Schizophrenia

Question 1

What is Schizophrenia?

Answer 1

Schizophrenia is a major psychotic disorder (disorder where there is a separation/breakdown from reality) that causes a variety of psychological symptoms, but is typified by a lack of contact with reality
The word ‘schizophrenia’ comes from Greek words
This does not mean that people with schizophrenia have split personalities (a common misconception) but rather there is some loss of contact with reality and disconnected thought processes
- this can interfere severely with very day tasks

Question 2

Facts about Schizophrenia

Answer 2

1 in 100 people are effected by schizophrenia in their life time
It’s not true that “someone with schizophrenia can appear perfectly normal one moment and change into a different person the next”
- it’s not a personality disorder
Drugs and alcohol cause far more violence than people with sz
Auditory hallucinations can be critical and abusive
Thought to be caused by higher activity in part of the brains immune system
People with sz die 15-20 years earlier than the rest of the population
Only 8% of people with schizophrenia are employed
13% of people in the UK have sz
Medication can reduced the risk of relapse to 10%
30% of the NHS spending goes towards sz
220,000 people with sz are treated by the NHS each year

Question 3

Classification & Diagnosis

Answer 3

Classification is the process of organising symptoms into categories based on which symptoms cluster together in patients
This then allows us to distinguish one disorder from another
A diagnosis of a disorder is then possible because we can identify the symptoms a patient has and decide what disorder they have based on their symptoms
This is the medical approach to mental illness

Question 4

Symptoms

Answer 4

Individuals sz may have very different symptoms from each other
In order to try and make sense of the array of behaviours that people with sz may show, Kurt Schneider (1959) suggested categorising the symptoms into positive and negative symptoms

Question 5

Positive Symptoms

Answer 5

(Despite the name positive, they aren’t “good” symptoms)
Positive symptoms and symptoms of behaviours that a person is exhibiting in addition to ‘normal’ behaviours
- if they didn’t have sz, they wouldn’t have this symptom
They include:
- hallucinations
- delusions
- disordered thinking
- disorganised behaviour

Question 6

Hallucinations

Answer 6

Perceptions that are unreal - very hard/impossible to distinguish between reality
Many people with sz report auditory hallucinations, such as hearing sounds or voices - these are the most common type of hallucination, but sz patients can have any type
Hallucinations can present themselves in any sensory mortality
E.g. Kathryn Lewandowski et al (2009) estimated that 20% of people with sz have tactile hallucinations, whereby they are perceiving sensation as if someone or something is touching them
- formication is common - sensation of insects in/under/on the skin

Question 7

Delusions

Answer 7

Beliefs that are unreal but you are convinced that they are the truth
They are experienced with no evidence to offer in support of the delusions
There are many possible types of delusions, but most commonly held delusions are of persecution (belief that a person, group or organisation want to harm the individual) and of grandiose (belief that the individual is special in some way, e.g.they have superior knowledge or the assume the identity of a powerful figure, such as Winston Churchill)
Other delusions include control, guilt, paranormal, appearance, thought broadcasting are other examples

Question 8

Disordered Thinking

Answer 8

This is often evident through examining the speech (or reading their writings) of those individuals with schizophrenia
It is sometimes described as derailment or knight’s move thinking (taken from the movement of knights in chess)

Question 9

Disordered Behaviour

Answer 9

The person with schizophrenia many show a range of behaviours
For example, they may:
- move for no discernible purpose
- energetically pace
- wander in circles
- show fast, repetitive, useless movements
- make unexpected gestures
- emit loud utterances
Echopraxia may also occur
- mimicking others movements unpredictably and causes observer discomfort

Question 10

Negative Symptoms

Answer 10

Symptoms or behaviours that are inhabiting people with sz from demonstrating ‘normal’ behaviour
- something is lacking and taken away
Include:
- Alogia
- avolition
- anhedonia
- flatness of affect
- catatonic behaviour

Question 11

Alogia

Answer 11

Refers to the poverty of speech (don’t talk as much)
Apart from the reduction in the total amount of speech produced, people with sz lack meaning
- even simple, short answers can be a problem

Question 12

Avolition

Answer 12

Distinct lack of goal-directed behaviour
- don’t have the desire/motivation to do things, even though they need to be done
- people who are unaware of the diagnosis may perceive as disinterest

Question 13

Anhedonia

Answer 13

An individual does not react appropriately to pleasurable experiences
- lack of enjoyment and pleasure

Question 14

Flatness of affect

Answer 14

They may conserve without the usual emotion intonation and show little to no facial emotional expressions such as smiling or grimacing
Behaviour can be interpreted by others as being unsympathetic
Speech patterns are very monotonous and do not rise and fall as normal speech patters do

Question 15

Catatonic Behaviour

Answer 15

Individual may remain immobile for prolonged periods of time in seemingly uncomfortable postures and demonstrate waxy flexibility if moved
- almost freeze
Waxy flexibility - when a person is moved, they will maintain that position for prolonged periods of time
- named this because the human body can ‘be distorted like candle wax’

Question 16

Classification & Diagnosis

Answer 16

2 major classification systems for mental disorders APA Diagnostic & Statistical Manual (DSM-5 —> produced in America) and the WHO International Classification of Disease (ICD-10)
There are slight differences in how the DSM-5 and ICD-10 classify sz
For example, the GSM-5 says at least 2 symptoms must be present for at least a month and at least one symptom has to be a positive symptom
However, the ICD-10 says that one of the following symptoms must be present for at least 1 month is enough:
- thought delusions - e.g. thought insertion or withdrawal
- delusions of control
- hallucinatory voices
- biz are delusions
In addition, the ICD-10 says that 2 negative symptoms are sufficient for a diagnosis of SZ (catatonic behaviour plus once other of the negative symptoms)

Question 17

Issues in classification & diagnosis

Answer 17

There are potential issues when classifying and diagnosing sz
6 of these issues include:
- reliability
- validity
- co-morbidity
- gender bias in diagnosis
- culture bias in diagnosis
- symptom overlap

Question 18

Reliability

Answer 18

Consistent, trustworthy data that’s gets the same result each time
A psychiatric diagnosis is said to be reliable when:
- different diagnosing clinicians reach the same diagnosis for thr same individual (inter-rater reliability)
AND
- same clinician researches the same diagnosis for the same individual on 2 occasions (test-retest reliability)
Before publication of the DS<-5 in 2013, reliability for the diagnosis of sz was low, but this has been improved
- for example, Osorio et al (2019) reported excellent reliability for the diagnosis of sz in 180 individuals using the DSM-5
- there was a correlation co-efficient of +0.97 for diagnosing clinicians reaching the same diagnosis for the same individual and a correlation co-efficient of +0.92 for the same clinician reaching the same diagnosis for the same individual on 2 occasions
- these correlations show a strong positive correlation
- this tells us that the reliability of the sz diagnosis is very high
- this is a strength of classification and diagnosis of sz, as it means the diagnosis is dependable and trustworthy

Question 19

Validity

Answer 19

2 types
Internal validity - does the researcher actually and accurately measure what it claims to measure
External validity - can the research be legitimately generalised beyond the setting of the study
In this situation, we are especially interested in internal validity
- does the diagnosis of the sz diagnosis actually fit the symptoms being displayed
We can do thus by looking at the criterion validity
- i.e. asking if the criteria we are using to diagnose are actually accurate
Research in 2009 suggested that the criterion for sz is low
- Cheniaux at al found that when 100 patients were assessed using the ICD-10, 63 were diagnosed with sx, however the same 100, only 39 of them were diagnosed when being assessed using the DSM-4
These findings suggest that sz is either under or over diagnosed, depending on which diagnostic system used, which in turn suggests that criterion validity is low and diagnosis using the criteria set out in the classification systems is not accurate
However, in the Osorio reliability study, we saw that there was an excellent agreement when the same classification system in used, suggesting that criterion validity is actually good when it takes place within a single diagnostic system (although this may be a result of an improved criteria from the DSM - Cheniax used the DSM-4 whereas Osorio used the DSM-5
***

Question 20

Co-morbidity

Answer 20

Refers to the occurrence of 2 disorders or conditions together, e.g. an individual having both sz and depression together
Sz is very commonly diagnosed with other conditions
- according to Buckley et al (2009) around 50% of patients with sz also had depression ad 47% had substance abuse issues
PSTD occurred in 29% of cases and OCD in 23% of cases
- shows sz commonly occurs alongside other mental illnesses and the disorders are co-morbid
This is a problem because when 2 conditions are frequently diagnosed together it calls into question the validity of the classification of both illnesses
This could be a problem for some poeple diagnosed with sz because they might have have sz at all, but instead have unusual cases of other conditions such as depression
- this would be an issue for people who have experinced this because they my be put on sz specific medication (anti-psychotics) whic his a very harsh medication
- they also won’t get treatment for the mental health condition they actually have

Question 21

Gender bias in diagnosis

Answer 21

More commonly diagnosed in men
In 2017, the ratio was at 1.4:1
It could be that women are just less likely to develop sz, e.g. they may be biologically less vulnerable
However, reserach does not show this to be the vase
- it is more likely that women are just less likely to develop sz as men but are able to function between because they have closer social support networks compared to men
As a result of appearing to function more adequately, women are under diagnosed
This is an example of alpha gender bias
- differences between men and women are exaggerated
This is a disadvantage to women because it prevents them from getting the diagnosis they need to access help and treat t to help and manage their condition

Question 22

Culture bias in diagnosis

Answer 22

Since the 1970s, stats have shown that higher than expected numbers of individuals of Afro-Caribbean descent are diagnosed with sz
For example:
- Blake (1973) found that clinicians are more likely to diagnose a patient with sz from a written case study if they are described as Afro-American
- McGovern & Cope (1987) carried out as case study in Birmingham and found that 2/3 of psychotic patient held in hospitals were African-Caribbean compared to only. 1/3 who were white or Asian
- Cochran et al (1995) found black A-C immigrants in the UK are up to 7 times more lielly to be diagnosed with sz
- Nazroo (1997) found that black A-C immigrants in the UK sre 3 times more likel to be diagnosed than white British people
This data cannot be explained by genetics because the increased risk is not apparent in studies conducted in the Caribbean (Mahy et al, 1999) c
Therefore, the additional stress induced through migration to a different culture was suggested as being a reasonable explanation for these studies
However, the increases risk ad diagnosis rates were not only found in 1st gen migrants, but higher rates were also being noted in the children of A-C migrants in the UK (Harrison et al, 1998)
This suggests that there may be a stereotype within psychiatry that A-C people are more likely to have sz and therefore they are more liekly to jump to it as the diagnosis and conclusions

Question 23

Symptom Overlap

Answer 23

A final limitation in sz diagnosis is symptom overlap with other conditions
For example, there are similarities between sz and OCD
- both include thoughts or beliefs that are disconnected from reality, sz = disconnected thinking, ocd = obsessions
- both include repetitive behaviours, sz = disorganised behaviour, OCD = compulsions
As with co-morbidity, symptom overlap means that it is hard to distinguish sz bewteen other disorders
It may be because sz does not exist as a distinct condition and that even if it does, it is hard to diagnose
Therefore, both its classification and diagnosis are flawed

Question 24

Genetic Basis of SZ

Answer 24

The idea that mental illnesses such as sz are inherited

Question 25

Family studies

Answer 25

There is a lot of evidence that sz does have a genetic basis, as shown by family studies
- family studies look at the likelihood that 2 people in the same family share the behaviour
- in this case specifically, the same mental illness, sz
- they look at correlations and concordance rates
Gottesman Family Study Findings:
General population = 1%
Third degree relatives, 12.5% related:
- first cousins = 2%
2nd degree relatives, 25% related:
- uncles/aunts = 2%
- nieces and nephews = 4%
- grandparents = 5%
- half siblings = 6%
First degree relatives, 50% related:
- parents = 6%
- siblings = 9%
- children = 13%
- fraternal twins = 17%
100% related
- identical twins =- 48%
We can conclude sz does have a genetic basis
We are seeing positive correlations, the higher the concordance rate, the more closely related you are to someone with sz
But it isn’t purely genetic
It if was, identical twins would have 100% concordance rate

Question 26

Candidate genes

Answer 26

Next logical step is to identity candidate genes
Early research into this area looked for a single genetic variation with the belief that one faulty gene could explain sz
However, it appears that a number of different genes are involved in sz
- it is polygenic
This isn’t surprising as sz is a very complex condition, so makes sense it has a complex cause
Saying it only has one gene would be simplistic
There is also a massive range on symptoms that people can experience, with positive and negative symptoms
The most likely genes thought to be involved were those coding for neurotransmitters such as dopamine, as since the 1970s dopamine hypothesis was proposed as explanation for sz
However, in 2014, the Schizophrenia Working Group of the Psychiatric Genomics Consortium (a group of over 300 scientists from 35 countries) reported that there were 108 genetic loci associated with sz
This finding was presented as a result combining all previous data from genome studies of sz
- this is a meta analysis
- bigger set of results - increases population validity
This shows that although there may be genetic basis for sz, it is a complex matter
- more than just a few abnormal dopamine genes
It tells us sz is aetologically heterogenous (i.e. different combination of factors, including genetic variations, can lead to sz)

Question 27

The role of mutation

Answer 27

Sz can also have a genetic origin in the absence of a family history of the disorder
There could be a mutation in parental DNA which can be caused but factors such as radiation, poison or viral infection
One factor is ‘the season of birth’ influence
There is an increased risk in developing sz if you are born in winter
- found a statistically significant increase risk
This increase can ve as high as 5-15%
It is specifically in the earlier months of the year (i.e. January and February)

Question 28

Strengths of genetic explanations

Answer 28

Strong evidence base. This evidence base is objective and scientific
For example, family studies such as Gottesman (1991) study showed that risk of sz increases with genetic similarity to a family member with sz, with 2% concordance rate for cousins, 6% for parents and 48% for mz twins
The Hikler et al (2018) twin study found 7% concordance rate for DZ twins compared to 33% for MZ twins
There have also been adoptions studies (such as Heston 1966 and Tienari 2004) in which adoptees with genetic predisposition to sz had higher rates than those without genetic link, showing environment can’t be only factor
There is a wide range of evidence to support genetic link, covering a range of different backgrounds , from different centuries and large sample sizes (can be generalised). Adds validity to hypothesis

Practical applications
Genetic counselling has been developed. If a couple wants to have children but they are worried about family history of sz, they can talk to a genetic counsellor who will talk through concordance rates, symptoms and what developing it can mean and treatments
Allows for potential parents to be reassured about having a child and allow them to look out for symptoms in their children as they grow so early treatment can be sought if it develops
However, this can also be seen as a limiations
Nothing can be done about the child’s risk of SZ and genetic counselling may scare them probably unnecessarily given genetic concordance rates are generally very low

Question 29

Limitations of genetic explanations

Answer 29

Limitation of family studies and twin studies to investigate the role of genetics in sz is that it is hard to separate out the effects of nature (genetics) and nurture (environment) as families and twins are generally raised together. There is clear evidence to show that environmental factors also increase the risk of developing sz, especially those around childhood traumas
One example of such a case study is the Genian quadruplets, 4 identical daughters who all were diagnosed with sz by age 25. May suggest that genetics played a key role, as all of the sisters were genetically identical, but all were raised in a household with an alcoholic father who sexually molested at least 2 of his daughters and a mother who ignored their plight and it is widely believed that their terrible upbringing contributed at least in part to their psychotic breakdowns
Further supported by more recent research in 2017 which found that 67% of people with sz and other related psychotic disorders reported at least one childhood Rama as opposed to 38% of a matched group with non-psychotic mental health issues
Means that genetic factors alone can’t provide a complete explanation for sz
However, by carrying out the adoption studies (Heston and Tienari), thy do still show there is a genetic link

Question 30

Neural correlates of sz

Answer 30

This is the idea that mental illness such as sz are caused by abnormalities in the brain structure and/or function
This looks specifically at roles of neurotransmitter dopamine (DA) as this is one of the best-know and well-researched neural correlate in sz
- it could be that abnormal dopamine activity has agentic cause

Question 31

Initial hypothesis

Answer 31

Initially, the dopamine hypothesis was quite a basic concept
It proposed that individuals with sz simply had too much of of the neurotransmitter dopamine, and as such they demonstrated symptoms related to high levels of dopamine
This initial hypothesis was supported by research
For example, 1968 Griffith induced psychosis in non-sz volunteers with the administrations of dextroamphetamine (a drug that increases the amount of dopamine in the brain), finding that the volunteers demonstrated a generally abrupt onset of paranoid delusions and demonstrated a cold and detached emotional response
However, the initial dopamine hypothesis was identified as being too simple, confirmed by the fact that administering drugs that reduce the levels of dopamine had little or no effect on those individuals who suffered mainly with the negative symptoms of sz

Question 32

Second hypothesis

Answer 32

The situation was also complicated by he discovery of several subtypes of dopamine receptor sites, D1-D5
Of particular interest was D2 receptor
Research into the impact of antipsychotic drugs showed that this specific type of report was blocked by drugs
As D2 receptors are found primarily in sub optical regions, the lambic system, and its related anyways and its related pathways became the main focus of the dopamine hypothesis
There are 2 main pathways associated with sz
Mesolimbic pathway:
- dopamine is a major neurotransmitter in the mesolimbic pathway
- too much dopamine (hyper function), either from the neurones that fire too often or too quickly, cause overstimulation and ultimately positive symptoms such as hallucinations of delusions
- the mesolimbic pathway goes from the NA (nucleus accumbers) to the VTA (ventral legmental)
- this pathway involves the D2 receptors
Mesocortical pathway:
- again, dopamine is a major neurotransmitter in the mesocortical pathway
- this pathway carries signals from the VT (ventral tegmental area) to the frontal lobe area of the cortex
This nerve pathway is vital in emotional responses (flatness of effect), motivation, conditions and motor function (catatonic behaviour)
Too little dopamine (hypofunction) is evident in D1 receptors of the frontal lobe of many individuals with the cognitive impairments and negative symptoms of sz
Makes sense because under activity of these functions would explain negative symptoms

Question 33

Strengths of neural correlates

Answer 33

A strength of the dopamine hypothesis it that it is supported by reliable research evidenced
In 1968 Griffiths induced psychosis in non-sz volunteers with the administration of dextroamphetamine (drug that increases dopamine levels in the brain) and he found that volunteers demonstrated a generally abrupt onset of paranoid delusions and detached emotional responses
Research in 1950s looked at role of dopamine in Parkinson’s disease, a neurological condition which causes tremors and slow, imprecise movements. It was discovered that the drug L-DOPA increased the amount of dopamine in the brain and reduced Parkinson’s symptoms. However, what was also observed when people were given L-DOPA were behaviours similar to that of individuals similar to that of individuals with sz
This is a strength because it shows that high dopamine levels do cause sz symptoms even in those without the conditions and have had it induced synthetically. This adds internal validity to the dopamine hypothesis. We also have further scientific findings with D1 and D2 receptors

One strength is that it has led to the development of anti-psychotic drug therapies. Antipsychotic drugs essentially work by acting as antagonists i.e. they reduce the action of dopamine by blocking dopamine receptors in the brain
There is evidence to support that antipsychotics can lead to moderately effective control of sz. Ben Thornleyet et al. (2003) reviewed studies comparing the facts of chlorpromazine to control conditions. Data from 13 trials, totalling 1121 ppts, showed that it was associated with better overall functioning and reduced symptom severity compared to the placebo. There is also evidence for other antipsychotics. Herbert Melter (2012) concluded that clozapine is more effective than typical antipsychotics and had been effective for 30-50% treatment resistant cases where typical antipsychotics had failed
Shows that there is multiple research supported antipsychotics medications that have proved to be effective in people. This means that there are multiple options that help treat and support individuals with sz

Question 34

Limitations of neural correlates

Answer 34

Biological explanations for sz, such as dopamine hypothesis can be criticised for being biologically reductionist. This means the approach ignores nature aspects of our life, which can have an effect on developing sz
Other non biological factors can play a role in developing sz, such as abuse in childhood, drug use and even infections that the mother may have during pregnancy, urbanism can pose risks for people developing sz
Biological approach to sz ignores the other important environmental factors, when both biology and experiences should be taken into account

Although the dopamine hypothesis proposes that dopamine imbalances cause sz, it could also legitimately be proposed that sz causes the dopamine imbalances. Are the dopamine discrepancies seen in some people with sz just another symptom of it rather than a cause of it?
Research using PET scans (e.g. Copolov & Crook, 2000) hasn’t yet been able t detect differences in the dopamine activity of the brain of individuals with sz and those without it, let alone whether imbalances in dopamine activity are the cause of sz or a symptom of sz
We can’t establish cause and effect relationship and establish ‘which comes first’ - the abnormal dopamine activity or the sz
This is a difficult issue to overcome because to obtain a definitive answer, a prospective study would have to be carried out. This would be very expensive and time consuming, where there is no guarantee that people will ever develop sz, even if they have a very strong family history. There is only a 48% concordance rate seen in mz twins.

Question 35

Biological therapies - drugs therapy

Answer 35

The most common treatment for sz involves use of antipsychotic drugs
The term ‘antipsychotic’ refers to psychosis
A person with psychosis experiences some loss of contact with reality, e.g. through hallucinations or delusions
Psychosis is a defining characteristic of sz and related disorders
Antipsychotics may be required in short or long term
Some people take them short term and then stop their use without the return of symptoms
Other people may require them for life or else face the likelihood of recurrence of sz
Antipsychotics can be divided into typical (traditional) and newer atypical or second generation drugs

Question 36

Typical antipsychotics

Answer 36

Have been around since 1950s and include chlorpromazine which can be talked as tablets, syrups or injection
If taken orally it is administered daily up to a max of 1000 mg although daily doses are much smaller and for most people the dosage is gradually increased to max of 400 to 800 mg
Typical prescribed doses have declined over last 50 years (Liu and de Haan 2009)
Dopamine antagonists:
There s a strong association between use of typical antipsychotics like chlorpromazine and the dopamine hypotheis
They work by acting as antagonists in domaine system
Antagonists are chemicals which reduce action of a neurotransmitter
Dopamine antagonists work by blocking domaine receptors in the synapses of the brain, reducing the action of dopamine
Initially when an individual begins taking chlorpromazine, the dopamine levels build up, but then production is propduced
According to dopamine hypothesis of sz this dopamine-antagonist effect normalises neurotransmission in key areas of the brain (e.g. mesolimbic pathway) reducing symptoms like hallucinations
Sedation effect:
As well as having antipsychotic properties chlorpromazine is also an effective sedative
This is believed to be related to its effect on histamine receptors but it is not fully understood how this leads to sedation
Chlorpromazine is often used to calm indivuals not only with sz but also with other conditions
This has often been done when patients are first admitted into hospital and are very anxious
Syrup if absorbed faster that tablets so it tends to be given when chlorpromazine is used for sedative properties

Question 37

Atypical antipsychotics

Answer 37

Have been used since 1970s
The aim in developing newer antipsychotics was to maintain or improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and also minimises the side effects of the drugs used
There are a range of atypical antipsychotics and they don’t all work in the same way
in fact we don’t know how some ofn them work
Clozapine:
Developed in 1960s and first trialed in early 70s
It was withdrawn for a while in 70s following deaths of some patients from a blood condition called agranuclocytosis
However, in the 80s, when it was discovered to be more effective than typical antipsychotics, clozapine was remarketed as a treatment for sz to be used when other treatments failed
It is still used in this way today, and people taking it have regular blood tests to ensure they aren’t developing agranulocytosis
Because of its potentially fatal side effects is isn’t a viable as an injection
Daily dosage it a little lower than chlorpromazine, typically 300-450 mg a day
Clozapine binds to dopamine receptors in the same way that chlorpromazine does, but in addition it acts on serotonin and glutamate receptors
It is believed that this action helps improve mood and reduce depression and anxiety in patients and that it may improve cognitive functioning
The mood-enhancing effects mean that it sometimes prescribed when an individuals is considered at high risk of suicide
This is important as 30-50% of people with sz attempt suicide at some point
Risperidone:
More recently developed atypical antipsychotic
Been around since 90s
It was developed in an attempt to produce a drug as effective as clozapine but without its serious side effects
Like chlorpromazine, risperidone can be taken in form of tablets, syrup or injection that lasts for around 2 weeks
In common with other antipsychotics, a small does is initially given and this is built of to a typical dose of 4-8 mg and a maximum of 12 mg
Like clozapine, risperidone is believed to bind to dopamine and serotonin receptors
It binds more strongly to do around receptors than clozapine and is therefore effective in much smaller doses than most antipsychotics
There is some evidence to suggest that this leads to fewer side effects than other antipsychotics

Question 38

Antipsychotic strengths

Answer 38

One strength of using typical antipsychotics to treat sz is that there is a large body of scientific evidence to show that they are an effective treatment for sz
Cole (1964) gave some patients typical (conventional) anti-psychotics and some patients a placebo. The findings suggest that psychiatrists could treat mental disorders in the same way as physical ones. He found that 75% of those given a conventional antipsychotic were considered to be ‘much improved’ compared to only 25% of placebo. In addition, non of the patients given the antipsychotic got worse, compared to 48% of the placebo
In addition, Thornley et al. (2003) reviewed studies, comparing the effect of chlorpromazine to control conditions. Data from 13 trials with a total of 1121 ppts showed that it was associated with better overall functioning and reduced symptom severity compared to the placebos
Shows early researchers and doctors that sz can be treated, as it was previously considered to be untreatable, and allowed for further research and development of newer even more effective atypical antipsychotics

To further develop this point, a second strength is that atypical antipsychotics also have a number of controlled, double-blind placebo trials that show that these also help people with sz
Meltzer (2012) found that atypical antipsychotic clozapine is more effective than typical antipsychotics and can help in 30-50% of cases where the typical antipsychotics failed to help. More recent study published in 2019 by Huhn et al (largest meta analysis on effectiveness of antipsychotics with over 400 studies and over 50,000 ppts) also found that newer antipsychotics were effective at reducing symptoms of sz
This is a strength because it means that, as far as we can tell, antipsychotics work and help people with sz function more adequately and have a better quality of life

Question 39

Antipsychotics limitations

Answer 39

However, despite these pieces of research evidence suggesting that anti-psychotics are effective, one limitation is that there are problems with these studies
One major problem with assessing effectiveness of antipsychotics medications is non compliance. It is a particular issue for those with chronic sz because many of these individuals tend to lack necessary insight into their own condition. They don’t believe they have a problem and therefore don’t take the medication. Maria Rettenbacher and colleagues (2004) found full compliance in only 54.2% of individuals with sz, partial compliance in 8.3% of individuals and non compliance in 37.5%
Healy (2012) has suggested serious flaw with evidence for effectiveness. For example, most studies are of short term effects only and some successful trials have had their data published multiple times, exaggerating these size of evidence base for positive effects. Also, because antipsychotics have powerful calming effects, it is easy to demonstrate that they have some positive effects on people experiencing sz. This isn’t the same as saying they really reduce the severity of psychosis
Suggests that in the real world antipsychotics aren’t as effective as they seem to be in the highly controlled clinical trials that are used to investigate effectiveness

One weakness of using antipsychotics are the negative side effects
Typical antipsychotics can cause dizziness, agitation, sleepiness and weight gain. Longer-term use can result in tardive dyskinesia (caused by dopamine super sensitivity and causes involuntary facial movements such as lip smacking and grimacing) and Parkinsonism (tremors and instability). The most serious side effect is neuroleptic malignant syndrome (NMS) which is thought to be caused when the antipsychotic blocks dopamine action in the hypothalamus. As the hypothalamus is associated with the regulation of our body systems, NMS can cause delirium, coma and death and is estimated to occur in 0.1-2% of patients
This is a weakness because it means psychiatrists have to consider if the benefits offered to the individual with sz are worth the potential costs of the side effects as they can do harm as well as good and a patient experiencing these negative side effects may then avoid treatment. It is also worth noting that in some instances e.g. if the individual has been sectioned, they may be given antipsychotics without their valid consent, meaning any resulting side effects are definitely not their choosing

Question 40

Family dysfunction introduction

Answer 40

Psychologists have attempted to link sz to both childhood and adulthood experiences of living in a dysfunctional family
Three types of family dysfunction:
1. The schizophrenicgenic mother
2. Double-blind theory
3. Expressed emotion

Question 41

The schizophrenicgenic mother

Answer 41

This explanation is based on ideas that:
- our childhood experiences are key to our future behaviours, personality and mental health
And
- the mother-child relationship is to be one of the crucial factors in the development of sz (the word ‘schizophrenicgenic’ translates to ‘schizophrenia-causing’)
Developed by psychiatrist Frieda Fromm-Reichmann in 1940s and was based on the accounts she heard form her patients about their childhood
She noted many of them spoke of a particular type of parent she then called the schizophrenicgenic mother
This concept proposed that the mother of individuals who develop sz are overprotective and controlling but at the same time rejecting and distant

The mother’s overprotection = stifles child’s emotional development
Her emotional distance = deprives child from personal security
This creates a family climate = characterised by tension and distrust
This distrust later = developed into paranoid delusions and ultimately sz
In other words , mothers with their own psychological problems ‘gave birth to healthy children and literally drove them mad’
“The schizophrenic is painfully distrustful and resentful of other people due to the serve early warp and rejection he encountered in important people in his infancy and childhood, as a rule mainly inn a schizophrenicgenic mother”
- Freida Fromm-Reichmann, 1948

Question 42

Schizophrenicgenic mother strength

Answer 42

Quite a popular concept from the 1930s to 70s and it was the focus of much psychiatric literature with some supporting research published
Early research included one study by Kasain et al (1934) who examined hospital case records and reported evidence of maternal overprotection was found in 33 out of 45 cases of sz. Further studies published in 50s and 60s seemed to confirm the theory
Theory that dysfunctional and overprotective mothers can cause sz does seem to have supporting research evidence

Question 43

Schizophrenicgenic mother limitation

Answer 43

Research is, at best, tenuous
A closer look at findings of the Kasain study shows us that almost a third of cases didn’t have an overprotective mother, making it rather unconvincing evidence. Furthermore, the judgements may have been biased as the researchers weren’t ‘blind’ to the hypothesis and so it my have lacked objectivity as they may have been more likely to categorise normal behaviour of concerned parents as ‘overprotection’
Suggests that mother can’t be ‘schizophrenia-causing’. It also isn’t particularly objective. Bias from the researchers when looking at mothers of people in hospital because the mothers might have been overprotective because their children are in hospital
It wasn’t until the mid-70s that the concept of the schizophrenogenic mother lost favour
In 1982, Australian psychiatrist Gordon Parker published a review of schizophrenogenic mother research, concluding that, while the distant and controlling mothers provably exist, there was no evidence that they were more likely than anyone else to have schizophrenic children

However, the ‘wrongness’ of the idea that schizophrenogenic mother doesn’t that parenting and the family environment play no role in children’s mental health
This is where we look at the other 2 theories

Question 44

Double-blind theory

Answer 44

Bateson et al (1956) proposed that the symptoms seen in individuals with sz were the result of communication difficulties within the family, especially between the parents and their children he believed that children who receive contradictory messages from their parents are more likely to develop sz
E.g. a mother tells her child that she loves them but then turns her head away in disgusts
Bateson called these conflicting messages double-blind communicating as the parent is communicating 2 opposing messages
Bateson was clear that this was neither the main type of communication in the family of sz suffers nor the only factor in developing sz, just via risk factor
However, long-term exposure to these sorts of communication contradictions means that the child learns to perceive the world in terms of contradictory input from their environment and that they are unable to discriminate between contradictory messages, as they have internalised the double-blind situation
He believed that this eventually could lead to the manifestation of symptoms of sz as a means of escaping the contradictory demands of the double blind situation
E.g. delusions or hallucinations -> you are in your “own world”, flatness of effect -> don’t responds to the situation, don’t feel the emotions

Question 45

Double blind theory strength

Answer 45

Supporting research evidence
Berger (1965) carried our retrospective study in which a questionnaire was administered to a group of 20 individuals with sz and a control group of 40 college students. Consisted of 30 double blind statements. Ppts asked to rate on 4 point scale how frequently they recalled their mothers using such statements. Group with sz consistently reported a higher incidence of recall of such
Findings fit in with the prediction of double-blind theory, suggesting it has validity

Question 46

Double blind theory limitations

Answer 46

Contradictory research
Liem (1974) found that the communications offered in a structure task by the parents of 11 sons withy sz and were no more disordered that the communications offered by parents of 11 ones who did not have sz
Findings don’t fit the prediction of double-blind theory, suggesting it is invalid
Liem suggested that those studies that did find a difference in parental communications may actually just be detecting parents having to adapt their communication styles when dealing with a sz child. This suggests that the communication difficulties on which double blind theory is based on is really just an effect of sz rather than the cause

Question 47

Expressed emotion

Answer 47

When George Brown joined the Medical Research Council Social Psychiatry (MRCSP)unit in London in 1956, the antipsychotic drug chlorpromazine was being widely used to treat sz
After being stabilised with medication, patients were released but many were soon readmitted due to relapse of symptoms
Brown (1956) investigated 156 men with sz after they had been discharged to investigate this
He conducted interviews with patients and their families and observed their communications in their home
Based on his findings, he proposed that adverse home environments that have high levels of expressed emotion (EE) are negative and produce stress which exceeds the patient’s coping mechanism and therefore triggering a relapse
High EE is a negative family communication style including:
- critical comments about behaviour
- hostility from capers as they get angry or irritated with the individuals with sz because they feel they can control their behaviour (this usually results in rejection of the person with sz)
- emotional over-involvement where parents and acres blame themselves for the person’s illness and therefore show high leaves of emotion such as severe sadness or being over-protective
- lack of warmth
- lack of unconditional positive regard
Early reserach offered clear support for the role of expressed emotion in relapse rates
For example, Vaughn and Leff (1976) found that 53% of those individuals with sz who had a high EE relatives released within 9 months, whereas only 12% of those with low EE relatives relapsed

Question 48

EE limitations

Answer 48

Contradicting research
McCreadle and Philips (1998) failed to find higher subsequent 6 and 12 month relapse rates among individuals with sz living in high EE homes
Suggests EE theory lacks validity as results aren’t reliable or consistent

Question 49

General psychological explanation limitations

Answer 49

Ethical issues
Put blame on the family, e..g schizophrogenic mother
Blaming families will add more stress to them in an already stressful situation

Families share genes (nature) as well as dysfunctional environments (nurture)
Schizophrenogenic mother may be behaving this way due to having sz herself
Means the child might have inherited sz, lowering internal validity

Question 50

Family therapy intervention

Answer 50

Family therapy takes place with families as well as the identified patient
NICE guidance for family therapy for sz states that:
Family intervention should:
- include the person with psychosis or sz if practical
- be carried out for between 3 months and 1 year
- include at least 10 planned sessions
- take account of the whole family’s preference for either single-family intervention or multi-family group intervention
- take account for the relationships between the main carer and the person with psychosis or sz
- have specific supportive, educational or treatment function and include negotiated problem solving or crisis managing work (2009)
This is followed by the NHS
The overall aim of family therapy is to improve the quality of communication and interaction between the family members
There are a range of approaches to family therapy
- we will look at family intervention and how this can be put into practise with Burbach’s (2018) model of practise

Question 51

Family intervention

Answer 51

Aims to reduce levels a of negative EE in the family and develop a trusting and co-operative relationship within the family

Reducing negative emotions:
- the family and the person with sz are encouraged to share their experiences of living with the ilness
- it is a petered that the family might sometimes feel angry, frustrated and impatient
- might be due to feelings of helplessness, loneliness or loss, negative symptoms are frustrating
Ways of expressing these emotions without resorting to high EE patterns of behaviour are considered
Instead, the family learn more constructive ways of interacting with each other
- e.g. improving communication style, adjusting expectations of the family member with sz

Improving the family’s ability to help:
It involves an educational element where the therapist provides information about the cause, course and symptoms of sz and ways of managing and coping worth the everyday difficulties that arise
- e.g. ensuring medication is taken
The family and the individual are also trained to recognise the early signs of relapse so that they can respond early and reduce its severity
In addition, the family will think about how they can achieve a balance between caring for the individual with sz and maintaining their own lives

Question 52

Burbach’s 2018 model of practise

Answer 52

Phase 1 - staring basic information
- length of sz, symptoms, medications, providing emotional and practical support

Phase 2 - identifying resources, including what a family can and cannot offer
- e.g. Time, transport

Phase 3 - creating a safe space for all family members to express their feelings
- encourager mutual understanding

Phase 4 - identifying unhelpful patterns of interaction

Phase 5 - skills training
- e.g. learning stress management techniques

Phase 6 - relapse prevention training

Phase 7 - maintenance for future

Question 53

Family therapy strengths

Answer 53

Large body of reliable evidence showing its effectiveness
Anderson et al. (1991) found 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 they were both used together with the medication. A meta-analysis by Pharaoh et al. (2003) found family interventions help the patient to understand their illness and to live with it, developing emotional strength and reducing rates of relapse. More recent review by McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments available for sz. Relapse rates found to be reduced by typically 50-60%. Also concluded that using family therapy as mental health starts to decline is particularly promising
Shows family therapy is a beneficial treatment for sz, especially in reducing relapse

Doesn’t only help the individual with sz but also benefit whole family, who provide bulk of the care
Lob an (2013) reported that other family members felt they were able to cope better thanks to family therapy. By strengthening the functioning of a whole family, family therapy lessens the native impact on other family members and strengthens ability of the family to support the person with sz
Means family therapy has a wider benefit beyond the obvious positive impact on the identified patient

Economically friendly
Tarrier et al (1991) compared family therapy with standard care and concluded that family therapy is significantly less costly than standard care. 2 analyses compared family intervention with individual supportive therapy (Goldstein 1996, Lieberman et al. 1987). They concluded that the treatment costs of fall intervention are higher than those of individual therapy, but cost savings relating to other health care costs (e.g. reduced hospital stays as rates of relapse are reduced) offset extra treatment costs.
Makes therapy more financially accessible to everyone

Question 54

Family therapy limitations

Answer 54

May not be helpful to everyone
Patients may not live with their family. Sz may have put such a strain on the family and therefore they moved out or their delusions are leading them to believe they need to be on their own. Won’t be as effective as family can’t implement the techniques that they are taught on a daily basis. Therapy may also stress patient out. Strained relationships may make therapy hard or they may be having delusions making them believe that their family is agains’t them.
Can’t help everyone, may be counterproductive