Characteristics

• There are two categories of schizophrenia symptoms as suggested by Schneider (1959):

  • Positive - Symptoms or behaviours exhibited in addition to normal behaviours.

  • Negative - Symptoms or behaviours that inhibit schizophrenic individuals from demonstrating normal behaviour.

Prodromal symptoms

• These often occur before the onset of typical SCZ symptoms, and can last between weeks and months.

  • This often occurs in young people.

• Common symptoms include:

  • Loss of interest in normal activities.

  • Avoiding the company of others.

  • Staying away from work or school.

  • Being irritable or oversensitive.

  • Lack of interest in hygiene or appearance.

  • Generalised anxiety.

  • Mild degrees of depression.

Positive

Hallucinations

• Unreal perceptions, which can include:

  • Auditory - Hearing voices or sounds.

  • Tactile - When a person feels they are being touched. An example is formication, the feeling of insects crawling on or under the skin.

  • Visual - Seeing objects or people.

• Lewandowski et al. (2009) estimated around 20% of schizophrenic people have tactile hallucinations.

Delusions

• Unreal beliefs, which can include:

  • Persecution - A belief that someone or something is attempting to harm the individual, such as a friend or MI5.

  • Grandiosity - A belief that one is special in some way or assumes the identity of a famous person, such as believing they are connected to or are Queen Elizabeth.

  • Reference - A belief that environmental stimuli, such as adverts and newspapers, are communicating hidden messages.

Disordered thinking

• Sometimes described as derailment or knight’s move thinking.

• An individual’s thoughts and speech move from one topic to another, for no reason with no logical flow. This is sometimes referred to as a word salad.

  • Their speech may be muddled and incoherent, which can make communication difficult.

• Individuals also report that the thoughts in their head don’t belong to them, which is known as thought insertion.

  • An individual may believe these thoughts have been inserted by another person.

  • This can cause them to be misdiagnosed with DID.

Negative symptoms

Alogia

• This means a poverty of speech.

• Individuals with schizophrenia will talk less overall and lack meaning.

Avolition

• Individuals seem indifferent and unconcerned with their surrounding, and lack the desire to engage in activities.

  • This can include work or personal activities previously enjoyed by the individual.

• There is also a lack of goal-directed behaviour, which may be perceived as disinterest.

• This can cause schizophrenia to be misdiagnosed as depression.

Anhedonia

• An individual does not react appropriately to pleasurable experiences.

• This can cause schizophrenia to be misdiagnosed as depression.

Flatness of effect

• When an individual appears to have no emotion.

• This can be conversing without emotional intonation (tone) or without any facial expressions.

  • This can be interpreted by others as being apathetic.

• Their speech patterns are often monotonous.

Catatonic behaviour

• This can range from fast and repetitive movements to no movement at all.

  • They may move for no reason, such as pacing, and make unexpected gestures and loud noises.

  • Echopraxia can also occur, where they mimic the movements of those around them.

  • They may remain immobile for long periods of time in uncomfortable positions, and when moved may resist or demonstrate waxy flexibility - their limbs and body is movable but their posture remains rigid and unnatural.

  • They may also adopt unnatural facial contortions.

ICD-11 vs DSM-5

• Both have further classifications dependent on whether it is an individual’s first episode, multiple episodes, or whether remission is apparent.

• DSM-5 requires the existence of prodromal or residual symptoms for 6 months alongside the one month of psychotic symptoms.

Biological explanations

Schizophrenic genes

Description

C4 gene

• McCarroll, and other scientists across MIT and Harvard, analysed the genomes of 65,000 people, 700 post mortem brains and used mouse genetic engineering to find the strongest genetic risk of schizophrenia.

  • They found the complement component 4 gene (C4) which is utilised in synapse pruning, which eliminates synapses. This occurs in teens - early adulthood, which is often the time of schizophrenia onset.

  • C4 works by depositing a sister protein known as C3, marking it to be pruned.

  • C4 was discovered to be unusually variable, but it has two main forms. The higher the expression of one form, known as C4A, the higher the risk of developing schizophrenia.

  • The researchers suggest this could be used to develop treatments that counteract the overactive C4.

  • It is located on chromosome 6, and towers far above other risk factors.

  • It has been suggested the link between schizophrenia and chromosome 6, which is associated with the immune system, means schizophrenia may be associated with immune system dysfunction.

    • More research into this is needed.

Genetic link studies

• Gottesman (1991) researched concordance rates (amount of pairs that share an attribute, in this case both being schizophrenic or non-schizophrenic) based on European twin studies between 1963-1987.

  • He found it was higher for monozygotic twins (48%) than dizygotic twins (17%).

• Joseph (2004) pooled data for all schizophrenic twins studied prior to 2001.

  • Found a concordance rate of 40.4% for monozygotic twins, and 7.4% for dizygotic twins.

• Varma et al. (1997) looked at first-degree relatives of 1,000 schizophrenics and 1,000 non-schizophrenics.

  • He found psychiatric illness was found in 16% of relatives of schizophrenics, and in 7% of the control relaties.

  • However, psychiatric illness does not mean schizophrenia and may suggest they had similar environments.

• Tienari et al. studied Finish adoptees, comparing 164 adoptees with schizophrenic mothers to 197 control adoptees.

  • They found that 6.7% of those with schizophrenic mothers developed schizophrenia, compared to 2% of the control.

• APA (1994) found that if one identical twin has schizophrenia, there is a 40-60% chance their twin will suffer too. This drops to 17% in non-identical twins.

Evaluation

Gene research issues

• Inheritance studies:

  • Family studies:

    • Will be highly influenced by the environment, especially when considering children and parents.

    • Highly subject to social desirability, as people may not want to admit their family issues.

  • Twin studies:

    • Twins often grow up in extremely similar environments, therefore this can have an impact.

    • If studied from children, valid consent becomes an issue.

    • Even MZ are not completely identical genetically - de novo mutations occur after the egg has split in utero.

    • Additionally, blind diagnoses where researchers are unaware if participants are DZ or MZ have lower MZ concordance rates, perhaps suggesting researcher bias is a factor.

  • Adoption studies:

    • May have high attrition rates as are longitudinal.

    • Valid consent of the children is an issue.

    • Can ignore the influence of the adoptive family's influence.

No single genes

• Many other genes have been identified as potentially causing schizophrenia:

  • O’Donovan et al. found 108 specific locations in the human genome that are linked with schizophrenia.

  • 83 of these had not been reported before.

  • These genes had roles in brain function, but also immune system functioning.

  • This means that different people could have genetic schizophrenia, but from different genes.

  • Alternatively, it may be a combination of genes required to become schizophrenic.

• Additionally, there are likely many genes that are not yet identified, making genetic links hard to determine.

• Schizophrenia is also likely polygenic, meaning it is a condition multiple genes influence.

Reductionist

• This theory states that all cases of schizophrenia are due to genes, and considers no other factors.

• If this was the case, all monozygotic twins would have schizophrenia as they have the same genes.

• It also ignores the impact of environmental factors, such as stressors.

• The diathesis stress model could be seen as combining these two ideas:

  • People have genetic predispositions to schizophrenia, but schizophrenia only appears when a stressor occurs.

  • This could explain why not all monozygotic twins are schizophrenic, they may have different responses to stress or experience different stressors. For example, one twin may have a close friend die.

Concordance rate

• If schizophrenia was fully genetic, you would expect to see a 100% concordance rate between MZ twins, which is not seen.

• There are two possible explanations for this:

  • Epigenetics - This is when environmental circumstances affects gene expression, by switching a gene on or off, such as DNA methylation.

  • Diathesis-stress model - This is when a condition is assumed to be inherited via a genetic predisposition, but this is not a guarantee.

    • Only when combined with an environmental stressor, sometimes known as a stressor, will the condition arise.

Treatment applications

• The discovery of SCZ genes could improve screening techniques, allowing people to understand whether they are at risk of the gene.

  • This could allow them to notice the arisal of prodromal symptoms and seek help earlier, preventing the disease from worsening.

• Additionally, genetic causes such as the C4 gene could have specific treatments designed to combat it, such as suppressor genes, therefore preventing the disease from developing.

  • This, alongside genetic screening, could allow individuals to stop the disease entirely.

Dopamine hypothesis

Description

Initial hypothesis

• This stated that those with schizophrenia have too much dopamine, and this caused their symptoms.

• Griffith et al.(1968) gave dextro-amphetamines (a drug which increases dopamine in the brain) to non-schizophrenics.

  • This induced psychosis, with participants experiencing paranoid delusions and a cold, detached emotional response.

• However, drugs which reduce dopamine (antipsychotics) had no effect on individuals suffering from negative symptoms.

Receptor sites

• This initial theory was complicated with the discovery of five different receptor sites (D1-5). These are distributed in and underneath the cerebral cortex - in the limbic system.

• Seeman and Lee found that antipsychotic drugs had a large impact on D2 receptors, making them the focus for research.

  • As they are primarily found in the limbic system, this became the main focus of the overall hypothesis.

Limbic pathway

• The limbic system has many functions, including emotion, memory and arousal.

• It has two main pathways associated with schizophrenic, the mesolimbic and mesocortical:

  • The mesolimbic pathway carries signals from the ventral tegmental area to the nucleus accumbens.

    • Too much dopamine, from neurons firing too often or too quickly, is hypothesised to cause overstimulation and positive symptoms, such as hallucinations and delusions.

    • Antipsychotics work by reducing this transmission, therefore reducing dopamine in the pathway and positive symptoms.

  • The mesocortical pathway carries signals from the ventral tegmental to the frontal lobe, and is used for emotional responses and cognition.

    • Davis et al.(1991) found that too little dopamine, hypofunction, is evident in D1 receptors of the frontal lobe of schizophrenics with cognitive impairments and other negative symptoms.

Evaluation

Gene link

• Many argue that dopamine imbalances by have a root in genetic causes.

  • Schizophrenia is certainly shown to be genetic (Joseph, Tienari et al.).

• However, there is not one single gene for schizophrenia, with O’Donovan finding 108 specific locations on the human genome linked to schizophrenia.

  • The major risk factor identified is the C4 gene, which is associated with neural pruning, not dopamine release.

Measuring dopamine

• Most research into dopamine releases measures metabolites - what dopamine is broken down into.

• Homovanillic acid (HVA) is measured in cerebrospinal fluid obtained from lumbar punctures, which could be seen as unethical due to discomfort.

  • HVA levels are highly influenced by diet and drug use, and can vary widely between participants.

• Therefore, neurotransmitter research that uses this can be inaccurate.

• Lindstroem et al. instead radioactively labelled chemicals needed to produce dopamine, and found that schizophrenia sufferers use these up faster than non-sufferers.

Serotonin

• This is another neurotransmitter identified as linking to schizophrenia, and is targeted by atypical antipsychotics alongside dopamine.

  • Older typical antipsychotics only targeted dopamine.

  • Atypical also have less movement related side effects.

• This suggests dopamine is only a partial explanation.

Cause or effect

• This hypothesis suggests dopamine imbalances cause schizophrenia, however it may be schizophrenia that causes these imbalances.

• Copolov and Crook (2000) were unable to detect dopamine activity differences in the brains of those with and without schizophrenia. This makes it difficult to research this issue.

Individual differences explanations

Psychodynamic approach

Explanation

Freud

• Freud based his theory of SCZ from the memoir of a man with SCZ - Schreber.

  • He was specifically fascinated with his ability to keep working once developing the disease.

  • Schreber died in asylum while attempting a legal case for his release.

  • He also was not diagnosed with SCZ, but dementia praecox, as SCZ was seen as an early form of dementia.

• Freud believed that SCZs formed a fixation on the first one to two months of the oral stage of development.

  • This would be caused by too much satisfaction (overindulgence) or under satisfaction (frustration).

  • During this stage, the main way to satisfy the libido is breastfeeding, meaning the blame for this would be put on the mother.

  • When the SCZ individual occurs stress, they then regress to this stage of development again.

    • Regression is an ego defense mechanism when a person returns to an earlier stage of development.

  • This is seen as returning them to the mental state of a newborn.

• At this age, the ego is not well developed and the superego does not exist. This means the id’s impulses are hard to control, and therefore dominate the mind.

  • This means all attachments are lost other than those focused on the self, and disengage from the outside world.

  • The detachment from reality combined with possession of an active mind leads to the creation of alternative fantasies not part of the real world.

  • As the Id has total control, this leads to self-centred narcissistic delusions.

  • Hallucinations are caused by a need to interact with something external, but distrust of all that is real, causing an alternate reality to form.

Schizophrenogenic mother

• Fromm-Reichman was a Neo-Freudian, meaning she was a trained psychoanalyst but developed her own theories.

• She suggested SCZ was triggered by mothers who were overly dominant in the home, especially towards the child, meaning they were controlling and overprotective.

  • They were also cold and distant.

  • This stifles childhood development, and leaves the child feeling emotionally insecure.

  • This type of mother is known as schizophrenogenic.

Evaluation

Lack of evidence

• No psychodynamic theories have scientific support, including the id, ego and superego which this theory is based upon.

• Kasanin et al. (1934) examined hospital case records and found maternal overprotection in 33 out of 45 cases (73.3%).

  • This means a third of cases were not explained by the SCZG mother, making it unconvincing.

  • Additionally, this was based on hospital records, meaning bias may be present both in the doctors and researchers, who were not double-blind.

  • Additionally, this overprotection could be explained by their child’s illness.

• Additionally, Waring and Ricks (1965) found that mothers of SCZs tended to be more anxious, shy, withdrawn and incoherent rather than controlling.

• Wild et al. (1975) found that fathers of those with SCZ played a more dominant role than the mothers

No treatment application

• Freud believed those with SCZ could not be treated by psychoanalysis, as they lacked the insight necessary.

• Later, Rosen (1947) proposed that SCZ could be treated by psychoanalytical techniques.

  • However, Strupp et al. (1977) found that these techniques could harm a SCZ individual rather than benefit them.

  • This could be due to psychoanalysis requiring experiencing distressing memories, which is worsened as a SCZ individual will struggle to distinguish between reality and hallucinations.

• If it cannot treat SCZ, this suggests it has not adequately explained it.

Cause and effect

• It could be as Fromm-Reichman suggests, and the SCZG mother causes it.

• It could be that having a child with SCZ causes the mother to be more protective and emotionally distant

• It could be those who develop SCZ are more difficult children, making it harder for the mother to bond with them.

• It could be this behaviour is caused by genetics - the mother may herself be exhibiting SCZ symptoms.

Sexism

• This theory specifically focuses on mothers, not just the SCZG mother but the fact the mother is the one supposed to satisfy the oral stage of development.

• This makes the theories highly out of date, as:

  • Mothers are often not always home.

  • Mothers are not always primary caregivers.

• This theory caused great harm, by causing mothers of SCZ children to feel responsible.

Not full explanation

• While this explains positive symptoms, it cannot explain any of the negative symptoms.

  • Sterling and Hellewell (1999) argued that SCZ behaviour does not resemble that of infants, as infants are usually highly expressive and emotional.

• It does not explain all cases of SCZ.

  • Some individuals may have warm and kind mothers - how do they develop SCZ?

• Freud used one man - Schreber - who he never met, to form his explanation of SCZ, making it highly ungeneralisable.

Cognitive approach

Explanation

Hallucinations

• Claiborn (2009) estimates that 2.5-4% of the general population has experienced hallucinations, most not diagnosed with a psychiatric problem.

  • This raises the question, what causes those with SCZ to develop the rest of the symptoms alongside these hallucinations.

  • Another consideration is not all those with SCZ hallucinate - consider in evaluation, not in description.

• There are two main explanations:

  • Morrison (1998) proposes that triggers, such as sleep deprivation, causes some individuals to hear maladaptive voices.

    • Individuals then appraise (evaluate) these voices inappropriately, such as coming from aliens.

    • This elicits behaviours such as social isolation or self harm, which leads to negative emotions.

    • These emotions reinforce the messages from the voices, causing them to be perpetuated in a cycle.

  • Frith (1992) proposes that those with SCZ have an abnormal inner voice.

    • Everyone has an inner voice, and most people believe they have control over it.

    • Those with SCZ fail to monitor their own thoughts, and misattribute them to the outside world.

    • Voices heard by those with SCZ are therefore their own inner speech being misinterpreted.

    • He speculated these were linked to irregularities in neural pathways running between the septo-hippocampal system and the prefrontal cortex.

    • McGuire et al. (1996) supported this theory, by finding those with SCZ had reduced activity in the parts of the brain involved in monitoring inner speech.

Negative symptoms

• Beck linked his negative cognitive triad, which was originally linked to depression and used to develop CBT, to these negative symptoms.

• Beck et al. proposes that the individual endorses dysfunctional beliefs about their performance and ability to experience pleasure.

  • This leads to a cynical and gloomy view of the future.

  • Their mental filter also only allows them to process negative (irrational) thoughts, leading to a deficit in information which bolsters their negative views.

  • This leads to flatness effect, avolition and anhedonia, and perhaps even delusions.

Lack of preconscious filters

• Frith (1979) developed the Attention Deficit Theory of SCZ.

  • SCZ is seen as a result of the breakdown of thought filtering processes due to abnormalities in parts of the brain that use dopamine

  • This prevents them from effectively filtering out non-pertinent information from their preconscious thought - which is thought without awareness.

  • The most important incoming information is then sent into our conscious thought, which allows individuals to make sense of the information.

  • These filtering issues can cause disordered thinking, due to issues categorising information due to it overloading an individual.

    • This can also be seen as causing issues with memory recall, as those with SCZ are not able to properly process their environmental information, leading to incomprehensible memories.

  • Additionally, attentional biases can cause information to be seen as more important than it is, leading to delusions of persecution and reference.

  • Frith believed this was caused by abnormalities in areas of the brain that use dopamine, especially the prefrontal cortex.

    • His research shows that those with SCZ have reduced blood flow to these areas during certain cognitive tasks.

    • This indicates lessened activity, but does not directly correlate to dopamine activity.

  • Bentall (1994) argued that those with SCZ have an attentional bias to threatening and emotional stimuli, such as that related to pain and violence.

    • This means stimuli is seen as threatening when it isn’t, explaining paranoid delusions.

      • However, not all SCZ individuals experience these, so what explains grandiose delusions?

Comprised theory of mind (ToM)

• Everyone possesses this - which is the ability to understand everyone has their own minds, and separate desires, knowledge and ideas.

• Frith (1992) argues those with SCZ have this impaired, meaning they are not able to distinguish between internal and external actions.

• He believes SCZ is the result of disorders within 3 separate cognitive systems:

  • Disorders of willed action - This is when a person cannot plan and carry out a behaviour, forgetting what tasks they have done and need to do.

    • This can explain some negative symptoms.

  • Disorders of self monitoring - This is when a person is unaware of their own intentions and the effort behaviour requires. They are only able to monitor behaviour via consequences.

    • This leads them to blame their actions on external forces, such as a person with SCZ drinking water because they are thirsty being attributed to messages from the TV.

    • This can explain hallucinations and delusions.

  • Disorders of monitoring others - This is when a person is unable to monitor and interpret the behaviour of others, leading to misunderstandings that can cause delusions of persecution.

Evaluation

Supporting research

• Supporting Firth’s theory of hallucinations:

  • McGuire et al. (1996) found those with SCZ had reduced activity in the parts of the brain involved in monitoring inner speech.

• Supporting Firth’s theories of filtering:

  • Barch et al. (1999) compared Stroop test results between those with SCZ and those without.

    • They found those with SCZ were slower and made more mistakes, showcasing the difficulty they have processing information.

Causal statement

• Frith posits that the faulty operation of cognitive mechanisms is due to a disconnection of the functions within the frontal cortex - involved in decision making and action - and the more posterior areas - involved in perception.

  • He has even produced some supporting evidence, finding people with SCZ had changes in cerebral blood flow when completing cognitive tasks.

• Some critics, however, argue this is reductionist as it downplays a complex experience to the functioning of brain circuits.

Limitations

• It is criticised for only explaining cognitive symptoms of SCZ, and not issues such as catatonic behaviour.

• It is also criticised for not explaining the origin of cognitive deficits.

  • Therefore it explains the proximal (cause of current symptoms) but not the distal causes (the origins).

  • Therefore, it is not a single explanation.

• Claiborn (2009) estimates that 2.5-4% of the general population has experienced hallucinations, most not diagnosed with a psychiatric problem.

  • What causes those with SCZ to misappraise these voices, as Morrison claims to maladaptive causes.

• The cognitive triad by Beck was originally designed for depression, therefore it may be generalisable to SCZ.

Integrated model

• Frith uses cognitive neuropsychology in his explanations of hallucination and ToM.

• Murray and Howes have described another integrated model of SCZ:

  • It is caused by genes or early life factors, which combine with life events or social stressors.

  • This provokes the dopamine system to overly release dopamine, which causes issues with cognitive processes.

  • This causes a vicious cycle, where the stress induced by experiencing these symptoms provokes more dopamine to be released.

Treatment applications

• Cognitive theories lead CBT to be used to treat those with SCZ, which is recommended for treatment by NICE.

• Kuipers et al. (1997) randomly allocated those with SCZ to one of two conditions; standard care and CBT + standard care. These individuals had a positive and distressing medically resistant symptom.

  • After nine months, control group had one suicide, 3 individuals who had worsened and 31% of individuals who had improved.

  • The CBT group had only 1 individual who had worsened, and 50% of improved individuals.

Social psychological explanations

Sociocultural factors

Explanation

Urbanicity

• Humans have changed over time to mainly live in urbanised areas, which could be argued goes against our evolution.

  • By 2050, the UN estimates 66% of the world’s population will live in an urban area.

• Schizophrenia is more prevalent in urban populations over rural ones.

  • Faris and Dunham (1939) found this, but also that schizophrenia rates were increased in the more densely populated areas of Chicago.

    • These rates were also increased for areas with high levels of social conflict and social mobility - people move in and out frequently.

  • Krabbendam and Van Os (2005) suggest that this could link to other explanations of schizophrenia.

    • Urbans areas have high rates of socioeconomic adversity and poverty, which could cause stressful home lives and affect familial relationships, increasing the levels of expressed emotion.

    • They also labelled overcrowding, drug use, environmental pollution and exposure to toxins and infectious agents as possible causes.

  • Maternal stress during pregnancy has linked to increased risks of illness in childhood.

    • Herman et al. (2006) found the stress of unwanted pregnancies can increase the risk of a child being schizophrenic. This is linked to poverty.

  • Zammit et al. (2002) found that cannabis usage doubled the risk of schizophrenia in Swedish men.

    • Drug use is more common in urban areas.

  • Bebbington et al. (2004) found that sexual abuse leads to a 3x increased rate for schizophrenia.

    • Childhood abuse is more common in poverty stricken households.

• Pederson et al. (2006) found that being raised in an urban environment increases SCZ risk, but being born in an urban environment doesn’t.

Social isolation

• Schizophrenics are often extremely socially isolated - more likely to live alone, be estranged from family and have little friends.

  • This could be due to their disturbing behaviour and struggles with communication.

  • It could also be self-imposed.

• Faris (1934) suggested that those with schizophrenia withdraw as they find communication stressful.

  • This cuts the individual off from feedback about what behaviours and thoughts are appropriate, leading to a positive feedback loop of strange behaviour.

• Jones et al. (1994) conducted a longitudinal study on children born in a single week of March.

  • There were 30 diagnosed cases of SCZ, and researchers found those diagnosed were more likely to have solitary play preferences at 4-6, and rate themselves less socially confident at 13.

• Van Os et al. (2010) found that people were more likely to be schizophrenic if they were foreign born, unemployed or welfare dependent, but only if many of their neighbours were not foreign born, unemployed or welfare dependent.

  • Single people also have a higher likelihood of SCZ if they live in an area with a small number of single people.

  • They also found a 0.5% increased rate of SCZ for those born and raised in urban areas.

Ethnicity and discrimination

• Cochrane and Sashidharan (1995) found Afro-Caribbean immigrants in the UK are 7x more likely to be diagnosed with SCZ.

  • This could be due to them being more likely to be labelled as mentally ill due to racism, or the stress of discrimination.

  • Ineichen (1984) found that they are more likely to be forcibly admitted to psychiatric hospitals, perhaps due to stereotypes of aggression.

  • This cannot be attributable to genetics, as similar studies in the Caribbean (Mahy et al. 1999) had no increased risk.

• Cantor-Grace et al. (2005) conducted a meta-analysis on previous studies in migration and SCZ.

  • They found that those who were immigrants or had a family history of immigration had a higher risk of SCZ.

  • In fact, children of immigrants had a higher risk of SCZ.

  • This suggests it is the stress of being an immigrant, likely racism, that causes an increased risk of SCZ.

    • This could affect children more as SCZ usually develops in late adolescence, and they would experience this their entire childhoods.

• Boydell et al. (2004) found that migrant groups had an increased risk of SCZ when they formed a small proportion of the community.

  • This could be due to increased chances of racial abuse.

• Immigrants are also more likely to be socially isolated and live in poverty-stricken urban areas.

Evaluation

Urbanicity

• Too many factors in a city to label just one; cities cause social isolation and are more likely to have higher immigrant populations.

• City dwellers tend to be healthier and better educated than rural counterparts.

  • This may suggest city dwellers are more likely to be diagnosed and noticed with symptoms of schizophrenia than those in rural areas.

• There is a cause and effect issue:

  • The social drift hypothesis suggests that people experience a decrease in socioeconomic status once diagnosed with SCZ, causing them to drift to cheaper urban areas.

    • This is supported by Sartorius et al. (1986) who found that schizophrenia rates are consistent across cultures, including those who are mostly urban.

    • This suggests this is not an overall effect on SCZ rates, but on SCZ distribution.

  • The social causation hypothesis suggests that living in a city causes SCZ.

    • This is supported by Pedersen and Mortensen (2001) found that those at high risk of psychotic disorders, such as SCZ, reduced their likelihood of developing these if they moved to a more rural environment.

• There is barely any attempt to distinguish between socioeconomic status, as city dwellers can range in living status.

  • Those who are poor likely have a very different life to those extremely rich.

• There may be a cultural bias, as researchers have often never experienced poverty and may make assumptions about the people who live there, and how it affects them.

• However, those who live in social areas have a higher level of social capital - by communicating with more people and acting more effectively with other people.

  • McKenzie et al. (2002) proposed that high levels of this social capital may protect people from stress.

Social isolation

• This also has cause and effect issues:

  • It is either isolation causes SCZ:

    • van Os et al. (2000) found that single people have a higher likelihood of SCZ if they live in an area with a small number of single people.

  • Or isolation is a symptom of SCZ:

    • Jones et al. (1994) conducted a longitudinal study on children born in a single week of March.

      • There were 30 diagnosed cases of SCZ, and researchers found those diagnosed were more likely to have solitary play preferences at 4-6, and rate themselves less socially confident at 13.

• It could have treatment applications, as interventions can be made for social isolation, especially from younger ages.

Ethnicity and discrimination

• This could be due to clinician bias, and not an actual increase:

  • Immigrants may be more suspicious of mental health professionals, and be seen as more suspicious.

• Boydell et al. (2001) notes that SCZ rates increase in ethnic minorities when the proportion of ethnic minorities in the locality fell, suggesting that social isolation contributes to this.

• However, we will be unable to understand the effects of racism until we live in a world without racism.

Dysfunctional families

Explain

Double bind theory

• This theory was put forward by Bateson (1956), who believed that families of schizophrenics acted in ambiguous ways that could cause SCZ.

• This involves a parent saying something to a child, but using conflicting paralanguage (non-verbal communication).

  • For example, saying “I love you“ with an annoyed tone, or asking how their day was while reading a newspaper.

• This means a child receives two conflicting messages, and cannot adequately respond to or ignore them.

  • Children also often cannot metacommunicate (communicate about past communication) due to their reliance on the parent, leaving them confused.

• Bateson et al. emphasised that this type of communication was just a risk factor, and did not necessarily need to be the only form of communication to cause this risk.

  • He did suggest it could cause individuals to be unable to discriminate between contradictory message due to this communication, so they may be unable to understand sarcasm or jokes.

    • They will also be unable to communicate effectively, as they will believe this is a normal way to communicate by modelling their parent.

    • R.D. Laing even suggested that SCZ is a reasonable response to an insane world, which is definitely suggested by alterations to how they perceive the world.

  • Maladaptive thinking could be caused by these misunderstandings, especially delusions of reference and avoidance of other people.

  • He believed that hallucinations and delusions also developed as a form of escapism away from these conversations.

Expressed emotion (EE)

• Brown (1959) came up with his theory during his work in the Medical Research Council Social Psychiatry in London.

  • Once stabilised with medication, he found SCZ patients often readmitted after release due to a relapse of symptoms.

• To investigate this, he studied 156 SCZ men after release, finding relapse was highly connected to their location of release.

  • Men discharged to parents or wives had higher relapse rates than those who were discharged to siblings or lodgings.

  • To further investigate this, Brown interviewed the wives and parents of SCZ individuals, and concluded that high levels of EE increased the likelihood of relapse.

• High EE has 3 main traits:

  • Critical comments about the individual with SCZ, such as calling them lazy.

    • Low EE individuals recognised this as part of their illness.

  • Hostility was present while communicating with these individuals, which Brown labelled as due to unmanageable anger, irritation and rejection of the patient.

  • Emotional overinvolvement (EOI) is shown through high levels of happiness, sadness, excessive self-sacrifice and extreme overprotectiveness towards the SCZ individual.

    • This was more evident in parents, who expressed guilt for their child’s illness which led them to excessively attempting to reparative efforts.

  • Low EE has 2 main traits:

    • Warmth, measured by vocal qualities, smiling and empathy expressed when discussing the individual with SCZ.

    • Positive regard, which measures the number of reinforcing statements which express support and appreciation of the individual with SCZ.

Evaluation

Evidence

• Double bind theory:

  • Berger (1965) interviewed those with SCZ, and found they had higher recall of double bind statements by their mothers than non-SCZ controls.

    • This focuses on only mothers.

  • Mischler and Waxler (1968) found that mothers communicating with their SCZ daughters were aloof and unresponsive, while they responded in a normal way to their non-SCZ daughters.

    • This didn’t specifically investigate SCZ statements, but can still be seen as supporting the double bind theory.

• Expressed emotion:

  • Kavanagh (1992) found that those with SCZ in a high EE family were 4x more likely to relapse then low EE families.

  • Vaughn and Leff (1976) found that 53% of those with SCZ with a high EE relative relapsed within 9 months, compared to 12% of those with low EE relatives.

Cause and effect

• Liem (1974) studied communications during a structured task between 11 parents of male SCZ sufferers, and compared to a non-SCZ control.

  • He found no difference in parental communications.

  • Using this, he suggested that previous studies may have detected parents adapting their communication styles when dealing with SCZ children.

  • This makes it a cause, not an effect, of SCZ.

• For EE, it could be suggested that high EE in families is triggered by the stress of having an SCZ child.

Double bind

• This could be seen as offering an alternative explanation to familial SCZ risks, as parents often learn parenting skills from their own parents, and parent all their children the same.

  • However, not all children from one family inherit SCZ, which could be explained by parents singling out one child for some reason; being youngest or oldest, being accidental or being perceived as more difficult.

• Ringuette and Kennedy (1966) suggest double bind statements are highly subjective.

  • They tested this by having experts and non-experts in the theory make judgements about letters written to those with SCZ, and identify double bind statements.

    • They found experts and non-experts were equally as likely to identify these statements.

  • However, the double bind theory addresses the contrast between verbal and paralanguage cues, not written communication, making the study lack validity.

  • Schuman (1967) argued that the difficulty of defining these statements has caused the lack of research support for the theory.

EE

• Most evidence for this theory focuses on relapse rates, and not on whether it can originally trigger SCZ.

• Cuttings et al. (2006) found that SCZ patients were unable to understand criticisms and this would lead to more stress and negatively affect their wellbeing.

  • However, they were not as perceptive of emotional overinvolvement, suggesting it has a lesser impact.

  • However, this could suggest it is more harmful as SCZ sufferers are able to recognise and label it as harmful, as not recognising the harms doesn't mean you aren’t harmed.

• Additionally, it could be seen as ignoring other factors that can cause relapse.

  • McCreadie and Phillips (1998) failed to find higher relapse rates at 6 and 12 months post-release for those living in EE households.

  • This suggests there may be other factors that can cause relapse.

Sexism

• Many studies into these effects, especially those into the double-bind theory, focus on the mother as the main cause of the issues.

• This can be seen as due to Bowlby’s effects, but also show these studies have a bias as they do not investigate the effects fathers or other family members have.

• This can also be seen as a cultural bias, as the mother as a primary caregiver is a Western viewpoint.

Blame

• This theory could place blame on the parents, which could cause increases in high EE and worsen the emotional state of a parent.

• This can be seen as unjustified, especially as double bind theory was acknowledged as solely a risk factor, and there are many other explanations.

Treatment applications

• Family interventions could be used.

• Clinical psychologists, such as Pharoah et al. (2000) have suggested using these in order to reduce relapse rates. These sessions would include:

  • Forming an alliance with the carer.

  • Lowering the emotional climate by reducing the stress and burden on relatives.

    • This could lower EE.

  • Helping the carer to anticipate and solve problems.

  • Reducing the carer’s expressions of guilt and anger.

  • Maintaining expectations for the actions of the SCZ individual.

  • Forming boundaries between the carer and the SCZ individual.

  • Promoting changes in the carer’s beliefs and behaviours, when positive.

• To show the effectiveness of this, Pharoah et al. (2010) reviewed 53 randomised control trials, and concluded that family intervention decreased relapse frequency and hospital admissions.

• Additionally, families identified as having high SCZ rates could undergo parenting classes to avoid engaging in these behaviours, therefore lowering the risk of their child having SCZ.

Methodological issues

• Most studies use self reports, which are subject to issues such as the social desirability bias but also memory issues.

  • SCZ individuals would be more vulnerable to leading questions due to their warped sense of reality, making this an increased issue.

• Another method is controlled observations of familial interactions, either in their own home or a lab.

  • This lowers ecological validity, and is also subject to social desirability biases.

Methods of modifying behaviour

Antipsychotics

Explanation

Conventional, or first generation antipsychotics

• They were first developed in the 1950s.

• They work by:

  • Acting as an antagonist to the D2 receptors sites, but has also been found to block D1, D3, D4 and D5 receptor sites.

    • Additionally, it has been found to affect serotonin receptors (5-HT1 and 5-HT-2)

  • Dopamine is released from presynaptic vesicles, and the antipsychotic occupies receptor sites in the postsynaptic neuron.

  • While dopamine activity is reduced, the presynaptic neuron temporarily increases the release of dopamine into the synapse.

  • However, production of dopamine then drops as stores are depleted, decreasing the amount in the synaptic cleft.

• Reduction of this activity in the mesolimbic pathway should reduce positive symptoms.

• The first antipsychotic was Chlorpromazine, which was extremely low potency.

  • A later antipsychotic haloperidol, which is around 50x more powerful than Chlorpromazine.

Atypical, or second generation antipsychotics

• They also act as a dopamine antagonist, but the mechanisms are not as clear.

• There are many visible effects:

  • They are received at less D2 receptors and more D1 and D4 sites.

  • Many antagonise the serotonin receptor 5-HT2A as much as they antagonise the D2 dopamine receptor gene.

    • This can cause increases in dopamine in the mesocortical (affective problems) and nigrostriatal (motor control) systems, therefore balancing the dopamine antagonism.

    • This causes less severe side effects.

  • Seeman et al. (2002) reported the fast-off theory - atypical antipsychotics bind more loosely than typical, meaning it does not last long enough to cause movement related side effects.

  • They also have a lower half-life, only last on the receptors for less than 24 hours, while atypical last past 24 hours.

• Examples include clozapine and aripiprazole.

  • Aripiprazole works as a partial agonist.

  • In areas where dopamine is too high, it attaches to receptors and gives a partial reduced response, but where it is too low it boosts dopamine activity.

    • This means it is less likely to cause side effects linked to lowered dopamine, such as weight gain.

Evaluation

Effectiveness

• Typical antipsychotics:

  • Cole et al. (1974) found that 75% of those given a conventional antipsychotic were considered to be much improved, with only 25% of those given a placebo considered to have improved to this level.

    • Additionally, none of the antipsychotic patients had gotten worse, while 48% of those given a placebo had be.

• Atypical antipsychotics:

  • Ravanic et al. (2009) compared the effectiveness of clozapine (atypical), chlorpromazine and haloperidol (atypical) antipsychotics.

    • They found that, over five years, clozapine had fewer adverse effects (0.9) compared to chlorpromazine (3.2) and better psychometric score results.

  • Lobos (2010) compared clozapine with a number of other atypical antipsychotics, finding it reduced positive symptoms the most but many dropped out due to the risk of serious side effects.

    • It also did not work very well in patients resistant to treatment, so it is often paired with another antipsychotic - however there is limited evidence as to whether this reduces symptoms further.

• However, as there is not one successful drug for each individual with SCZ, it may be considered pointless to compare them.

  • While atypical are more commonly given, there are still those who respond better to typical, meaning they still need to be created.

  • The process of finding the right antipsychotic can be seen as largely trial and error.

• However, there are high rates of non-compliance in those with SCZ.

  • This can be due to the severe side effects, they feel normal and so stop taking it, may be unable to plan their own behaviour and may forget to take their tablets, may have paranoid and persecutory delusions and not trust the medication.

  • This is a major issue as clinical trials likely would have the drugs taken in a controlled area, whereas in the real world they may not be adhered to as strictly.

  • Rettenbacher et al. (2004) found full compliance in only 54.2% of those with SCZ, partial compliance in 8.3% and non-compliance in 37.5%.

  • Valenstein et al. (2004) performed a study on those with SCZ taking antipsychotics.

    • Found that 40% had poor adherence to antipsychotics, however clozapine only had 4.6% showing poor adherence.

    • This could suggest this is a more effective antipsychotic, as it may reduce memory issues.

    • Also found that adherence to medication varied across groups, young people and African Americans were less likely to adhere than old people and White Americans.

Ethical

• Side effects:

  • Clozapine requires a special monitoring service as it can cause agranulocytosis (a life threatening drop in white blood cells).

    • Regular blood tests, weekly and then fortnightly, are necessary to monitor any blood problems.

    • This could cause large amounts of stress to an individual with SCZ.

  • Tardive dyskinesia is a condition where your face, body or both make sudden, irregular movements which you cannot control.

    • It is caused by both atypical and typical antipsychotics, but less by atypical.

  • Parkinsonism is a condition that causes tremors and instability.

  • Seizures.

  • Psychiatrists should therefore do a cost benefit analysis of whether the side effects outweigh the positive symptoms.

• Additionally, finding the ideal medication can mean many different antipsychotics are taken, and doses, which can be extremely stressful.

• Antipsychotics are also seen as controlling, sometimes referred to as chemical straitjackets.

  • Psychiatrists such as Szasz argued that physical treatments for mental disorders are akin to demonology, and the concept of mental illness simply excludes non-conformists from society.

  • If antipsychotics are given to keep an individual normal and quiet, this could be seen as ethically wrong.

  • However, those with SCZ suffer greatly during episodes, meaning they also benefit from these drugs.

• This treatment is also lifelong, meaning it could be seen as an addiction. (https://www.washingtonpost.com/national/health-science/a-psychiatrist-thinks-some-patients-are-better-off-without-antipsychotic-drugs/2013/12/06/547f5680-48aa-11e3-a196-3544a03c2351_story.html)

  • Whitaker (2011) looked at studies for long term outcomes for those on antipsychotics indefinitely, finding those who don’t stop taking them become less likely to return to work, develop meaningful relationships and even experience brain shrinkage.

  • Steingard argues that pharmaceutical companies hide side effects, and only care about selling their drug, not improving it.

    • She decided to tell patients the full story of risks, ignoring concerns that surround people with SCZ not being able to make proper decisions - which can be seen as highly ableist.

    • However, only 6% abruptly stopped the drug, 62% opted for a dose reduction and 34% decided to remain with their current doses.

    • She also argued to prioritise patients quality of life and not just symptom reduction - some find meaning in their hallucinations, some learn to communicate with them and calm themselves down.

      • Some may prefer these techniques, learned through treatments such as CBT, to symptoms of antipsychotics such as becoming overweight and fatigued.

  • Wunderink et al. (2013) split individuals with SCZ into two groups, those who remained on drugs and those who stopped when symptoms stopped and restarted when they arose.

    • They found those who didn’t continuously take the drugs were more likely to get a job and resume regular life activities.

    • Additionally, those on drugs relapsed just as much as the other group over the 7 years.

• Additionally, the mechanisms by antipsychotics work are completely unknown, meaning it could be having unknown effects to an individual.

Social

• Antipsychotics were a big deal as they allowed those with SCZ to not be condemned to life in an asylum, and instead be able to live normal lives in the community.

  • Asylums were often cruel, and sedated any rebellious patients.

  • Additionally, they cost a lot of money to maintain, and those with SCZ were unable to benefit society or the economy.

  • However, a meta analysis by Ajnakina et al. (2019) found that in Europe 58.1% of patients were hospitalised during follow up appointments, only the only decrease has been in length of stay.

    • Additionally, black people and those who had gone longer without treatment were more likely to have longer stays, suggesting high levels of bias.

• However, it could be argued those with SCZ are more dangerous to themselves and others.

  • Valdo Calocane was a schizophrenic who killed 3 people, who had been unmedicated and out of touch with psychiatric services for 12 months before the killings.

    • This could suggest it is inaccuracies in mental health treatment that causes violence, not just SCZ.

  • Tiihonen et al. (2006) found a 37 fold increase in suicide risk for patients who stopped taking their medication.

  • Witt et al. (2014) found that suicide attempts and threats were linked to violence, perhaps suggesting it is only a small group of those with SCZ who engage in these behaviours.

  • Webb et al. (2011) found suicide was more common in males with SCZ, and that past violent behaviour was a risk factor for suicide in males.

    • This could suggest that only men show this elevated risk of violence, and therefore this risk could be attributed to different treatments or symptoms, and not just SCZ.

• Costs is another concern.

  • It can cost up to £5,000 for a stay in a psychiatric hospital, which could be seen as a huge burden to the NHS.

  • Antipsychotics could be seen as helping people stay out of these hospitals.

  • However, the cost of treating the side effects such as high blood pressure and diabetes could outweigh these benefits.

  • Antipsychotics cost the NHS 33 billion in 2022, perhaps suggesting that a treatment such as CBT may be more cost effective in the long run.

Cognitive Behavioural Theory (CBT)

Explanation

Irrational thinking

• CBT is done to help identify, organise, understand and modify irrational thoughts.

• This allows a person to understand that irrational thoughts come from themselves, and allows them to understand how this can worsen their illness.

• While this focuses on positive symptoms, it can help negative symptoms by allowing the person with SCZ to be more independent and to gain confidence.

Key components of CBT

• CBT occurs for around 5-10 sessions, weekly or fortnightly, and aims to trace back the origins of symptoms to understand their development.

• NICE recommends that every adult with psychosis or SCZ should be offered CBT.

• Smith et al. (2003) identified 5 key treatment components:

  • Engagement strategies - This is when a client and the therapist discuss key concerns, including symptoms and general fears.

    • A rapport is aimed to be established, as those with SCZ may have elevated paranoia if they have past negative experiences with practitioners.

    • They will also discuss an individual’s coping strategies the client is using, empowering the client.

  • Psychoeducation - This teaches a client the characteristics of their illness, allowing the symptoms to be decatastrophized, increase the client’s understanding and assess their client’s past understanding of their symptoms and illness.

  • Cognitive strategies - These are methods to help them to deal with cognitive symptoms, and there are many examples:

    • Verbal challenging, such as Ellis’ ABCDE model - Activating event leads to an irrational Belief which causes harmful Consequences.

      • This is then Disputed by the therapist, and the Effect is that this becomes rational.

    • Homework activities, such as a thought diary where they record how they felt, what they did and how they thought.

      • They are challenged to think differently about the event by recording potential alternative views.

      • These diary entries are then discussed.

    • Behavioural experiments - Clients are asked to identify situations or actions they could employ to lessen symptoms, such as listening to music.

      • They are then asked to rate the severity of the voices, allowing them to see a direct improvement.

    • Socratic questioning - Series of curiosity driven questions asked during therapy sessions.

      • This aims to identify evidence the individual with SCZ has.

      • This therefore undermines the strength of irrational behaviours.

  • Behavioural skills training - This allows them to cope with SCZ symptoms, comorbid anxiety and depression, and side effects of the antipsychotic medications.

    • This can include relaxing, activity scheduling, distraction and problem solving.

    • Problem solving involves 5 steps:

      • Identifying and defining a problem.

      • Generating probable solutions.

      • Evaluating alternatives.

      • Deciding on a solution.

      • Evaluating the outcome.

  • Relapse prevention strategies - This allows them to identify earlier indicators of relapse, such as thoughts, feelings and behaviours.

    • They are also asked about alterations to their relationships, and what people they are close to noticed.

    • They then develop plans on what to do when these factors are noticed, such as how to communicate with those close, what support they can access and what actions they can take.

Evaluation

Effectiveness

• There is lots of research into the effectiveness of CBT:

  • Kuipers et al. (1997) randomly allocated SCZ individuals with a medically resistant positive symptom into two groups; treatment as usual (TAU) and TAU + CBT.

    • After nine months, the TAU group had a 31% improvement rate, 3 people who had worsened, and 1 suicide.

    • In the TAU + CBT group, there was a 50% improvement rate and only 1 person had worsened.

    • This makes it significantly better than TAU.

  • Jauhar et al. (2014) reported only a small therapeutic effect from using CBT on clients with SCZ.

    • This is still a positive effect.

  • Morrison et al. (2014) reported that psychiatric symptoms were greatly reduced in those with SCZ after CBT.

• Antipsychotics are often necessary alongside CBT, as patients need to recognise you have SCZ in order to understand they are symptoms.

  • Due to this, those who receive CBT already have less severe symptoms due to the drug treatments.

• The effectiveness has been criticized as short term.

  • Tarrier et al. (2004) studied individuals who received CBT shortly after their diagnosis, or TAU.

  • 18 months later, they were found to have the relapse rates, suggesting the effects are short lived.

  • However, those who received CBT seemed to be less negatively affected by their symptoms than the TAU group.

• CBT is based on willingness to participate and engage, meaning those who participate need to engage to get the most out of the programme.

  • This is not the same for antipsychotics, as they work just by being taken.

  • This could show that CBT is more difficult for an individual with SCZ, and potentially harm any study as only those active and willing properly complete the programme.

Ethics

• CBT could be argued to psychologically harm participants.

  • This is because the therapy involves listening and understanding delusions and hallucinations, which can be scary.

  • Kuipers et al. (1997) reports clients were generally satisfied with their experience of CBT, and they thought it was an appropriate way to deal with problems.

• Due to the fear of psychological harm, psychiatrists are selective with the patients they refer onwards.

  • This is usually based on a client not believing or accepting their diagnosis, but can also be based on a belief they would not engage, or even a belief that antipsychotic medication is doing well enough.

  • Kingdon and Kirschen (2006) report that only 49% of individuals with SCZ were reported onwards for CBT.

  • This could suggest clinicians are responsible for limiting CBT access, which is a major ethical issue as they can be highly susceptible to bias.

• CBT does not have side effects, however, it can cause psychological harm.

  • Additionally, as antipsychotics are required to try the therapy, it could be argued that the side effects have to occur for the therapy to take place.

• CBT is also completely consensual and can be stopped at any time, making it highly ethical.

  • Additionally, those with SCZ do not become reliant on the therapy - they are able to stop at any time.

• CBT does not address root causes.

  • Bentall et al. (1994) argues that CBT puts too much emphasis on controlling, rather than understanding, their own thought processes.

  • The root of hallucinations and delusions may come from a traumatic experience, meaning that if this is not addressed the symptom will not alleviate.

Social

• Without therapeutic treatments such as CBT, those with SCZ are forced to be reliant on antipsychotics and may never develop proper coping mechanisms, which can cause relapse.

• Access to CBT is often determined by area in the UK, in the National Audit of Schizophrenia, the Royal College of Psychiatrists found significant variations in amount of CBT offered across the NHS trusts.

  • This ranged from 14% to 67%, with an average of 50% being referred.

  • This could be argued to be a cultural issue - different areas across the UK may have different outlooks towards therapy, or those with SCZ, skewing their treatments.

  • This also contrasts NICE guidelines.

• There are also financial issues:

  • CBT can cost the NHS around £100 a session, which can seem cost inefficient compared to the cost of antipsychotics.

  • However, Kuipers et al. (1998) analysed costs of antipsychotics and CBT, and concluded that money spent on CBT was offset by the reduced usage of service costs in the future.

    • This includes services such as inpatient wards.

  • However, NHS budgets deal with immediate care requirements, and often it is different teams that deal with inpatient budgets to CBT budgets.

• As CBT teaches individual coping mechanisms, it could be argued it further integrates those with SCZ back into society, allowing them to benefit the economy.