PSYA4: Schizophrenia

> Kraepelin divided mental illnesses into exogenous disorders, which he felt were caused by external conditions and were treatable, and endogenous disorders, which had such biological causes as organic brain damage, metabolic dysfunctions, or hereditary factors and were thus regarded as incurable.

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TYPE 1: Distortion of normal function

•  Delusions
• Hallucinations
• Disorganized speech
• Control under alien force 
• Disordered thinking 

EVALUATION

> Positive symptoms can be affected by cultural differences

> Tend to have greater weight when diagnosing

> Hard to measure objectively

TYPE 2: LACK OF NORMAL FUNCTION

• Apathy
• No emotion
• Flat effect
• Social withdrawal
• Alogia (poverty of speech)
• Anhedonia (inability to feel pleasure)
• Avolition (lack of motivation) 

EVALUATION

> Start before positive symptoms

> Less affected by cultural factors

> More objectively measured 

• PARANOID: Delusions, persecution, hallucinations
• CATATONIC: Immobile, catatonic stupors; wild, uncontrollable movements
• DISORGANIZED: Giggling, pulling faces, flat effect
• RESIDUAL: Low level positive symptoms but psychotic symptoms present
• UNDIFFERENTIATED: Does not fit into any of the above 

• Little consistency in how diagnosis has been applied over the years
• Inconsistency between different early classifcation symptoms and vagueness of the DSM led to very low reliability in diagnosis
• DSM: Should provide an exhaustive system that includes all types of abnormal behaviour
• Boundaries between different catagories should be clear.

• Validity is concerned with the appropriateness of the classification catagories
• Schizophrenia-like disorders: Some show similar symptoms to those seen in SZ but do not fit the criteria; difficult to diagnose an individual presenting these symptoms. Some doubt about the validity of classification systems.
• Dimension or categorical disorder?: Some psychologists believe SZ to be a dimensional disorder; classification should relate to the degree to which problems are experienced, not simply the presence or absence of such problems. 
• SZ as a multiple disorder: Difficult for clinicians to distinguish between SZ and other syndromes; certain prescribed and recreational drugs can cause psychotic behaviour and can be difficult to distinguish drug-induced psychosis and SZ.
• Dual diagnosis: Fairly common for people to be diagnosed with more than one disorder, called co-morbidity (i.e. SZ with depression); important for the clinican to make a dual diagnosis so that the individual is given appropriate treatment for both disorders. 
• Cultural variations: Consistent findings in the UK + USA; SZ is diagnosed more frequently in African-Americans and African-Caribbean popns than in other groups (Harrison et al) - not sure whether this reflects greater genetic vulnerability, psychosocial factors associated with being part of a minority group or misdiagnosis.

ICD-10

• Published in 1991 by the WHO (World Health Organisation)
• 21 chapters of which only one is devoted to psychiatry
• Mental disorders were not included until 1952
• International and available in world languages

Catagories of  Mental Disorder in ICD-10

• Organic, symptomatic, mental disorders (e.g. dementia in Alzheimer's disease)
• Mental and behavioural disorders due to psychoactive substance abuse (e.g. those arising from alcohol abuse)
• SZ, schizotypal and delusional disorders
• Mood (affective) disorders (e.g. recurrent depressive disorder)
• Neurotic, stress-related and somatoform disorders (i.e. anxiety disorders)
• Behavioural syndromes associated with physiological disturbances and physical factors (anorexia nervosa)
• Disorders of adult personality and behaviour
• Mental retardation
• Disorders of psychological development 
• Behavioural emotional disorders 

• Developed in America and only available in English
• More widely used than ICD
• Early versions were heavily influenced by psychodynamic approach; later editions unbiased and contained much more detailed criteria in order to improve the reliability of diagnosis
• DSM is multi-axial - Clinicians have to assess a patient in five separate axes before making a diagnosis; these areas provide information about the biological, psychological and social aspects of a person's condition and so lead to a more informed decision by the clinician.

Reliability

• Early editions of DSM were vague descriptions and lacked reliability; clinicians not able to agree on diagnosis. DSM-IV was compiled very carefully and based on extensive research.Compilers excluded some catagories which have proven to be unreliable, included news ones and modified existing modules. Carried out field trials involving many clinicians and researchers to make sure that they were reliable.

Validity 

• DSM-IV is still criticised by people who believe that some of the criteria and catagories lack validity

• Rosenhan's study was done in two parts. The first part involved the use of healthy associates or "pseudopatients" (three women and five men) who briefly simulated auditory hallucinations in an attempt to gain admission to 12 different psychiatric hospitals in five different States in various locations in the United State. All were admitted and diagnosed with psychiatric disorders. 
• After admission, the pseudopatients acted normally and told staff that they felt fine and had not experienced any more hallucinations. All were forced to admit to having a mental illness and agree to take antipsychotic drugs as a condition of their release. The average time that the patients spent in the hospital was 19 days.
•  All but one were diagnosed with schizophrenia "in remission" before their release. The second part of his study involved an offended hospital challenging Rosenhan to send pseudopatients to its facility, whom its staff would then detect. 
• Rosenhan agreed and in the following weeks out of 193 new patients the staff identified 41 as potential pseudopatients, with 19 of these receiving suspicion from at least 1 psychiatrist and 1 other staff member. In fact Rosenhan had sent no one to the hospital.
• The study concluded "it is clear that we cannot distinguish the sane from the insane in psychiatric hospitals" and also illustrated the dangers of dehumanization and labeling in psychiatric institutions.
•  It suggested that the use of community mental health facilities which concentrated on specific problems and behaviors rather than psychiatric labels might be a solution and recommended education to make psychiatric workers more aware of the social psychology of their facilities. 

Criticism

• 'The myth of mental illness': Believed that this approach encourages us to interpret problems of living as if they are illnesses-
• Removes all responsibility from individuals for solving their own problems and run the risk of adminstering inappropriate, even damaging, treatments.
• If the concept of mental disorder itself controversial, any classfications of mental disorders are likely to be controversial aswell.

Response

• Szaz's view is not accepted by many psychologists 
• Considerable evidence for the existence of certain distinct syndromes (e.g. SZ)
• Little support for the idea that such a devastating condition can be brought about simply be stressful living.

Criticism

• Placing a patient in a diagnostic catagory distracts us from understanding that person as a unique human being with an individual set of difficulties.
• This can lead to stigma whereby an individual with a 'mental illness' is wrongly judged.
• Some sociologists hace suggested that labelling socially deviant behaviour as illness simply increases the individual's difficulties.

Response

• Not the diagnostic label that leads us to stigma; people were stigmatized long before modern diagnostic catagories were used
• Stigma will only be reduced when there is true nature of some mental illnesses.
• Clinicians working within psychopathology should only be diagnosed in the presence of a range of symptoms, not solely in terms of socially deviant behaviour.

Criticism 

• Individuals do not all fit neatly into the diagnostic catagories; some meet the criteria for more than one and others do not fit into an existing catagory at all

Response

• It is true that a few individuals do not fit into the existing catagories, but this is not a good reason to abandon classification systems for the majority who do

Kendler et al (1985): Evidence from family studies

• 1st degree relatives share an average of 50% of their genes, and 2nd degree share approx 25%.
• To investigate genetic transmission of SZ, studies compare rates of SZ of relatives in diagnosed cases with relatives of controls.
• There is now a considerable body of research that suggests that the closer the biological relationship, the greater the risk of developing SZ.
• Kender et al have shown that 1st- degree relatives of those with SZ are 18x more at risk than the general popn.

Evaluation:

• Family studies often inconclusive because conducted retrospectively (comparing a cross section of people who have already been diagnosed).
• A prospective (longitudinal) study can provide more reliable data; follows same group of people over a period of time and allows for comparison before and after any signs of illness.

• Prevelance is 1% worldwide
• Supports biological view as does not vary with environment
• There are variations within geographical areas.
• Turrey (2002) found high rates of SZ in Ireland; 4% of population have the disorder - incidence is also high in Croatia and Scandinavian countries but low in Spain and Italy and very low in parts of Africa

• Studies establish genetic links by comparing concordance rates for identical (MZ) and fraternal (DZ) twins
• Both share same environment, but only MZ twins have identical genetic makeup.
• Research shows that MZ have higher concordance rates.
• Gottesman and Shields used Maudsley Twin Register (210 MZ twins, 319 DZ twins) and found that 58% were concordant for SZ (7/12 MZ twins reared apart). 
• Severe MZ twins had 75-91% concordance rates.
• DZ concordance rates only 9-26%.
• May be greater genetic loading in severe types. 

Danish Adoption Study

• Kety et al took national sample across Denmark, found high rates of diagnosis for chronic SZ in adoptees whose biological parents had the same diagnosis, even though they had been adopted by 'healthy' parents.

Finnish Adoption Study

• Tienari (1969) identified adopted-away offspring of biological mothers who had been diagnosed with SZ (112 index cases), plus a matched control group of 135 adopted-away offspring of mothers who had not been diagnosed with any mental disorder.
• Adoptees ranged from 5-7 yrs at the start of the study and all had been separated from their mothers before the age of 4.
• The study found that 7% of the index adoptees developed SZ, compared with 1.5% of the controls.

EVAL: Twin studies

• Even in the rare case where MZ twins are reared apart, they still share the same environment in the womb before birth, so the contribution of environmental factors cannot be discounted
• Small sample - not entirely representative; very few MZ twins have SZ.

EVAL: Adoption studies

• Prospective study, so has indicated a strong genetic link for SZ
• Tienari showed that the risk for developing SZ was 4X greater in adopted children with bio mothers with SZ than in adopted children with mothers who do not have mental disorders.
• Wahlberg et al (2000) re-examined the same data and found that there was a strong interaction between genetic and environmental factors; only children who were adopted into families with poor communication were at an increased risk of developing SZ.
• Another problem in these longitudinal studies is that diagnostic criteria for SZ are continually being updated and changed.

• Related to the dysfunction of several neurotransmitter systems (Dopamine, 5-HT, Serotonin, Glutamate) all thought to play a part of SZ.
• SZ is said to be caused by excessive DA activity, causing abnormal function of DA-dependent brain systems, resulting in schizophrenic symptoms
• DA can increase/decrease depending on which part of the brain you are looking at.

Process of neurotransmitter release

1. Synthess and stroage of neurotransmitter molecules

2. Release of neurotransmitter molecules into synaptic cleft

3. Binding at neurotransmitter sites on post-synaptic membrane

4. Inactivation (by enzymes) or removal of neurotransmitter

5. Re-uptake of neurotransmitters sponged up by pre-synaptic neuron

Drug studies 

•  Amphetamines lead to increase in DA levels. Large quantities lead to delusions and hallucinations; if given to SZ patients their symptoms get worse.

Post-Mortems

• Falkai et al: Autopsies have found that people with schizophrenia have a larger than usual number of dopamine receptors. Increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen). Concluded that DA production is abnormal for schizophrenia.

PET Scans

• Lindstroem at al (1999): Radioactively labelled chemical L-Dopa and administered to people with and without SZ. L-Dopa was taken us more quickly in SZ patients. This suggests that they were producing more DA than the control group.  

• Not clear whether increases (i.e increased dopamine activity) are a cause or result of SZ. 
• Given these findings are from post-mortems, and assuming that dopamine is the important factor in the action of antipsychotic drugs, then it would be expected that dopamine metabolism is abnormal in patients with SZ.
• PET scan research - Wong et al (1986) revealed that dopamine receptor density in the caudate nuclei is indeed greater in those with SZ than in controls. 
• Unfortunately, neither PM/PS can reveal whether increased dopaminergic activity causes SZ, or whether SZ interferes with dopamine metabolism.

• Drugs alleviate positive symptoms; not so much negative systems - possible that findings in studies merely reflect two different forms of SZ.
• Amphetamines worsen positive symptoms and lessen negative symptoms associated with chronic SZ, whilst phenothiazines alleviate positive symptoms, but are not so effective with positive symptoms.
• Some people with SZ who do not respond at all to neuroleptic drug, which suggests a faulty dopamine system is not always a causal factor.
• One of the most effective drugs in treating SZ is clozapine; drug affects serotonin system rather than dopamine system, suggesting that neurotransmitterss could also be causal factors in SZ.
• Dopamine unlikely to be only causal factor in SZ; been implimented in other mental disorders.

• Brown et al: Decreased brain weight and enlarged ventricles, which are cavities in the brain that hold cerebrospinal fluid.
• Flaum et al: Also found enlarged ventricles, along with smaller, thalamic, hippocampal and superior temporal volumes.
• Buchsbaum: Found abnormalities in the frontal and pre-frontal cortex, the basal ganglia, the hippocampus and the amygdala.
• Structural abnormalities have been found more in neg/chronic symptoms; lending to the support that there are two types of SZ. 
• Critical period of onset is before adolescence; if abnormalities precede the onset of clinical symptoms, this confirms the view that SZ is a developmental disorder.
• Weinburger: Claims that despite much research, evidence is still inconclusive as to whether there are progressive structural changes prior to the onset of SZ or whether they follow the onset of clinical symptoms.
• Restricted to humans: Castner et al (1998) - researchers subjected monkeys to brain-damaging x-rays during foetal development, no ill effects during childhood compared with control, but at puberty they developed symptoms of SZ: damage during foetal devel caused symptoms.

Winter births

• Since late 1920's, overwhelmingly high proportion of people diagnosed with SZ were born in Winter and early Spring (Hope-Simpson 1981).
• Bradbury and Miller: Reviewed evidence and found that this was borne out of most countries in the N hemisphere.
• More recent study in England and Wales shows that this has remained consistent for the latter half of the century - Procopio and Marriott.

Viral infections

• Jones and Cannon: Young children who had viral infections were 5x more likely to develop SZ than those who did not.
• Also suggested that viral infections during pregnancy could be a casual factor (e.g. measles, polio, scarlet fever, influenza A)

• Some evidence shows that taking cannabis can lead to SZ.
• Cannabis raises dopamine levels in the brain and could trigger psychotic episodes
• Henquet et al: Meta-analysis found that heavy, young users of cannabis were 2x more likely as non-users to develop SZ.

Evaluation of link between substance abuse and cannabis

• Many studies show a link; however, seems likely that the increased risk occurs in young people who have a certain genetic predisposition - Caspi et al 2005.
• It has also been suggested by Peralta and Cuesta that people with early SZ symptoms might take cannabis as a form of self-therapy to deal with their negative experiences, suggesting that cannabis is not a causal factor.

• Links biological vulnerability to environmental stressors is the diathesis-stress model.
• Reasoning is that certain individuals have a constitutional predisposition to the disorder, but will only go on to develop SZ if they are exposed to stressful situations.
• Predisposition may be genetic/result of illnesses or damage in early life.
• Stressful events in the environment, such as major life events, traumatic experiences, or dysfunctional families may then act as a 'trigger' in a high stress situation.

Evaluation of D-S model

• Longitudinal studies provide support for model - shown that SZ did not always develop in those thought to be genetically vulnerable. This lead researchers back to the environment in search for precipitating factors.
• Isreali High Risk Study (Marcus 1987): Investigated environmental factors by assessing parents on hostility, inconsistency and over-involvement. All the reported cases of SZ had poor parenting rating. However, all of these cases also showed signs of neuropsychological abnormalities at the time of pre-initial assessment (13yrs) which raises the question whether these abnormalities had influenced the parent/child interaction. 

• The behavioural approach: Explains SZ in terms of conditioning and observational learning. It is difficult to see how the bizarre and complex pattern of SZ behaviour can be acquired through these simple proceses, although once diagnosed, it is possible that people with SZ are unintentionally reinforced for their odd behaviour.

• Psychodynamic explanations: 'Schizophrenogenic family' > People with SZ cannot resolve conflict between the demans of the ID and the overwhelming guilt imposed by the superego, and so they regree to an earlier, infantile stage of development. No evidence to support this view and, as with the behavioural approach, it fails to explain the complexity of the disorder. 

• Socio-economic status: SZ occurs in lower socio-economic groups- either status itself is a risk or people with SZ can no longer cope adaquately with jobs and relationships and so 'drift' down the social-economic hierarchy > Fox examined data from his own and others' studies and found no evidence for the so-called 'social drift hypothesis'.
• Migrant populations: SZ occurs more frequently in migrant populations; settling in a new and unfamiliar environment. Increased risk of diagnosis in african-caribbean popn in UK. Not entirely clear why this is the case, but it might reflect racial bias in diagnosis or factors associated with other migrant popns such as psychosocial adversity, stress of living with racial discrimination, cannabis use etc.

Evaluation: 

• Certainly evidence that acute life stresses can precipitate SZ, but it is unlikely that social class or economic status can be anything other than a contributory factor.

Schizophrenogenic families

• Patterns of communication may be a factor in the development of SZ - Fromm-Reichman used term to describe families with high emotional tension/close alliances/conspiracies.
• Bateson et al (1956): Double-blind hypothesis > Children given conflicting messages who express care, yet at the same time appear critical leads to confusion, self doubt and eventual withdrawal.
• Lidz et al (1965): 'Marital Schism' > abnormal family pattern where discord between parents was associated with SZ in offspring

Evaluation

• Methodologically flawed studies: did not include control groups and used poorly operationalized definitions of SZ.
• Major problem was that families were studied retrospectively, long after the person's mental disorder may have affected the family system.
• Routines are disrupted; suggesting that they have caused the disorder is unhelpful, if not highly destructive.

• One episode of SZ makes it more likely to have another.
• Set up prospective studies studies to investigate the degree if relapse in people who have already been diagnosed.
• Acts to maintain SZ rather than as a causal factor. 
• BROWN (1972): Patients who had SZ who returned home with a high level of EE acted as a greater tendency to relapse.
• VAUGHAN AND LEFF: Similar results; 51% relapse in high EE homes/13% in low EE homes. Concluded that time spent in face-face contact with relatives after discharge after discharge corresponded with increased rate of relapse in those with high EE. Those who went to work/care centre (<35 hrs work) significantly less likely to relapse.

• EE has now become a well-established model of SZ and many prospective studies support the hypothesis across many countries and cultures (Miklowitz 2004)
• Many patients with SZ are either estranged from their families or have minimal contact, so it is argued that they do no experience high EE and yet there is no evidence that such people are less prone to relapse - Goldstein 1988.
• It should also be remembered that relationships within the family should work both ways and there is some evidence that certain aspects of high EE behaviour are assoicated with the patient (Miklowitz)
• High EE is less common in the families of first-episode patients than in those with frequent re-admissions . This suggests that high EE may well develop as a response to the burdens of living with a person suffering from SZ.

• Thought that mechanisms that operate in normal brains to filter and process incoming stimuli are somehow defective in the brains of people with SZ - most people are able to focus attention selectively.
• Suggested that people with SZ cannot filter information in this way and they simply let in too much irrelevant information.
• This means that they are inundated by external stimuli, which they are unable to interpret appropriately, and so they experience the world very differently from the rest of us.
• Such ideas are supported by evidence that shows that some people with SZ are poor at lab tasks that require them to pay attention to some stimuli, but to ignore others

• Hemsley suggested that the central deficit in SZ is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.
• As a consquence, the individual cannot make sense of context; they don't know what incoming information and needs attention and what should be ignored.  They do not know what to expect next.
• This means that superficial incidents might be seen as highly relevant and significant and could explain symptoms such as delusions.
• Hemsley further suggests that internal thoughts are sometimes not recognized as arising from memory and are so attributed to an external source and experienced as auditory hallucinations.

• People with SZ are unable to distinguish between actions that are brought about by external forces and those that are generated internally.
• He believes that most symptoms from SZ can be explained in terms of deficits in three cog processes:
• 1) Inability to generate willed action
• 2) Inability to monitor willed action
• 3) Inability to monitor the beliefs and intentions of others.
• Three processes are all part of a 'meta-representation' that allows us to be aware of our goals and intentions of others.
• Faulty operation of this mechanism is due to a functional disconnection between frontal areas of the brain concerned with action and more posterior areas of the brain that control perception.

• Cog psychologists are attempting to find evidence for genetic links by examining whether malfunctioning is a family trait.
• Park et al (1995): Identified working mem. deficits in people with SZ, and in their 1st degree non-SZ relatives, a study has been supported by Faraone et al.
• Faraone et al and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to SZ and are even bold enough to claim that these are the cause of SZ.
• They admit, however, that their data cannot explain why some relatives do not develop SZ, even though they have the pre-disposing genes.
• Further work is needed to establish why some people have a 'low dose' of the genes,or, alternatively, whether they have not been exposed to any environmental agents that may trigger the disorder.
• Cannon et al: Identified verbal memory and attention deficits in people with SZ and their non-SZ siblings, suggesting that the mediating factors that determine the expression of these genes are birth complications.

• Cog theories do not explain the causes of SZ - simply describe symptoms in cognitive terms .In order to explain the origins of SZ, they need to be combined with the biological model. May not be able to offer a full explanation of SZ, but they may help to explain the origins of particular symptoms.
• Hemsley has tried to link the cognitive model to an underlying neurological system, in particular the hippocampus and related brain structures - there is very little clear cut empirical evidence.
• Frith's theory has provided a comprehensive framework for the symptoms of SZ. However, research is far from conclusive and the theory is still regarded as speculative.
• Theory is too reductionist, in that it fails to take into account environmental factors.
• Cognitive impairments thought to have a genetic origin have been implicated in a number of different mental disorders, e.g. attention deficit disorder. As an explanation for SZ, this is a new area of research and as yet, it is not possible to explain the validity of such a link.

• One of the early forms of treatment, first performed by Moniz in 1935, was the pre-frontal lobotomy, a form of psychosurgery in which sizeable portions of brain tissue were destroyed.
• This surgery was carried out extensively on a range of mentally ill patients, many of whom met the criteria for SZ.
• No evidence that this drastic treatment was effective, but plenty of evidence to show that it caused serious, even life-threatening side effects and was so abandoned as a therapy for SZ in the 1950's, when antipsychotic drugs were discovered.

• Drug therapy is the most common treatment for SZ, uses antipsychotic drugs. Some of these are called 'conventional/typical' antipsychotic drugs are used to reduce the effects of dopamine.
• Other drugs, called 'atypical' antipsychotic drugs also work on reducing serotonin activity.

Blocking dopamine receptors

• Phenothiazines (neuroleptics) alleviate the positive symptoms of SZ by acting on the neurochemical dopamine in the brain. Most frequently used phenothiazine is chlorpromazine.
• Produce maximum benefits in the first six months.

Blocking serotonin receptors

• Antipsychotic drugs such as clozapine have been introduced.
• Seem to take their effect by blocking serotonin rather than dopamine receptors.
• More effective than the conventional drugs.

Effectiveness

• The management of SZ has been revolutionized by antipsychotic drugs, which can rapidly reduce the most disturbing symptoms and can decrease the amount of time spent in hospital.
• Both conventional and atypical antipsychotic drugs have been shown in many studies to be an effective form of treatment.
• Produce a sedative effect and can significantly reduce psychotic symptoms of hallucinations and delusions.
• This enables patients to leave a relatively normal life in the community and has transformed SZ from a hospital 'long-stay' to a hospital 'short stay condition'
• Conventional drugs are not effective in reducing negative symptoms - atypical drugs seem to improve negative symptoms (deLima et al, 2005)
• If found that symptoms often return if patients stop taking the drugs (Rzewuska) and patients sometimes have to be kept on maintenance doses for long periods of time. This increases the risk of serious side effects. 

• One is the development of symptoms similar found to those in Parkinson's, such as stiffness, immobility and tremors. In it's most serious form, it leads to a condition called 'tardive dyskinesia' which includes uncontrollable sucking and smacking of the lips and facial tics.
• It is thought that this is caused by phenothiazines destroying parts of the brain. 
• This occurs in 30% of those taking the drugs and the risk increases with prolonged usage (Gualteiri).
• Other side effects include low blood pressure, blurred vision and constipation.
• Newer drugs are more effective than the conventional drugs. However, Clozapine has a potentially life-threatening side effect in damage to the immune system. Atypical drugs are also very expensive and can cause unwanted weight gain.
• Research has indicated that if antipsychotic drugs are stopped abruptly, then symptoms recur (Davis et al) - leading to a 'revolving door syndrome' of continual discharge into the community followed by readmission to hospital.
• Long-lasting injections can be given to patients, so that they do not have to take drugs continually. 

• Aims to reduce the level of negative expressed emotion in the family. 
• This type of treatment programme requires the involvement of several family members as well as the individual with SZ.
• Also involves an educational element where family members are given informaation about the disorder and ways of managing it - e.g. improving communicatin skills, lowering EE, adjusting expectations and expanding social networks.

Evaluation of family interventions

• A meta analysis (Pharoah et al) found that family interventions of this type were effective in significantly reducing rates of relapse and of admission to hospital in people with SZ.
• May also be appropriate because it can improve compliance with taking medication, which, as we saw before, contributes to effective outcomes from drug therapy.
• However, the analysis revealed a wide range of outcomes so the results are not conclusive. 
• Therapy is widely used in current practice, but is clearly most suited to patients who still live with/close contact with families.

• Individuals with SZ have a number of problems with social skills, e.g. social interactions, self-care, coping with stressful situations, self-awareness, managing symptoms and appraising social situations.
• Social skills training problems aim to teach complex interpersonal skills so that people with SZ can manage their lives more effectively.

Evaluation of social skills training

• Results of these interventions are generally positive, but it seems likely that the gains are not always maintained after the programme has ended.
• This kind of approach also seems to work better, and therefore be more appropriate, in conjunction with other therapies.
• Hogarty (2002) found that patients on medication who had also recieved social skills training adjusted to living in the community and avoided re-hospitalization more successfully than other groups on medication or social skills alone.

• Used to be thought-appropriate only for those who are capable of gaining reasonable insight into their problems. 
• CBT is based on the idea that people with mental disorders have irrational and unrealistic ways of thinking.
• The goal of CBT is to adjust thinking patterns and alter inappropriate beliefs.
• One particular type of cognitive intervention, called belief modification, teaches strategies to counter delusional beliefs and hallucinations and involves a process called cognitive challenge.
• Clients are taught to regard their negative responses to particular situations as hypotheses, rather than reality.
• They learn to challenge their initial negative interpretations. 

• Several controlled trials have shown that CBT can be effective in treating SZ. Turkington et al, found CBT to have a significant effect on both P + N symptoms of SZ and also that it could be effectively delievered via brief intervention programmes delievered by community psychiatric nurses.
• Belief modification is a relatively new approach - Jones et al carried out a meta-analysis on trials of belief modification and found that it reduced both frequency and the intensity of hallucinations. 
• BM is less effective in changing delusional beliefs but it did seem to reduce the accompanying distress.
• Drury et al reported on a study in which BM formed part of the treatment programme - immediate and short term gains were encouraging, but in a five-year follow up the treatment group showed no advantage over a control group. 
• This suggests that interim cognitive interventions might be required in order to achieve long-term benefits. 

• Although some studies have shown that CBT can improve certain symptoms of SZ, and new cognitive treatments continue to be developed, CBT does not offer a cure but rather a way of 'normalizing' symptoms.
• CBT is a colloborative therapy and involves the active cooperation of the client. For this reason it often avoids the criticism made of drug therapy that the client becomes a passibe recipient of treatment.