughts and behaviour. This allows an insight into our own intentions and goals. It also allows us to interpret the acions of others.
• Central control is the cognitive ability to suppress automatic repsonses while we perform deliberate actions instead. Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.

- Evidence for biological factors is not adequately considered: Psychological explanations for schizophrenia can be hard to reconcile with biological explanations. It could be that both biological and psychological factors can seperately produce the same symptoms, which raises the question of whether both outcomes are really schizophrenia. Alternitavely, we can view this in terms of the diathesis-stress model where the diathesis may be biological or psychological.

+Strong evidence for dysfunctional information processing: Stirling (2006) compared 30 patients with a diagnosis of schizophrenia with 18 non-patient controls on a range of cognitive tasks including the stroop test, in which participants have to name the ink colours of colour words, suppressing the impulse to read the words in order to do this task. In line with Frith's theory of central control dysfunction, patients took over twice as long to name the ink colours as the control group.

- Weak evidence for family-based explanations: There is almost no support to the importance of the schizophrenogenic mother or double bind. Both these theories are based on clinical observations of patients and early evidence involved assessing the personality of the mothers of patients for 'crazy-making characteristics'.

Most common treatment is antipsychotics- drugs used to reduce the intensity of symptoms, in particular the positive symptoms, of psychotic conditions.

Typical antipsychotics- The first generation of antipsychotic drugs, having been used since the 1950s. They work as dopamine antagonists and include chlorpromazine. There is a strong association between the use of chlorpromazine and the dopamine hypothesis. Chloropromazine acts as an antagonist. Antagonists are chemicals which reduce the action of a neurotransmitter. Dopamine antagonists work by blocking dopamine receptors in the synapses of the brain, reducing the action of dopamine.

Atypical antipsychotics- Drugs for SZ developed after typical antipsychotics. They typically target a range of neurotransmitters such as dopamine and serotonin. Examples include clozapine and risperidone. Clozapine was developed in the 1960s, and in 1980 was discovered to be more effective than typical antipsychotics, and was remarked as a treatment for SZ. Clozapine binds to dopmine recpetors in the same way chlorpromazine does, but in addition is acts on serotonin and glutamate receptors. Risperidone- Binds to dopamine but binds more strongly that clozapine so more effective and fewer side effects.

+ Evidence for effectiveness: Thornley (2003) reviewed studies comparing the effects of chlorpromazine to control conditions in which patients recieved a placebo so their experiences were identical except for the presence of chlorpromazine in their medication. Data from 13 trails showed that chlorpromazine was associated with better overall functioning and reduced symptom severity.

- Serious side effects: Typical antipsychotics are associated with a range of side effects including dizziness, agitation, sleepiness and weight gain. Long term use can result in tardive dyskinesia which is caused by dopamin supersensitivity and manifests as involuntary facial movements such as blinking and grimacing. Can also cause neuroleptic malignant syndrome which can be fatal. Atypical antipsychotics include agranulocytosis but side effects are reduced.

- Chemical cosh: Widely believed that antipsychotics are used in hospitals to calm patients down and make them easier for staff to deal with, rather than for benefits of the patient. This practice is seen by some as human rights abuse.

CBT- A method for treating mental disorders based on cogntive and behavioural techniques. From the cognitive viewpoint the therapy aims to deal with thinking, such as challenging negative thoughts. The therapy also includes behavioural techniques. CBT helps patients to make sense of how their delusions and hallucinations impact their feelings and behaviour. Just understanding where symptoms come from can be hugely helpful to some patients.

Family therapies- A psychological therapy carried out with all or some members of a family with the aim of improving their communication and reducing the stress of living as a family. Pharoah (2010) identified a range of strategies by which family therapists aim to improve the functioning of a family with a member suffering from SZ. Suggested that these strategies work by reducing levels of stress and expressed emotion, whilst increasing the chances of patients' complying with medication. This combination of benefits tends to result in a reduced likelihood of relapse.

Token economies- Reward system used to manage the behaviour of patients with SZ. The idea is that tokens are given immediately to patients when they have carried out a desirable behaviour that has been targeted for reinforcement. Tokens can then later be swapped for rewards such as cigarettes or privilages such as a walk outside.

- Ethical issues: Token economy has proved controversial, the main issue being that privileges become more available to patients with mild symptoms of SZ and less for those with more severe symptoms that prevent them from complying with desirable behaviours. This means that the most severely ill patients suffer discrimination and some families of patients have challenged the legality of this.

- Treatments improve quality of life but do not cure: Aim to make SZ more managable and in some way improve patients' quality of life, and so the failure to cure SZ is a weakness of psychological treatments.

+ Evidence for effectiveness: Jauhar (2014)~CBT, Pharoah~family therapy, McMonagle and Sultana (2009)~token economies.

Interactionist approach- a broad approach to explaining SZ, which acknowledges that a range of factors, including biological and psychological, are involved in the development of SZ.

Diathesis stress model- An interactionist approach to explaining behaviour. For example, SZ is explained as the result of both an underlying vulnerability and a trigger, both of which are necessary for the onest of SZ. In early versions of the model, vulnerability was genetic and triggers were psychological. Nowadays both genes and trauma are seen as diathesis and stress can be psychological or biological in nature. Meehl (1962)- if a person does not have the schizogene then no amount of stress would lead to SZ.

Modern understanding of diathesis- Read (2001) propsed a neurodevelopmental model in which early trauma altes the developing of the brain. Early and severe through trauma can seriously affect many aspects of brain devlopment.

Modern understanding of stress- Houston (2008) Although psychological stress, including that resulting from parenting may still be considered important, a modern definition of stress includes anything that risks triggering SZ.

The model is associated with combining antipsychotic medication and psychological therapies, most commonly CBT. Turkington (2006) said it is possible to believe in biological causes of SZ and still practice CBT to relieve psychological symptoms. However, this requires adopting an interactionist model; it is not possible to adopt a purely biological approach and tell patients that their condition is purely biological and there is no psychological significance to symptoms, and to simultaneously treat them with CBT.

In Britain it is increasingly standard practice to treat patients with a combination of antipsychotic drugs and CBT. In USA there is more of a history of conflict between psychological and biological models of schizophrenia and this may have led to slower adoptation of an interactionist approach.

It is unusual to treat SZ using psychological therapies alone. CBT, family therapy and the use of token economies with sufferers of SZ are usually carried out with patients taking antipsychotics.

+ Evidence for role of vulnerability and triggers: Teinari (2004) investigated the combination of genetic vulnerability and parenting style. Adopted children from 19,000 Finnish mothers with SZ between 1960 and 1979 were followed up. A child-rearing style characterised by high levels of conflict and low levels of empathy was implicated in the development of SZ but only for the children with high genetic risk but not in the control group. This suggests both genetic vulnerability and family-related stress are important in development of SZ.

- Don't know exactly how diathesis and stress work: There is strong evidence to suggest that some sort of underlying vulnerabiliity coupled with stress can lead to SZ. We also have well-informed suggestions for how vulnerabilities and stress might lead to symptoms. However, we do not yet fully understand the mechanisms by which the symptoms of SZ appear and how both vulnerability and stress produce them.

-Original model is simple: Multiple genes increase vulnerability to SZ, there is no single schizo-gene. Also stress can come in many forms, including but not limited to dysfunctional parenting. Therefore vulneravbilty and stress do not have one single source.