Schizophrenia

A severe mental illness where contact with reality and insight are impaired (1% of world population).

SZ does not have a single defining characteristic - 2 major systems for classification is ICD-10 and DSM-5 .ICD-10 recognises subtypes of SZ e.g. 

Disorganised type ( disorganised speech, and behaviour - cant act appropriately in situations, can’t start or finish task, flat/inappropriate affect - poor eye contact, lack of facial expressions).

Residual type (patient who is not presently experiencing prominent delusions, hallucinations, disorganized speech, or disorganized or catatonic behaviours. However, they are experiencing at least two of those symptoms to a lesser extent)

Catatonic type (severe motor abnormalities, doing opposite of what is being asked)

Paranoid type (involves delusions and hallucinations).                                                     

Undifferentiated type (variation between symptoms not fitting into a particular type).        

Symptoms are divided into postive/negative. Postive are additional experiences beyond our normal everyday ones. e.g. hallucinations, delusions. Negative are the loss of abilities and experiences e.g. avolition(loss of motivation to carry out tasks), speech poverty.

• Reliability - Inter-observer reliability (the extent to which different assessors agree on their assessments), so 2 or more professionals come to the same diagnosis for the same patient. Cheniaux had 2 psychiatrists diagnosing 100 patients using both DSM and ICD. Interobserver reliability was poor, one psychiatrist diagnosed 26 according to DSM and 44 to ICD. and the other 13 to DSM and 24 to ICD.
• Validity - Criterion validity do different assessments such as ICD and DSM arrive at the same diagnosis for the same patient. Cheniaux's study showed that SZ is more likely to be diagnosed using ICD than DSM.
• Co-morbidity - 2 or more conditions occurring together. SZ is commonly diagnosed with other conditions (Buckley) 50% of SZ patients also have depression, 47% substance abuse, 29% PTSD and 23% OCD.
• Symptom overlap - e.g both Sz and bipolar disorder involve symptoms like delusions and avolition.
• Gender bias - Longenecker reviewed studies and concluded that since the 1980's men have been diagnosed with SZ more than women. maybe men are more genetically vulnerable to developing Sz than women. However gender bias because female patients function better than men (more likely to work, good family life etc). This may explain why women may be less likely to be diagnosed even if they have the same symptoms men.
• Cultural bias - African American are more likely to be diagnosed than white people. maybe because positive symptoms such as hearing voices may be more acceptable in African cultures because of communication with ancestors and when reported to psychiatrist from another culture it will be seen as bizarre. Also, white psychiatrists tend to over-interpret symptoms and distrust honesty of black people.

Sz runs in families. Mz twins share 100% of genes. Parents and Dz twins share 50%. There is a strong relationship between the degree of genetic similarity and shared risk of sz - supported by Gottesman large-scaale family study. Candidate genes are individual genes that are belived to be associated with risk of inheritance however Sz is polygenic because a number of genes may cause it also different studies have identified different candidate genes so sz appears to be aetiologically hetrogeneous(different combinations of factors can lead to the condition). Stephen Ripke carried out a study combining all previous data from genome wide s of sz. The genetic makeup of 37,000 individuals was comapred to 113,000  controls and 108 seperate variations were associated with increased risk of SZ.

The dopamine hypothesis - The brains chemical messenegrs appear to work diffrently in the brain of a sz patient. Dopamine is widley belived to be involved. Hyperdopaminergia in the subcortex (high levels of dopamine). Hypodopaminergia in the cortex. Low levels of dopamine in the prefrontal cortex. Goldman-rakic have identified a role for low nlevels of dopamine (responsible for thinking and descion) in the negative symptoms.

Neural correlates - Many sz's have lower activity in this area which could be linked to delusions and disorganised thoughts. The basal ganglia is larger in sz which could show motor dysfunction. The amygdala is smaller in sz so can link to loss of emotion. Avolition which is the loss of motivation involves the ventral striatum. Abornormalities in this area may be involved in the development of avolition. Juckel measured levels of activity in the ventral striatum in sz and found lower levels of activity compared to control groups. Allen scanned brains of patients experiencing audiotory hallucinations and  comapred them to a control group. Lower activity levels in the superior temporal gyrus and anterior cingulate gyrus were found in hallucination group.

Adoption studies e.g. Tienari  studied the adopted children of schizorphrenic (biological) biological mothers and a matched control group.Particpants were between 5 and 57 at the start of the study and adopted before the age of 4. 7.5% of sz biological mothers developed sz as opposed to 1.5% of controls. So still at heightened risk of dveloping sz. Twin studies Kendler found concordance rates of 31% in mz twins and 6.5% in dz twins. Family studies - Kendler found that 1st degree relative of those with sz are 18x more at risk than general population.

Evidence for dopamine hypothesis - Dopamine agonists such as amphetamines which increase levels of dopamine make sz worse and can produce sz like symptoms in non-suffres (Curran). Anti-psychotic drugs woork by reducing dopamine levels. Radioactive labelling studies such as that by Lindstroem have found that chemicals needed to produce dopamine are taken up faster in the brain of sz sufferes, suggests they produce more dopamine. Some genes identified in the Ripke study code for the production of other neurotransmitters, alot of attention is now on the neurotransmitter called glutamate - Clozapine works on serotonin aswell and is effective.Studies of the dopamine hypothesis are correlational because they show an association and not a direct cause and effect. The drugs given to test this hypothesis may effect other neural correlates, this is a weakness because yoi cant directly manipulate dopamine levels.

Role of psychologoical environment - There is evidence to suggest an important role for environmental factors included psychological ones such as family functioning during childhood. After all 50%risk of developing sz if identical.

Causality - Cause and effect cannot be established with brain abnormalities, it is uncertain whether structural abnormalities predispose sz or acutally having these symptoms causes these changes in the brain. A strength is that the research has reliability. carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. This suggests that if this research was tested and re-tested the same results would be achieved.

The sz mother - Fromm-Reichmann said the shizophrenogenic mother is cold. rejecting and controlling and tends to create a family climte characterised by tension and secrecy. This leads to distrust that later develops into paranoid delusions and then sz. 

Double bind theory - Batesons theory says that by communicating with their children in contradictory ways, parents predispose them to sz. e.g. a mother might tell her son she will always love him but when the child makes a mistake he is faced with a consequence which contridicts this. Therefore the child develop a coherent construction of reality and zsz develops because they see the world as confusing which is reflected in symptoms such as delusion. This is just a risk factor.                                                                                                                                                                              Expressed emotion is the level of emotion in particular negative emotions expressed towards a patient by their carers. Such as verbal criticsm, hostility and emotional over involvement. These cause high levels of stress for the patient and is a primary explanation for relapse in patients. Teh source of stress can also trigger the onset of sz in a person who is already vunerable (diathesis stress model).

Sz is characterised by disruption to normal thought processing, we have already seen reduced processing in the ventral striatum is associated with negative symptoms and reduced processing of info in the temproral and cingulate gyri is associated with hallucinations. Frith identified 2 kinds of dysfunctional thought processing - 1) metarepresentation - our cogntive ability to reflect on thoughts and behaviour. Dysfunction here would disrupt our ability to recognise our actions and thoughts are carried out by ourselevs and not by others.  2) Central control - 

Most people are able to focus attention selectively on things that matter. But people with sz cannot filter info and let too much irrelevant info in.

There is evidence to suggest that difficult family relationships in childhood are associated with increased risk of sz. Read reviewed 46 studies of child abuse and sz and concluded that 69% of women in patients with sz had a history of physical or sexual abuse - 59% for men. Adults with insecure attachments are more liekly to have sz. Inf about childhood expericnes from patients was gathered after the development of symptoms and the sz may have disorted patients recall of childhood experiences. 

Dysfunctional family explanations have led to parent blaming. Parents who already have suffered seeing thier child go through sz, would undergo further trauma by recieving the blame for the conditon.One strength of the double bind explanation comes from further empirical support provided by Berger (1965). They found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. However, evidence may not be reliable as patient’s recall may be affected by their schizophrenia. This suggests that there is wider academic credibility for the idea of contradictory messages causing schizophrenia.

Strong support that info is processed differently for sz patient. Stirling comapred 30 patients with 18 from a control group on a range of cognitive tasks incl the stroop test. Patients took twice a long to name the ink colours. Cognitive theories cannot however explain the origins of sz.

Direction of causality - It is unclear whether cognitive factors are a cause or a result of the neural correlates and abnormal neurotransmitter levels seen in sz. A second weakness of the cognitive model is that it is reductionist. The reason for this is because the approach does not consider other factors such as genes. It could be that the problems caused by low neurotransmitters creates the cognitive deficits. This suggests that the cognitive approach is oversimplistic when consider the explanation of schizophrenia.

Typical antipsychotics -e.g. chlorpromazine. Chlropromazine works  by acting as antagonists in the dopamine system (it acts against dopamine).  They work by blocking the dopamine receptors in the synapses of the brain, reducing the action of dopamine - initially the dopamine levels rise but then production is reduced. This reduces postive symptoms such as hallucinations.  Chlorpromazine is also an effective sedative so can be used to calm patients down.

Atypical antipsychotics - e.g. Cloapine was first trialled in the 1970's but then withdrawn because of the death of some patients from a blood condition called agranulocytosis.  But now it is used as an antipsychotic which is to be used when other treatments fail. Clozapine binds onto dopamine, serotonin and glutamte receptors. This improves mood and reduces anxiety and depression in patients and also improves cogntive functioning. Because of the mood enhancing effects it is prescried to patients who are considered at a high risk of suicide (30-50% of patients attempt suicide).

Risperidone also binds to dopamine and serotonin receptors. it binds more strongly to dopamine receptors than clozapine and is therefore much more effective in smaller doses. Some evidence to sugget that this leads to fewer side effects.

Effectiveness - Thornely reviewed studies comparing the effects of chlropromazine to control condtions where patients recieved a placebo. Data from 13 trials with a total of 1121 patients  showed that chlropromazine was associated with better overall functioning and reduced symptom severity. Davis also found that 53% of placebo patients relapsed whereas only 11% relapsed in the treatment group. Meltzer concluded that clozapine is more effective than typical and atypical drugs and that it is effective in 30-50% of treatment resistant cases where typical drugs have failed.

Side effects - Typical drugs have side effects such as dizziness, agitation, sleepiness and itchy skin. Long term use can result in tardive dyskinesia which is caused by dopamine supersensitivity and manifests as involuntary facial movements. Most serious side effects of typical drugs is NMS, this is caused becasue the drug bloaks dopamine action in the hypothalamus and this area regulate a number of body systems. NMS can result in high temperatures, coma. Atypical has fewerside effects but regular blood tests needed.

The dopamine hypothesis is the idea that there are higher levels of dopamine in the subcortex of the brain. However dopamine levels in the other areas of the brain may be too low and if this is true it is not clear how antipsychotics(which are dopamine antagonists) can help with sz if they reduce dopamine activity.

Problems - Healy has suggested that some successful trials have had their data published multiple times, exgaerting the evidence for positive effects. Also most studies assess the short term benefits rather than the long term ones. He also said that because they have powerful calming effects, it is easy to demostrate that they have positive effects on patinets, this is not the same as saying they reduce the severity of sz.

Antiposychotics are used in hospitals to calm patients downand make them easier for staff to work with rather than for the benefits of the patients themselevs. This is seen by some as human rights abuse.

CBT - aims to help patients identify their irrational thoughts and then challenge them and change them. This may involve an argument or discussion of how likely the patients beliefs are to be true. This will allow patients to cope with symptoms better. Patients may be set homework to help disprove thier delusions or make them less anxious about something. You could use the ABC model because the belief can be ratioanlised, disputed and chnaged. The therapist will try to normalise the symptoms so the patient feels less isolate and less judged. The therapist will use critical collabrative naalysis hwereby they question the patients thoughts to help undertsnad illogical ones.

Family therapy - Takes place with families and aims to improve the quality of communication and interaction between family members. Some therapists see the family as the root of the cause. However now most therapists are concerned with reducing the stress within the family that may contribute to relapse - it aims to reduce levels of expressed emotions. Pharoah carrie out family therapy by forming an therapeutic alliance with all family members, reducing the stress of caring for a relative with sz, improving the ability to solve and anticipate porblems, reduction of anger and guilt in family members, improving beleifs about sz.

Token economies - These are reward syststem used to manage behaviours of patients with sz, ecspecially those who have developed maladaptive behaviours through spending long periods in psychiatric hospitals. Common for bad hygiene or staying in pajamas all day. So modifying these habits leads to a better quality of life and makes it more likely they can live utside a hospital setting. They get tokens when they perform a diserable behaviour and they can exchnage the token (secondary reinforcer) for rrewards such as sweets or having a walk outside the hospital.

Effectiveness - Jauhar reviewed 34 studies of cbt and found cbt has a significant but fairly small effect on both positive and negative symptoms. Pharoah reviewed eveidence for the effectiveness of family therapy and concluded that there is moderate evidence to show that family therpy significanlty reduces hospital readmission and improves quality of life for patient and family. Howevr results of different studies were inonsistent and there was problems with the quality of some evidence - so weak evidence.  McMonagle and Sultana reviewed the eveidence for token economy and found only 3 studies where the patients were randomly allocated to condtions, random allocation is importnt in matching patients to treatment and control groups, only 1/3 studies showed improvement . A study by Anderson et al. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy or Social Skills training were used and the relapse rate was less than 5% when both were used together with the medication.

Treatments improve quality of life but do not cure - All these treatments makes sz more managebale. CBT allows patients to make some snese and in some cases challenge some of their symptoms. Family therpay helps by reducing stress for both patients and families. Token economies help by making patients behaviours more socilly acceptable.

Ethical issues - Token economy has proven constraversial because privelleges, rewards become more available to patiets with mid symptoms rather than those with more severe symptoms, these servere symptoms prevent them from complying with desirbale behaviours. So the most severly ill patients suffer discrimination.  Also CBT involves challenging a patienst paranoia but at what point does this interfere with an individuals freedom of thought.

Research by Kingdon and Kirschen (2006) found that CBT is not suitable for all patients, especially those who are too thought disorientated or agitated, who refuse medication, or who are too paranoid to form trusting alliances with practitioners.

This approach acknowledges there are biological, psychological and soceital factors in the development of sz.

The diathesis-stress model says that both a vunerability to sz and a stress trigger are necessary in order to develop the condition. Meehls model said diathesis (vunerability) was entirely genetic (result of a single gene). According to Meehl if the person doesnt have the sz gene then no amount of stress would lead to sz. However carriers of this gene, stress through childhood and adolescence could result in the development of the conditon. Now the modern understanding makes it clear that many genes appear to increase genetic vunerability (there is no single gene)(Ripke), Ingram and Luxton included that psychological trauma  is a daithesis rather than the stressor.  Read proposed a neurodevelopmental model in which early trauma alters the developing brain e.g. the HPA system can become overactive, making the person much more vunerable to stress.

Stress is seen as psychological in nature e.g. parenting. However a modern definitiincluded anything that risk triggering sz (Houston). Cannabis is a stressor because it increases risk of sz by 7x, because cannabis interferes with the dopamine system.

The model uses both antipsychotics and psychological therapies (CBT) for treatment. Turkington said it is possible to believe in biological causes of sz and still practise CBT to relieve symptoms - this requires adopting an interactionist model. In Britain it is increasingly standrad  to treat patients with a combinations of CBT and drugs however in the US it is more common for just medication to be given.

Evidence - There is evidence to support the role of vunerability and tress in the development of sz. Teinari ivestiagted the combination of genetic vunerability and parenting style. Children adopted from 19,000 finnish mothers with sz between 1960 and 1979 were followed up. Their adoptive parents were assessed for child-rearing style and the rates of sz were compared to those in a control group of adoptees without any genetic risk. Parenting techniques with high levels of criticism and low empathy were implicited in development of sz but only for children with high genetic risk but not in control group.

The orginial diathesis-stress model is over simple - Now we know multiple genes increase vunerability to sz so there is no signle schizogene.  Also stress can come in different forms. It is now beleived that vunerability can be a result of early trauma and stress can come in many forms incl biological. Houston found childhood sexual trauma emerged as a vunerbaility factor whilst cannabis was the trigger.

Effectiveness of both treatments - Tarrier dtudied 315 patients who were randomly allocated to a mdeiction+CBT or medication+supportive counselling or a control group (mdeication only).  Those in combination groups showed lower symptoms than those in the control group hwowver there was no difference in rates of hospital readmission.