Schizophrenia Mock Revision

A servere mental illness where contact with reality and insight are impaired, an example of psychosis.

Classification of schizophrenia

The process of organising symptoms into categories based on which symptoms cluster together in sufferers. DSM requires symptoms for 6 months and would diagnose with 1 positive symptom whereas the ICD only requires symptoms for 1 month and would only diagnose if 2 or more negative symptoms are present.

Positive symptoms

These are additionsal experiences beyond those of ordinary existence. They are atypical symptoms. These include both hallucinations which are sensory experiencesof stimuli that have either no basis in reality or are distortions of what is there and delusions which are irrational beliefs. ANTIPSYCHOTICS

Negative symptoms

These represent the loss of a usual experience such as loss of motivation or clear thinking. These are atypical experiences. They include avolition which involves the loss of motivation, Andreason identified 3 signs of avolition; poor hygiene, lack of persistence in work/education also a lack of energy and speech poverty which involves reduced frequency and quality of speech. COGNITIVE BEHAVIOURAL THERAPY

• EVALUATION Elie Cheniaux et al asked 2 psychiatrists to diagnose 100 patients with the DSM+ICD. Inter rater reliability=poor. 1 psych diagnosed 26 people with Sz according to DSM and 44 with Sz according to the ICD while the other psych diagnosed 13=DSM+24=ICD. Low validity also.
• Co-morbidity when 2+ conditions occur together. When 2 conditions are disgnosed together the validity is questioned as as it might be 1 condition. Buckley et al found almost half of those diagnosed with Sz are also diagosed with depression, It's likely that severe depression looks a lot like Sz= vice versa so they may be misdiagnosed
• Symptom overlap, also calls into question validity as in Sz+bipolar disorder the pos sympotom of delusions and neg of avolition is involved. Are they 1 in the same?

Genetics

Sz runs in families, however, relatives usually also share the same environment so there is weak evidence to suggest Sz=genetic. There have been systematic investigations of the extent to which greater similarity in genes correlates to liklihood to develp Sz. E.g We share 100% with identical twins etc. There=strong link between risk of development and genetic similarity. Gottesman suggested that identical twins have a 48% risk of developing Sz and twins=17% children=9%

Candidate Genes

Sz=polygenic(number of factors combined) and aetiologically heterogenous(different combinations of factors can lead to Sz). Ripke et al carried out a huge study combining all previous data from genome-wide studies(those looking into all human genes not just 1) of Sz. Genetic makeup of 37,000 patiets compared with 113,000 controls; 108 genetic variations associated with increased risk of Sz. These included those coding for the function of a number of neurotransmitters including dopamine.

The dopamine hypothesis

Neurotransmitters like dopamine appear to work differently in brains of those with Sz. Dopamine=important in the functioning of severl brain systems which maybe implicated in the symptoms of Sz. Originally dopamine hyp focused on the possible role of high levels or activity of dopamine in the sub cortex. Now however, it focuses on abnormal dopamine systems in the brains cortex. Goldman-Rakic et al have identified a role for low levels of dopamine in the prefrontal cortex (decision making) in negative symptoms. 

Neural correlates of Sz

Measurements of the structure/functioning of the brain that correlate with experience(Sz) both pos+neg symptoms have neural correlates. Neural correlates for negative symptoms= Avolition- involves anticipation of reward, which is in the ventral striatum, so abnormality of areas such as this maybe involved in development of avolition. Juckel et al measured activity levels in ventral striatum in Sz + found lower levels in controls. Neural correlates for positive symptoms- Allen et al scanned brains of those with auditory hallucinations compared to control while they identified if pre-recorded speech was theirs or not. Lower activation levels in superior temporal gyrus and anterior cingulate gyrus found in hallucigenic group, this group also made more errors.

GENETIC Very strong ev for genetic vulnerability to Sz Gottesman=Ev+ Adoption studies- Tienari et al shows how children of Sz suffers are still at hightened risk of Sz id adopted into families with no history of Sz + Kendler et al found that 1st degree relatives of those with Sz= 18xmore at risk, however, less than 50% of kids with parents who both have Sz develop it. The higher concordance rate between identical twins may be due to them being treated more similar than DZ=Nurture not genetics.

DOP HYP Seeman found increases in dopamine receptor density of between 60-110% compared to controls+ Lindstoem et al found in radioactive labelling that chemicals needed to produce dopamine are taken up faster in Sz brains, which suggests they must produce more dopamine. However, some genes identified in Ripke et al study for production of other neurotransmitters so dopamine=not the only NT associated with Sz Eg-glutamate.

NEURAL The ev for neural correlates leaves some important questions unanswered like does the unusual activity in a region of the brain cause the symptom? 

Family dysfunction

The schizophrenogenic mother->Frieda Fromm-Reichmann proposed a psychodynamic explanation for Sz based on her patients childhood. She noted that many of her patients spoke of a particular type of parent, which she named the SM, which literally means they are Sz causing. This mother is cold, rejecting and controlling, and tends to create a family climate characterised with tension and secrecy. This leads to distrust that later develops into paranoid delusions and ulimately Sz.

Double-bind theory->Bateson at al agreed with Frommetc but argued that the communication style  used within a family is vital. During a childs development they will be faced with situations where they may fear doing the wrong thing, but they receve mixed messages about what that may be. If the child is to listen to 1 response and follow that they will be neglecting the other response/s which suggests that the child will always respond in the wrong way meaning they will be unable to seek clarification. As the child is bound to be wrong in their response they are often punished by the parents by a withdrawl of love. This leads them to believe the world is confusing and dangerous whcih is reflected in symptoms such as paranoid delusions and disorganised thinking. 

Expressed emotion(EE) and Sz-> This is the level of emotion, especially negative emotion that is expressed to patients by their carers. EE elements;

• Verbal criticism of the patient, occasionally accompanied by violence
• Hostility towards the patient, including anger or aggression
• Emotional over-involvement in the life of a patient, including needless self-sacrifice.

Theses EE towards the patient causes stress, and this explains relapses. It has also been suggested that those who are already vulnerable to developing Sz could if placed in stressful situations such as these due to their genetic makeup (Diathesis stress model)

Cognitive explanations

Sz is associated with several types of abnorman mental processing, these can explain Sz as a whole. Sz=characterised by disruption to normal thought processing-this is shown in many of it's symptoms. Reduced processing in the Ventral striatum is associated with negative symptoms and reduced processing of info in temporal and cingulare gyri are associate with hallucinations. This suggests that Sz patients cognition may be impaired.

Frith et al identified 2 kinds of dysfunctional thought processing that could underline some symptoms.

• Metarepresentation-Cog ability to reflect on thoughts+behaviour + it allows us insight into our goals/intentions + interpret actions of others. Dysfunction in this would disrupt the ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else which may explain hallucinations of voices+delucsions like thought insertion.

• Central control-Cog ability to suppress automatic responses while we perform deliberate actions instead, Disorganised speech and thought disorder may result with the inability to supress automatic thoughts and speech triggered by other thoughts. Suffers with Sz tent to experience derailment of thoughts and spoken sentences because each word triggers associations, and the patient cannot suppress automatic responses to these.

FAM DYSFUNTION Read et al reviewed 46 studies of child abuse + Sz. They concluded that 69& of adult women in-patients with the diagnosis of Sz had a history of physical/sexual abuse for men=59%. Berry et al said that adults with insecure attachments to their primary caregiver=more likelyy to have Sz. However, info about childhood experiences is gathered after the symptoms are developed so they may effect/distort the patients recall them=Problem with validity.

FAM-BASED EXPLANATIONS There is almost no ev to support the importance on the schizophrenogenic mother ot double bind. Harrington-they are based on clinical observation of patients and looking into the mothers personality to identify if they have any crazy making characteristics which is an outdated approach. Also this theories have led historically to parent blaming which may be unfair.

DYSFUNCTIONAL INFO PROCESSING Stirling et al compared 30 patients with Sz against 18 controls on a range of cog tasks including the stroop test(Colourword) The patients took over 2x as long.-Linked to Central control being dysfunctional. Although links between symptoms and faulty cognition are clear, this does not tell us anything about the origins of those cognitions or of Sz.

This approach ignores the biological factors that influence Sz.

Antipsychotics-Drugs used to reduce the intensity of symptoms, in particular the posoty symptoms of psychotic conditions like Sz.

Typical antipschotics

1st gen of antipsychotics (1950's) They can be taken as tablets, syrup, or injections. Daily tratement of a max of 1000Mg(typically 400-600Mg) This form of antipschotic has decined over the past 50 yrs. Chlorpromazine is strongly associated with the dophyp it works by acting as antagunists in the dopamine system(They reduce the action of neurotransmitters) So it blocks the dopamine receptors in the synapses of the brain. Initaially by taking this dopamine levels build up but slowly it's production is reduced. It normalises neurotransmission in key areas of the brain and so reduces symptoms like hallucinations. It is also an effective sedative, and is often used to calm patients.

Atypical antipschotics

(1970's) They target a range of neurotransmitters such as dopamine and serotonin. Examples include Clozapine and Risperidone.

Clozapine->Trialled in 1970's but withdrawn due to deaths of patients from a blood condition called agranulocytosis and so can't be taken through injection. In 1980's it was remarketed as it was more effective than Chlorpromazine as a back up for when other treatments fail those who take it have to have regular blood tests. Clozapine binds to dopamine receptors like chlorpromazine does, but it also acts on serotonin and glutamate receptors, which helps inprove mood+reduce depression+anxiety, and so may help with cog functioning. It is often perscribed to those who are at risk of suicide. (30-50% commit suicide)

Risperidone->1990's. Developed to be as effective as clozapine but with less serious side effects. It can be takethrough tablets, injection or syrup. Like clozapine it is believed to bind to dopamine and serotonin receptors but more stronly to dopamine receptors than clozapine and so it is more effective in smaller doses.

It is widely believed that antipsychotics have been used in hospotal situations to calm patients and make them easier to work with, this means it is being used more for that staffs benefit than the patients. According to Moncrieff this to some can be seen as human rights abuse.

EFFECTIVENESS Thornley et al reviewed studies comparing the effects of chlorpromazine to control conditions in which patients recieved a placebo so their rexperiences were identical except for the presence of chlorpromazine. Data from 13 trials with a total of 1121 participants showed that chlorpromazine was associated with better functioning+reduced symptom severity. Data from 3 trials with 521 participants showed replapse rate=lower with chlorpromazine. Also Maltzer concluded that clozapine is more effective than typical antipsychotics and other atypical antipsychotics+that it is effective in 30-50% of treatment-resistant cases. However, Healey has suggested that some successful trials have had their data published multiple times, exaggerating the ev for positive effects. He also suggested that because antipsychotics have powerful calming effects, and claim this as being a positive effect which is not the same as reducing symptom severity.

SIDE EFFECTS Typical antipsychotics are associated with side effects such as dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. LT use can result in tardive dyskinesia. Most serious of all is neuroleptic malignant syndrome(NMS) which can be fatal. Atypical antipsychotics like clozapine can cause agranulocytosis.

Cognitive Behavioural Therapy

Commonly used in the treatment of Sz+takes 5-20 sessions either individual or in groups. The aim of CBT is to help patients identify irrational thoughts and trying to change them. This involves discussing the likelihood of the patients beliefs to be true and consideration of less threatening possibilities. Although it does not remove the symptoms of Sz, it helps patients deal with them. This is because they are able to make sense of how their delusions/hallucinations impact their feelings+behaviour. With explanations for their symptoms their anxieties can be reduced.

Family therapy

Aims to improve the quality of communication+interaction between family members. This helps to reduce stress, EE and the possiblity of relapsing. Pharoah et al identified a range of strategies by which fam therapists aim to improve the functioning of a fam with a member with Sz.

• Forming a theraputic alliance+balancing out care and maintaining own life
• Reducing the stress of caring after some1 with Sz+ anger+guilt of fam members
• Improving ability to solve+anticipate problems

Token economies

Reward systems used to manage the behaviour of patients, in particular those who have developed patterns of maladaptive nehaviour through spending long periods in psychiatric hospitals. Bad habits may have been picked up which can be modifyed, although this does not cure Sz, it improves the patients QOL

• Tokens->Given to patients who carried out a desirable behaviour that needs to be reinforced. E.g getting dressed in the morning/making a bed. Needs to be rewarded immediately..
• Rewards->Tokens can be swapped for rewards E.g sweets, cigarettes, room cleaning or walks outside the hospital. Token economies are a kind of behavioural therapy based on operant conditioning. Tokens=secondary reinforcers as they only have value once the patients has learned they can be used to obtain rewards.

There are actually other psychological therapies but they are less well known and often ignored, E.g the National Institite for Health and Clinical Excellence recommends art therapy, provided a qualified art therapist with experience of working with Sz sufferers is available.

EFFECTIVENESS CBT-Jauhar et al reviewed the results of 34 studies of CBT for Sz. They concluded that CBT has a significant but fairly small effect of pos+neg symptoms. FT-Pharoah et al reviewed the evidence for the effectiveness of fam therapy, they concluded that there is moderate ev to how that fam therapy reduces hospital readmission over the couse of a yr+ improved QOL. However, they also noted that results of different studies were inconsistent. TE-McMonagle+Sultana found only 3 studies where patients has been randomly allocated to conditions with only 110 patients. Random allocation=important in matching patients to treatments and control groups. Only 1 of the 3 showed improvements in symptoms. 

QOL/CURE None of the psychological therapies actually help cure Sz, they simply all increase QOL...

ETHICAL ISSUES Token economy systems have proved to be controversial. As those who have a milder Sz, they will find it easier to perform desirable behaviour than those with more servere Sz, which means that they will often be favoured, while others may find themselves being discriminated against for being 'rebellious'

Explaining the interactionist approach: The diathesis stress model

The DSM says that both a vulnerability to Sz and a stress-trigger are necessary in order to develop the condition. This vulnerability is biological it is also the diathesis part of the model, while the stress-trigger is environmental and therefore the stress part of the model.

Meehl's model->Original DSM, which stated that the diathesis was completely genetic, the result of a single 'schizogene'. This led to the development of a biologically based schizotypic personality, 1 characteristic of which is vulnerability to stress. Meehl stated that if a person does not have the schizogene then no amount of stress would lead to Sz. However, in carriers of the gene chronic stress during childhood or the presence of a schizophrenogenic could result in Sz.

Modern understanding of DIATHESIS->It is now clear many genes could increase genetic vulnerability, there is no one schizogene. Also now more than just genes is considered to be diathesis E.g pschoogical trauma. Read et al suggests that trauma could alter developing brains which could make them more vulnerable to stress. E.g over active hypothalamic-pituitary-adrenal

The modern understanding of STRESS->According to Houston et al this not includes anything that risks triggering Sz rather than just psychological factors(especially within development) 1 thing that is considered to trigger a Sz ep is cannabis usage. This is because cannabis interfers with the dopamine sytem.

Treatment according to the interactionist model

It is compatabile with both biological and psychological treatments. In particular the combination of antipsychotics with CBT. Turkington et al point out that it is perfectly possible to believe in biological causes of Sz and still practise CBT to relieve psychological symptoms. However, this requires adopting the interactionist model.

In Britain it is increasingly standard to treat patients with a combination of antipsychotics and CBT, it is actually unusual to treat patiets with psychological therapies alone. Turkington et al argue that there is a good logical fit between the interactionist approach and the combination of treatments but this does not necessarily mean the interactionist approach is correct.

EV FOR ROLE OF VULNERABILITY AND TRIGGERS Tienari et al invetigated the combination of genetic vulnerability and parenting style. Children adopted from 19,000 Finnish mothers with Sz between 1960-1979 were followed up. Their adoptive parents were assessed for child-rearing style, and the rates of Sz were compared to a control group of adoptees without any genetic risk. A child-rearing style characterised by high levels of criticism+conflict+low levels of empathy was implicated in the development of Sz, but only for the children with high genetic risk, not control. 

MEEHL'S MODEL=OVER-SIMPLE The orginal DSM is clearly over simple as it assumes only one gene a schizogene is responsable for the vulnerabilty to stress. Now we know multiple genes are responsible and all have a small effect on there own. Also stress can come in many forms not just dysfunctional parenting. 

EFFECTIVENESS FOR TREATMENT COMBINATION Tarrier et al 315 patients were randomly allocated to a medication+CBT group or medication+supportive counselling or a control group. Patients in the 2 combination groups showed lower symptom levels, however there was no difference in hospital readmission.

HOW DOES DIATHESIS AND STRESS WORK? We do not yet know the mechanisms by which the symptoms of Sz appear and how both vulnerabilit+stress reduce them.