Schizophrenia

define schizophrenia

a serious mental disorder characterised by severe disruptions in psychological functioning, which affects thoughts, perception, language, emotion + causes a loss of contact with reality.

what's the prevalence of schizophrenia

1%

what's the age of onset for schizophrenia

usually 15-45

what are positive symptoms

those where there is an addition or an excess to normal cognitive functioning (e.g. delusions or hallucinations)

what are negative symptoms

where there is a loss of normal functioning (e.g. affective flattening)

what are the positive symptoms of schizophrenia

delusions, hallucinations + disordered thinking

what are the negative symptoms of schizophrenia

avolition, speech poverty, affective flattening + catatonia

define delusions

fixed, untrue or irrational beliefs strongly held despite contradictory evidence. can be bizarre, paranoid (e.g being persecuted by government), grandiose (e.g. having superpowers) or delusions of control (believing their body is being controlled)

define hallucinations

unreal perceptions of the environment, usually auditory (hearing voices), can be visual (seeing people who don't exist), olfactory (smell), tactile (touch) or gustatory (taste)

define disordered thinking

inability to think logically. thoughts often show derailment, which may manifest as a conversation shifting rapidly from one topic to an unrelated topic, making it hard for listeners to understand

define avolition

inability to take part in goal directed behaviour. motivation is reduced + individual appears to be uninterested. signs include poor hygiene + grooming + lack of persistence in work or education

define speech poverty

reduction in amount + quality of speech sometimes with delayed verbal responses. speech becomes incoherent + may insert unrelated words in a sentence.

define affective flattening

lack of emotional expression. facial expressions, tone of voice + body language is reduced.

define catatonia

extreme loss of motor function. may hold rigid poses for hours, not reacting to any environmental stimuli.

outline how schizophrenia is classified

• characterised by positive + negative symptoms

• positive= symptoms where there’s an addition to functioning (e.g. hallucinations- unreal perceptions of environment such as hearing voices)

• negative= symptoms where there’s a loss of functioning (e.g. speech poverty where speech becomes less clear)

• according to ICD10, one first rank symptom must be present for majority of one month period for diagnosis to be made (e.g. thought echoes or auditory hallucinations)

• at least two second rank symptoms (e.g. catatonic behaviour) are required for diagnosis

describe the ICD10 diagnostic criteria for schizophrenia

• at least one 1st rank symptom needed for diagnosis:

  • thought echo

  • delusions of control

  • hallucinatory voices

  • persistent delusions

• at least 2 2nd rank symptoms needed for diagnosis:

  • persistent hallucinations

  • breaks in train of thought resulting in incoherent speech

  • catatonic behaviour

what are the ICD10 first rank symptoms of schizophrenia

• thought echo

• delusions of control

• hallucinatory voices

• persistent delusions

how many ICD10 first rank symptoms are needed for schizophrenia to be diagnosed

at least one

how many ICD10 second rank symptoms are needed for schizophrenia to be diagnosed

at least two

define classification

act of distributing things into different classes or categories of the same type

define diagnosis

the recognition + identification of a disease or a condition by its signs + symptoms

what are the two systems widely used in psychology to classify and diagnose mental illnesses

• ICD

• DSM

outline the diagnostic criteria for schizophrenia

3 diagnostic criteria must be met:

1. 2 or more characteristic symptoms each present for a large period of time during a 1 month period: delusions, hallucinations, disorganised speech which is a manifestation of formal thought disorder, grossly disorganised or catatonic behaviour, negative symptoms (blunted affect- lack or decline in emotional response, alogia- lack or decline in speech) or (lack or decline in motivation)

   if delusions are bizarre, or hallucinations consist of hearing one voice giving a running commentary on patients actions or hearing 2+ voices conversing with each other, only that one symptom is required above.

2. social or occupational dysfunction

3. significant duration: continuous signs of disturbance persist for at least six months. the six month period must include at least one month of symptoms.

what's the difference between the DSM and ICD in their classification of schizophrenia

DSM only includes hallucinations + bizarre delusions as 1st rank symptoms, whereas ICD has thought echo as well as these

what problems may arise as a result of the differences between the DSM + ICD

• someone may be diagnosed as schizophrenic using ICD but not with DSM

• so people may not get correct diagnosis + therefore correct trearment

outline Rosenhan's being sane in insane place experiment

• 8 healthy individuals faked auditory hallucinations to gain admission to 12 hospitals in 5 different states

• once admitted they stopped all symptoms, acted normally, said they felt well + asked to be released

• all were diagnosed as insane + admitted to hospital

• 7/8 diagnosed as schizophrenic

• 1/8 diagnosed as bi-polar

• took 7-52 days to be released

• no Drs or nurses ever identified participants as normal

• participants diagnosed as in remission on releases

what can be concluded from Rosenhan's being sane in insane places experiment

• psychiatrists aren't reliably diagnosing schizophrenia as different clinicians may arrive at different diagnoses for same patient or symptoms

• psychiatrists aren't validly diagnosing schizophrenia as they may not distinguish between real + pseudoparients

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): reliability

AO1:

• level of agreement on diagnosis by different psychiatrists across time + cultures

• measured using inter-rater relaibility: extent to which different mental health professionals agree on same diagnosis for a patient

• problem for reliability is that there are 2 different classification systems (DSM + ICD10) + DSM doesn’t include thought echoes as a first rank symptom

AO3:

• Cheniaux had 2 psychiatrists independently diagnose 100 patients using both DSM + ICD

• poor inter-rater reliability: one made 26 diagnoses using DSM whilst other made 13 + using ICD one diagnosed 44 compared to there only making 13

• shows low rate of inter-rater reliability in diagnosis

AO3:

• consequently, diagnosis may be unreliable

• could lead to person being diagnosed as schizophrenic when they’re not (false positive). This results in negative label due to stigma surrounding schizophrenia. This may lead to perosn losing personal relationships + they may start believing negative things about themselves, which could cause a self fulfilling prophecy where they become paranoid + withdrawn

• could lead to person with schizophrenia not being diagnosed (false negative), meaning they don’t get treatment they need + are likely to get worse over time

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): validity

AO1:

• extent to which schizophrenia is a unique syndrome with characteristic signs + symptoms

• extent to which psychiatrists are correctly identifying schizophrenia

AO3:

• Cheniaux had 2 psychiatrists independently diagnose 100 patients using both DSM + ICD

• poor inter-rater reliability: one made 26 diagnoses using DSM whilst other made 13 + using ICD one diagnosed 44 compared to there only making 13

• shows low validity in diagnosis

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): co-morbidity

AO1:

• 2 or more conditions occur together in same patient at same time, whcih causes problems with diagnosis as there may be confusion as to which disorder is being diagnosed

• problem for validity of diagnosis as it could be questioned as to whether schizophrenia is actually a separate + distinct disorder

AO3:

Buckley found:

• around half of schizophrenics also had depression

• PTSD occured in 29% of cases

• OCD occured in 23% of cases

• these results show a problem with validity- perhaps professionals aren’t very good at telling the difference between schizophrenia + other disorders (perhaps schizophrenia looks like severe depression or vice versa?)

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): symptom overlap

AO1:

• symptoms of schizophrenia appear in other disorders

• considerable overlap schizophrenia symptoms + bipolar disorder symptoms (both invlove positive symptoms like delusions + negative sysmtoms like avolition)

• calls into question validity of classification + diagnosis (are psychiatrists measuring schizophrenia symptoms or symptoms from a different disorder)

AO3:

• Ellason + Ross point out that people with dissociative identity disorder have more schizophrenic symptoms than people diagnosed as schizophrenic

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): cultural bias

AO1:

• schizophrenia is diagnosed much more frequently in African Americans + in African- Caribbean populations living in Britain

• rates of schizphrenia are no higher in Africa than other places, so there’s no biological or genetic vulnerability for these groups of people

AO3:

• Harrison suggests Western clinicians misinterpret cultural differences in behaviour + expression as symptoms of schizophrenia

• e.g. hallucinations like hearing voices may be more acceptable in African cultures because of cultural beliefs in communication with ancestors, so people are more likely to discuss these experiences. When reported to psychiatriasts from a different culture, these experiences are likely to seem bizarre + irrational

• specialists are misinterpreting cultural differences, which impacts validity

outline + evaluation of schizophrenia diagnosis + classification (AO1+ AO3): gender bias

AO1:

• there’s some disagreement between psychologists over the gender prevalence rate of schizophrenia

• accepted belief was that males + females were equally vulnerable to schizophrenia

• some argue that clinicians (majority of whom are men) have misapplied diagnostic criteria to women

• more recent studies show there may be up to 50% more female sufferers

AO3:

• one possible explanation is that female patients tend to function better than men, being more likely to work + have good family relationships (says Cotton)

• high functioning may explain why some women haven’t been diagnosed with schizophrenia where men with similar symptoms might have been

• women’s better interpersonal functioning may bias practitioners either because symptoms are masked altogether by good interpersonal functioning or because the high level of functioning makes the case too mild to warrant a diagnosis

• not diagnosing women who show the same symptoms as men means diagnosis is not consistent (reliable)

• also means they’re not diagnosing schizophrenia in a valid way as it confuses what schizophrenia is: is it a different thing for men?

positive evaluation of schizophrenia diagnosis + classification (AO3)

• despite problems for reliability + validity, manuals + diagnostic practice has been improved

• categories + definitions are more detailed + operationalised + psychiatrists now use standardised interviews when assessing patients

• ICD + DSM have been brought more in line with each other, so they’re now very similar

• Osario reported inter rater reliability of 97% + test retest reliability of 92% when DSM was used to assess 180 patients

• these improvements have led to people receiving reliable + valid diagnosis + timely + effective treatments

• many people with schizophrenia can recover a normal level of functioning + lead a full + happy life

what are the biological explanations of schizophrenia

• genetic explanation

• dopamine hypothesis

• neural correlates explanation

outline the genetic explanation of schizophrenia (AO1)

• schizophrenia is passed down to children from their parents via DNA or as a result of a genetic mutation

• Gottesman’s family study found the more genetically similar you are to a schizophrenic the greater the chance of you developing the disorder:

  • if both parents have it you have a 46% chance of developing it

  • if one parent has it you have a 16% chance of developing it

  • if one sibling has it you have an 8% chance of developing it

• later research suggests schizophrenia is aetiologically heterogeneous (can be caused by a number of different gene combinations)

• Ripke carried out a large scale review over 37,000 schizophrenia patients + found 108 seperate genetic variations associated with an increased risk of schizophrenia

• it’s not believed that there’s a single schizophrenic gene, but rather several genes are involved, which increase an individuals overall vulnerability to developing it (e.g. COMT gene)

• research from NIMH linked COMT gene on chromosome 22 to a near doubled risk of schizophrenia

• when COMT gene is abnormally expressed it depletes frontal lobe of dopamine + has been linked to problems regarding perception of reality (psychosis)

according to Gottesman’s family study, if both parents have schizophrenia what is the individuals chance of developing it

46% chance

according to Gottesman’s family study, if one parent has schizophrenia what is the individuals chance of developing it

16% chance

according to Gottesman’s family study, if one sibling has schizophrenia what is the individuals chance of developing it

8%

what does aetiologically heterogenous mean

can be caused by a number of different gene combinations

positive evaluation of the genetic explanation of schizophrenia (AO3)

• twin studies support genetic bases of schizophrenia. Gottesman reviewed over 40 twin studies + found concordance rates for monozygotic twins to be 48% vs 17% for dizygotic twins. Hilker found concordance rates for monozygotic twins to be 33% vs 7% for dizygotic twins. This is strong evidence of genetic factors as concordance rates for monozygotic twins are much higher than for dizygotic twins

• evidence from adoption studies supports genetic explanation. Tienari compared 155 children who were given up for adoption by a schizophrenic mother to a control group of 155 adopted children who didn’t have a biological parent with schizophrenia. Children in schizophrenic group were 10 times more likely to develop schizophrenia than control group, showing it’s transmitted genetically. This suggests genetics have a greater influence on development of schizophrenia than the environment

negative evaluation of the genetic explanation of schizophrenia (AO3)

• problem with using twin studies as support: twins share a very similar environment (more for identical twins as people respond to them in the same way). Higher concordance rates in monozygotic twins may be due to the similar environment/ experiences rather than due to shared DNA

• concordance rates for monozygotic twins aren’t 100%, so psychological influences also need to be considered. Morkved found 67% of schizophrenic patients reported at least 1 childhood trauma compared to 38% in a matched group with non-psychotic health problems. This suggests genetic factors alone can’t provide a complete explanation of schizophrenia

• issue with Tienari’s adoption studies: majority of children that developed schizophrenia came from an adopted home labelled as abnormal. This suggests schizophrenia may be a result of a genetic predisposition but that it won’t develop unless triggered by the environment

• interactionist approach to explaining schizophrenia may be more appropriate. This is one which suggests that schizophrenia is the result of a combination of biological predisposition (e.g. genes or brain abnormality) + an environmental trigger (e.g. family dysfunction or faulty cognitions)

outline the dopamine hypothesis as an explanation of schizophrenia (AO1)

• neurotransmitter dopamine appears to work differently in the brains of schizophrenics

• dopamine is important in the functioning of several different brain systems + so may cause the wide variety of schizophrenia symptoms

• hypothesis 1: schizophrenia is the result of hyperdopaminergia in the mesolimbic pathway + is responsible for positive symptoms (e.g. hallucinations). Hyperdopaminergia in regions in the subcortex (e.g. excess dopamine in Broca’s area which is responsible for speech production) may lead to speech poverty + auditory hallucinations

• hypothesis 2: brains of schizophrenics may be oversensitive to dopamine due to an abnormally high number of D2 receptors. This means more dopamine can bind to receptors, resulting in increased dopamine transmission. Dopamine neurons also play a key role in the transmission of messages relating to attention: too many attention messages will result in an inability to focus, which could result in disordered thinking or delusions (due to paying attention to irrelevant stimuli which seems to have importance)

• hypothesis 3: hypodopaminergia in mesocortical pathway causes negative symptoms (e.g. affective flattening). This area controls thinking + decision making + so could lead to avolition

what are the 3 parts of the dopamine hypothesis as an explanation of schizophrenia

Too much dopamine:

• schizophrenia is the result of hyperdopaminergia in the mesolimbic pathway + is responsible for positive symptoms (e.g. hallucinations)

• hyperdopaminergia in regions in the subcortex (e.g. excess dopamine in Broca’s area which is responsible for speech production) may lead to speech poverty + auditory hallucinations

Too much dopamine stimulation:

• brains of schizophrenics may be oversensitive to dopamine due to an abnormally high number of D2 receptors

• this means more dopamine can bind to receptors, resulting in increased dopamine transition

• dopamine neurons also play a key role in the transmission of messages relating to attention: too many attention messages will result in an inability to focus, which could result in disordered thinking or delusions (due to paying attention to irrelevant stimuli which seems to have importance)

Not enough dopamine:

• hypodopaminergia in mesocortical pathway causes negative symptoms (e.g. affective flattening)

• this area controls thinking + decision making + so could lead to avolition

explain how too much dopamine may cause schizophrenia

• hyperdopaminergia in the mesolimbic pathway results in positive symptoms (e.g. hallucinations)

• hyperdopaminergia in regions in the subcortex (e.g. excess dopamine in Broca’s area which is responsible for speech production) may lead to speech poverty + auditory hallucinations

explain how too much dopamine stimulation may cause schizophrenia

• brains of schizophrenics may be oversensitive to dopamine due to an abnormally high number of D2 receptors

• this means more dopamine can bind to receptors, resulting in increased dopamine transition

• dopamine neurons also play a key role in the transmission of messages relating to attention: too many attention messages will result in an inability to focus, which could result in disordered thinking or delusions (due to paying attention to irrelevant stimuli which seems to have importance)

explain how not enough dopamine may cause schizophrenia

• hypodopaminergia in mesocortical pathway causes negative symptoms (e.g. affective flattening)

• this area controls thinking + decision making + so could lead to avolition

what does hyperdopaminergia mean

too much dopamine

what does hypodopaminergia mean

not enough dopamine

positive evaluation of the dopamine hypothesis as an explanation of schizophrenia (AO3)

• Iverson conducted postmortems + consistently found unusually high levels of dopamine in the brains of schizophrenics, which suggests schizophrenia may be caused by increased dopamine

• Kessler compared brain activity in schizophrenics + non-schizophrenics using PET + MRI scans + found schizophrenics had significantly elevated dopamine receptor levels. This supports the view that they may be more sensitive to dopamine. Empirical, scientific methods + consistent findings suggest schizophrenia symptoms are caused by elevated dopamine levels + that the dopamine hypothesis is a reliable explanation

• implications from success of antipsychotic medication support the hypothesis. Medication found to be 60-75% effective in reducing positive symptoms. Believed to work because they block dopamine activity in the brain, reducing dopamine transmission. As a reduction in dopamine reduces schizophrenia symptoms, it could be assumed high levels of dopamine may be responsible for causing the symptoms

negative evaluation of the dopamine hypothesis as an explanation of schizophrenia (AO3)

• although it’s clear that increased dopamine transmission is linked to schizophrenia symptoms, the dopamine hypothesis doesn’t explain what causes the increased levels of dopamine. Therefore, it doesn’t give a full explanation for the illness

• most of the supporting evidence is retrospective correlational in nature, so it’s hard to establish cause + effect. We don’t know whether the changed dopamine activity occurs before or after the onset of schizophrenia. It could be that increased dopamine leads to development of schizophrenia, however it’s possible that the illness causes increased dopamine levels

outline neural correlates as an explanation of schizophrenia (AO1)

• idea that a particular brain area (structure or function) is correlated with schizophrenia

• fMRIs used to compare the functioning of schizophrenics brains with those of non-sufferers to identify brain areas linked to schizophrenia

• given tasks associated with types of functioning known to be abnormal in schizophrenics (e.g. social cognition, thought processing + memory)

Negative symptoms:

• avolition involves loss of motivation

• motivation involves complex thinking + decision making processes + these are carried out in the pre-frontal cortex

• hyperdopaminergia in the pre-frontal cortex means fewer messages are sent to this area, leading to an inability to take part in goal directed behaviour (avolition)

Positive symptoms:

• auditory cortex (in temporal lobe) is responsible for sensation of sound

• Wernicke’s area (in temporal lobe) is responsible for processing of speech

• abnormal activity levels in these areas are thought to cause people to hear voices that aren’t really there (auditory hallucinations)

• Hugdahl found reduced grey matter density in schizophrenics in an area of the cerebral cortex (which includes Broca’s + Wernicke’s area)

positive evaluation of neural correlates as an explanation of schizophrenia (AO3)

• Wilbe supports neural correlates for negative symptoms. They looked at grey + white matter in the pre-frontal cortex in a group of male schizophrenics + matched normal controls using MRI. Found no differences in grey matter between the 2 groups. Found significant reductions in white matter in the right pre-frontal cortex in the schizophrenic group, which correlated with negative symptoms. Supports idea that white matter in right pre-frontal cortex is a neural correlate for negative symptoms

• Allen supports neural correlates for positive symptoms. They scanned brains of patients experiencing auditory hallucinations + compared them to a control group whilst they completed a task to identify whether pre-recorded speech was theirs or others. Lower activation in auditory cortex + Wernicke’s area was found in hallucination group, who also made more errors than control group. Supports idea that auditory cortex + Wernicke’s area are neural correlates for auditory hallucinations

negative evaluation of neural correlates as an explanation of schizophrenia (AO3)

• research leaves important questions unanswered: does the unusual activity in a region of the brain cause the symptom? There are other possible explanations for the correlations: e.g. negative symptoms like avolition may cause less info to pass through ventral striatum causing the reduced activity. Neural correlates do exist, but tell us little about the causes of schizophrenia

• there’s evidence of environmental factors (e.g. family functioning during childhood) can also play a role in development of schizophrenia, something that the neural correlates explanation overlooks. Schizophrenia may be result of a combination of biological + psychological approaches, implying an interactionist approach may be more suitable for explaining schizophrenia

what are the psychological explanations of schizophrenia

all of these are family dysfunction explanations:

• schizophreniogenic mother

• double bind theory

• expressed emotion

schizophrenogenic mother AO1

• Fromm-Reichman noted that many patients spoke of a particular type of parent, the schizophrenogenic mother

• schizophrenogenic mother is cold, rejecting + controlling, + tends to create a family climate characterised by tension + secrecy

• leads to distrust that later develops into paranoid delusions + ultimately schizophrenia

double-bind theory AO1

• Bateson argued that family climate is important in development of schizophrenia

• he emphasised the communication style within the family

• double bind refers to contradictory messages children receive from their parent, usually on different communication levels (e.g. mother tells child she loves him but at same time turns her head away in disgust- child receives conflicting messages: one of affection on verbal level + one of animosity on non-verbal level)

• developing child regularly finds themselves in trapped situations where they fear doing the wrong thing, they receive mixed messages about what this is + feel unable to comment on the unfairness of the situation or seek clarification

• when they get it wrong, which is often, the child is punished by the withdrawal of love

• leaves child with an understanding of the world as confusing + dangerous + this is reflected in symptoms like disorganised thinking + paranoid delusions

• it also prevents the development of a coherant sense of reality + so could explain development of psychotic symptoms

expressed emotion AO1

• suggests that criticism + hostility lead to schizophrenia + relapse in patients

• expressed emotion is the level of emotion (mainly negative) expressed towards the schizophrenic patient + includes:

  • verbal criticism

  • hostility towards them, including anger + rejection

  • emotional over involvement

• high levels of expressed emotion cause stress in the patient which is a main reason for relapse in patients with schizophrenia

• expressed emtoion may explain the onset of schizophrenia in people with a biological predisposition

positive evaluation of pschological explanations of schizophrenia (AO3)

• evidence to suggest that family relationships in childhood are associated with increased risk of schizophrenia in adulthood: Read reviewed studies of schizophrenia + found a link between physical + sexual abuse in childhood + later development of schizophrenia. 69% of women in-patients with a diagnosis of schizophrenia had a history of physical or sexual abuse or both in childhood. They also found schizophrenia was the most common mental disorder for victims of sexual abuse. This supports the family dysfunction explanation as it shows schizophrenia may be influenced by negative family climate + family dysfunction

• evidence to support double-bind theory: Blotchky observed 15 families who had a child enrolled in a short-term residential treatment programme. They found that mothers communciated a larger proportion of messages in which verbal content was rated as being conflicting with non-verbal expression to the symptom bearing child than to other family members. This supports theory that double-bind communication can lead to development of schizophrenia

• Kavanagh reviewed 26 studies of expressed emotion + found mean relapse rate for schizophrenics who returned to live with high expressed emotion families was 48% compared with 21% for those who went back to live with low expressed emotion families

negative evaluation of pschological explanations of schizophrenia (AO3)

• weakness of evidence is that info about childhood experience was gathered after development of schizophrenia. Schizophrenia often affects memory recall + includes inaccurate perceptions of reality, so it’s difficult to establish what experiences from childhood were real. This creates a serious problem for the validity of the family dysfunction explanation

• problem establishing cause + effect with Blotchky’s research. Could be possible that mother’s contradictory communcation style led to development of schizophrenia. However, as mother only uses double-bind communication with affected child + not their siblings it’s equally possible that the mother’s communication style is the result of the child having abnormal behaviours

• most sufferers of schizophrenia haven’t suffered childhood abuse, they come from stable + supportive families. This shows there must be other factors which influence development (e.g. biology). The genetic explanation argues that schizophrenia is the result of DNA passed down from parents or as a result of a genetic mutation (supported by Gottesman’s family study- outline findings)

• there’s evidence for both biological + psychological factors, so diathesis-stress model may be a better explanation for development of schizophrenia. It proposes that schizophrenia is the result of a combination of biological predisposition (e.g. genes or brain abnormalities) + an environmental trigger (e.g. family dysfunction or faulty cognitions)

outline Blotchky’s research used to support family dysfunction explanations of schizophrenia

• evidence to support double-bind theory

• observed 15 families who had a child enrolled in a short-term residential treatment programme

• found that mothers communciated a larger proportion of messages in which verbal content was rated as being conflicting with non-verbal expression to the symptom bearing child than to other family members

• supports theory that double-bind communication can lead to development of schizophrenia

what is bad about Blotchky’s research used to support family dysfunction explanations of schizophrenia

• problem establishing cause + effect

• could be possible that mother’s contradictory communcation style led to development of schizophrenia

• however, as mother only uses double-bind communication with affected child + not their siblings it’s equally possible that the mother’s communication style is the result of the child having strange/ abnormal behaviours

outline Kavanagh’s research used to support family dysfunction explanations of schizophrenia

reviewed 26 studies of expressed emotion + found mean relapse rate for schizophrenics who returned to live with high expressed emotion families was 48% compared with 21% for those who went back to live with low expressed emotion families

outline the cognitive explnations of schizophrenia (AO1)

Dysfunctional thought processing:

• faulty cognitions (e.g. poor attention + memory + difficulties with language + disrodered thinking) may be responsible for symptoms of schizophrenia

• 2 most important examples of explaining schizophrenia are below…

• metarepresentation: cognitive ability to reflect on our own thoughts. Dysfunction may disrupt our ability to recognise our own actions + thoughts as being carried out by ourselves, possibly leading to hallucinationns + delusions

• central control: cognitive ability to suppress automatic responses while we perform deliberate actions instead. Dysfunction may lead to inability to supress automatic thoughts + speech. May lead to disorderd thinking + speech poverty

Attention deficit theory:

• Frith argues schizophrenia is result of a faulty attention system

• preconscious thought (thoughts that occur without awareness) contains a lot of info that is then usually filtered out

• if the filtering doesn’t occur, there’s sensory overload in conscious thoughts

• thoughts that would usually filtered out as irrelevant or unimportant are instead noticed + treated as more significant than they really are

• this accounts for positive symptoms like hallucinations, delusions + disordered thinking

• Hemsley suggests schizophrenia involves a breakdown in relationship between memory + perception

• people with schizophrenia have a disconnect between their schemata + waht they actually hear + see

• when they encounter new situations, their schemata aren’t activated, so they experience sensory overload because they don’t know which aspects of a situation to attend to + which to ignore

• also means they struggle to predict what will happen next

• leads to disorded thinking + behaviour that may manifest as avolition

define metarepresentation

• cognitive ability to reflect on our own thoughts

• dysfunction may disrupt our ability to recognise our own actions + thoughts as being carried out by ourselves, possibly leading to hallucinationns + delusions

define central control

• cognitive ability to suppress automatic responses while we perform deliberate actions instead

• dysfunction may lead to inability to supress automatic thoughts + speech

• may lead to disorderd thinking + speech poverty

outline dysfunctional thought processing (cognitive explanation) as an explanation of schizophrenia (AO1)

• faulty cognitions (e.g. poor attention + memory + difficulties with language + disordered thinking) may be responsible for symptoms of schizophrenia

• 2 most important examples of explaining schizophrenia are below…

• metarepresentation: cognitive ability to reflect on our own thoughts. Dysfunction may disrupt our ability to recognise our own actions + thoughts as being carried out by ourselves, possibly leading to hallucinationns + delusions

• central control: cognitive ability to suppress automatic responses while we perform deliberate actions instead. Dysfunction may lead to inability to supress automatic thoughts + speech. May lead to disorderd thinking + speech poverty

outline attention deficit theory (cognitive explanation) as an explanation of schizophrenia (AO1)

• Frith argues schizophrenia is result of a faulty attention system

• preconscious thought (thoughts that occur without awareness) contains a lot of info that is then usually filtered out

• if the filtering doesn’t occur, there’s sensory overload in conscious thoughts

• thoughts that would usually filtered out as irrelevant or unimportant are instead noticed + treated as more significant than they really are

• this accounts for positive symptoms like hallucinations, delusions + disordered thinking

• Hemsley suggests schizophrenia involves a breakdown in relationship between memory + perception

• people with schizophrenia have a disconnect between their schemata + what they actually hear + see

• when they encounter new situations, their schemata aren’t activated, so they experience sensory overload because they don’t know which aspects of a situation to attend to + which to ignore

• also means they struggle to predict what will happen next

• leads to disorded thinking + behaviour that may manifest as avolition

positive evalution of the cognitive explanations of schizophrenia (AO3)

• Stirling compared 30 patients with schizophrenia with 18 non-schizophrenics on cognitive tasks (e.g. Stroop test). Patients took over twice as long as control group to suppress the impulse to read the word + read the ink colour instead. Supports Frith’s theory of attention deficit theory as it suggests schizophrenics are less able to filter out irrelevant info. Also shows dysfunction in central control as schizophrenics found it harder to supress automatic response of reading the word

• Frith conducted PET scans (empirical measure of brain processes) to identify brain systems involved in some of the cognitive processes underlying symptoms associated with schizophrenia. Gave tasks to elicit cognitive processing whilst scanning schizophrenics brains. Schizophrenics had defects in willed actions + defects of self-monitoring were associated with abnormal activity in left hippocampus + frontal lobe. Suggests link between cognitive abnormalities described by Hemsley + development of schizophrenia

negative evaluation of the cognitive explanation of schizophrenia (AO3)

• cognitive explanations would predict schizophrenics would have extreme difficulty completing tasks requiring focused attention, however McKenna found schizophrenics were more sensitive than normal controls when judging whether photos of electric shocks being administered were genuine or not. Suggests attention deficit is too simplistic.

• difficult to conclude cause + effect. It’s possible that abnormalities in cognitive areas of brain cause schizophrenia, but it’s equally possible that schizophrenia causes the difficulties with cognitive processing. Cognitive deficits may be a symptom rather than the cause

• alternative biological explanations; many studies show high dopamine transmission in mesocortical pathways create positive symptoms like hallucinations. E.g. Iverson found unusually high levels of dopamine in the brains of schizophrenic when conducting post mortems. Research also suggests childhood trauma may be a contributing factor to development of schizophrenia. So diathesis-stress model is a more plausible explanation

what are the 2 cognitive explanations of schizophrenia

• dysfunctional thought processing

• attention deficit theory

outline drug therapy as a biological treatment of schizophrenia (AO1)

• antipsychotic drugs (tablets, syrup or injections) are most common treatment for schizophrenia

Typical antipsychotics:

• reduce effects of neurotransmitter dopamine

• according to dopamine hypothesis, schizophrenia symptoms are caused by abnormally high number of D2 receptors which increase dopamine transmission (hyperdopaminergia) in the subcortex (e.g. excess in Broca’s area may lead to speech poverty + auditory hallucinations)

• drugs (e.g. chlorpromazine) are dopamine antagonists, meaning they bind to dopamine receptors on post synaptic neuron, but don’t stimulate them, thus blocking dopamine transmission

• this reduces positive symptoms like auditory hallucinations

• bind to dopamine receptors for longer than atypical drugs, so have longer lasting effects

Atypical antipsychotics:

• clozapine binds to serotonin + dopamine receptors

• used to treat positive + negative symptoms

• bind to dopamine receptors on post synaptic neuron without stimulating them, allowing a more normal level of dopamine transmission

• bind temprarily then quickly dissociate, so have lower level side effects

• blocks serotonin receptors without stimulating them, reducing transmissions

• also induces release of glutamate

• these actions are thought to improve depression, anxiety + negative cognitive symptoms associated with schizophrenia

outline typical antipsychotics

• reduce effects of neurotransmitter dopamine

• according to dopamine hypothesis, schizophrenia symptoms are caused by abnormally high number of D2 receptors which increase dopamine transmission (hyperdopaminergia) in the subcortex (e.g. excess in Broca’s area may lead to speech poverty + auditory hallucinations)

• drugs (e.g. chlorpromazine) are dopamine antagonists, meaning they bind to dopamine receptors on post synaptic neuron, but don’t stimulate them, thus blocking dopamine transmission

• this reduces positive symptoms like auditory hallucinations

• bind to dopamine receptors for longer than atypical drugs, so have longer lasting effects

outline atypical antipsychotics

• clozapine binds to serotonin + dopamine receptors

• used to treat positive + negative symptoms

• bind to dopamine receptors on post synaptic neuron without stimulating them, allowing a more normal level of dopamine transmission

• bind temporarily then quickly dissociate, so have lower level side effects

• blocks serotonin receptors without stimulating them, reducing transmissions

• also induces release of glutamate

• these actions are thought to improve depression, anxiety + negative cognitive symptoms associated with schizophrenia

compare typical + atypical antipsychotic drugs

• typical reduces dopamine, whereas atypical reduces dopamine + serotonin

• typical has a longer lasting effect due to binding to dopamine receptors for longer, whereas atypical has a shorter lasting effect due to binding temporarily + then dissociating

• typcial have more side effects but they’re less serious, whereas atypical have less side effects but they’re more serious

positive evaluation of drug therapy as a biological therapy of schizophrenia (AO3)

• research supports effectiveness of antipsychotic drugs: Davis performed a meta analysis of >100 studies that compared antipsychotics with placebos. Drugs were more effective. More than 70% of sufferers treated with antipsychotics improved within 6 weeks. Less than 25% of placebo group improved. Suggests antipsychotics have a beneficial medical effect reducing schizophrenia symptoms. Drugs enable patients to live a more normal life.

negative evaluation of drug therapy as a biological therapy of schizophrenia (AO3)

• can cause many side effects (e.g. blurred vision, weight gain, seizures, motor problems, tardive dyskinesia + photosensitivity), so drugs aren’t appropriate for all sufferers. Studies found that tardive dyskinesia affects about 30% of those taking typical antipsychotic meds + that it’s irreversible in 75% of these cases. Lieberman found 74% of patients discontinued their treatment within 18 months due to intolerable side effects

• atypical antipsychotics produce fewer side effects, however some side effects are very serious (e.g. seizures + risk of agranulocytosis). So although antipsychotics were developed to reduce side affects, some still exist + this is a serious implication of antipsychotic drug therapies

• Ross + read argue that being prescribed meds reinforces the view that there’s something wrong with you, which prevents the individual thinking about possible stressors which might be a trigger for the disorder. Relying on drug treatments may reduce their motivation to look for another possible solution to their problems. So, psychological therapies or family therapy may be more effective as they focus on changing the thought preccesses that may be responsible for schizophrenia

• cause + effect: drugs don’t usually cure schizophrenia- if a patient stops taking their meds symptoms return (relapse). This suggests drugs are only tackling symotoms of the disorder + not tackling the root cause, limiting their success as a therapy.

what are the 3 psychological therapies

• cognitive behavioural therapy

• family intervention

• token economies

outline cognitive behavioural therapy as a treatment for schizophrenia (AO1)

• believe that distorted beliefs + disorganised thinking cause schizophrenia symptoms

• aim of CBT is to identify, understand + correct faulty thoughts, which will result in a change in behaviour

• patient is encouraged to trace back origins of their symptoms to get a better idea of how the symptoms developed, so they can be tackled

• reality testing techniques are used: find ways to test the validity of their faulty beliefs

• Chadwick reported a case of an individual who believed he could make things happen by thinking them. He was shown a video + asked to predict what would happen next. In over 50 trials he didn’t get a single prediction correct + he was able to understand he didn’t have the power to influence at all

• patients are set behavioural assignments with the aim to increase their general functioning (e.g. initiate social contact, which can help break down paranoid delusions like believing people want to harm them)

• therapist aims to introduce doubt as schizophrenics believe their delusions without question. Introducing doubt may start a process whereby the patient can see their views aren’t in line with reality (e.g. get a patient to list all other uses of white vans + they may start to realise that not all white vans are following them)

• normalisation: therapist helps patient understand origins of symptoms, making them less frightening + disabling, which can allow a more normal level of functioning

positive evaluation of cognitive behavioural therapy as a treatment for schizophrenia (AO3)

• Gould found a statistically significant reduction in schizophrenia symptoms when CBT was used in their meta analysis of 7 studies. This suggests it may be an effective treatment

• CBT works by trying to generate less distressing explanations for psychotic experiences, rather than trying to eliminate the experiences completely. Some negative symptoms can serve a useful function + can be seen as safety behaviours. E.g. expressing extreme emotions may lead to the person receiving treatment. If a person can see that some of their seemingly strange behaviours actually serve a purpose, they may experience less anxiety + it may reduce their symptoms

negative evaluation of cognitive behavioural therapy as a treatment for schizophrenia (AO3)

• most studies in CBT have been conducted with patients treated at the same time with antipsychotic medication, so it’s not possible to seperate the effectiveness of CBT alone. So it’s harder to make conclusions about the effectiveness of CBT

• Kingdon + Kirschen studied 142 schizophrenics + found many patients were deemed unsuitable for CBT as psychiatrists believed they wouldn’t fully engage with the therapy. They found older patients had less success with CBT, perhaps because it’s perceived as a new trend, or because their symptoms may be more severe or due to reduced plasticity

• it’s thought that CBT is only appropriate for those who can gain reasonable insight into their disorder (e.g. some patients delusions are supported by so much evidence that it’s difficult/ impossible for them to be disproved)

outline family intervention as a treatment for schizophrenia (AO1)

• aims to improve communication + interaction + reduce stress within the family that may contribute to patients risk of relapse

• Pharoah identified strategies used to achieve this:

  • forming a therpeutic alliance with all family members, agreeing on aims of therapy

  • reducing stress of caring for relative with schizophrenia

  • improving ability of family to anticipate + solve problems

  • reduction of anger + guilt family members may feel

  • helping family members achieve a balance between caring for schizophrenic + maintaining their own lives

  • improving families beliefs about + behaviour towards schizophrenia

• they suggested these strategies work by reducing levels of stress + expressed emotion, whilst increasing chances of patients complying with medication

• combination of benefits results in reduced likelihood of relapse + re-admission to hospital

• methods used include:

  • preliminary analysis: therapist conducts interveiws + observations to identify strengths + weaknesses of family members + identifies problem behaviours

  • information transfer: teaching patient + family facts about schizophrenia (e.g. causes, influence of drug abuse + effect of stress + guilt)

  • communication skills training: teach family to listen, express emotions in a healthy way + discuss things in functional ways. Taught skills like compromise + negotiation + requesting a time out. Aims to lower expressed emotion

outline the range of strategies used in family intervention as describe by Pharoah

• forming a therpeutic alliance with all family members, agreeing on aims of therapy

• reducing stress of caring for relative with schizophrenia

• improving ability of family to anticipate + solve problems

• reduction of anger + guilt family members may feel

• helping family members achieve a balnce between caring for schizophrenic + maintaining their own lives

• improving families beliefs about + behaviour towards schizophrenia

outline the 3 methods used in family intervention (AO1)

• preliminary analysis: therapist conducts interveiws + observations to identify strengths + weaknesses of family members + identifies problem behaviours

• information transfer: teaching patient + family facts about schizophrenia (e.g. causes, influence of drug abuse + effect of stress + guilt)

• communication skills training: teach family to listen, express emotions in a healthy way + discuss things in functional ways. Taught skills like compromise + negotiation + requesting a time out. Aims to lower expressed emotion

positive evaluation of family intervention as a treatment for schizophrenia (AO3)

• Pharoah reviewed evidence for effectiveness of family therapy for families of schizophrenia sufferes + concluded that there’s moderate evidence to show family therapy significantly reduces hospital readmission over the course of a year + improves quality of life for patients + their families

• McFarlane found family therapy to be one of the most consistently effective treatments for schizophrenia. Relapse rates were reduced by 50-60%. Found family therapy to be most effective when started early after diagnosis

• Anderson found a relapse rate of approx. 40% when patients had drugs only vs 20% when family therapy was used. But relapse rate was <5% when drugs + family therapy were used together

• economic benefits: family therapy is highly cost effective because it reduces relapse rates, so patients are less likely to take up resources + hospital beds

• Lobban reports that other family members were able to cope better thaks to family therapy. This is important as families often provide lots of care for the schizophrenic, so by strengthening the family as a whole, there’s more support for the schizophrenic

outline token economies (AO1)

• not a treatment but useful in management of schizophrenia

• form of behaviour modification used to try + reduce problematic behaviours (e.g. poor self-care, not socialising etc.)

• can improve the patients life during a hospital stay + help them adapt back to life in the community once discharged

• tokens are given to patients who carry out desirable behaviours (e.g. getting dressed)

• reward reinforces desirable behaviour + because it’s immediately given prevents delay discounting (reduced effect on desirable behaviour being repeated in future if reward is given some time after behaviour has been shown)

• tokens themselves have no value (secondary positive reinforcers) but they can be exchanged for tangible rewards (primary positive reinforcers)

• work on basis of operant conditioning: positive reinforcement increases likelihood of behaviour being repeated

• association (via classical conditioning) is made between desirable behaviour + reward

• frequent exchange periods increase frequency of target behaviours

• alleviates negative symptoms like poor motivation + nurses subsequently view patients more positively, which raises staff morale + has beneficial outcomes for patients

• reduce positive symptoms by not rewarding them but rewarding desirable behaviour instead (e.g. self-care + taking meds)

what approach forms the basis of token economies

learning approach

define discounting

a reduced effect on desirable behaviour being repeated in the future if the reward is given some time after the behaviour has been shown

positive evaluation of token economies (AO3)

• Paul + Lentz; token economies led to better overall patient functioning, fewer behavioural disturbances + were more cost effective than other methods of behavioural modification

• Upper + Newton found that the weight gain associated with taking antipsychotic medication was addressed with token economies. Chronic schizophrenics lost on average 3lbs of weight a week

negative evaluation of token economies (AO3)

• McMonagle + Sultana reviewed token economies over a 15 year period + found that it did reduce negative symptoms, though it was unclear if behavioural changes were maintained beyond the treatment programme. This shows token economies can be effective in changing mental state, but it’s unclear whether the effects are long lasting

• it’s hard to keep the benefits of token economies going once the patients are back home, where it’s difficult to monitor behaviour + provide immediate reinforcement. Kazdin found changes in behaviour achieved throught oken economies don’t remain when tokens are withdrawn, suggesting token economies address the effects of schizophrenia rather than the causes. It’s not a cure

• ethical concerns: seen as dehumanising, subjecting patients to regimes which take away their right to make choices. E.g. someone who likes to get up late + wear PJs all day won’t get tokens, whereas other who get up early + get dressed do get tokens. More seriously, it’s been suggested that token economies discriminate against the most ill patients, who may be too ill to perform desirable behaviours. Denying them simple pleasures may make their hospital stay even harder

outline the interactionist approach to explainimg schizophrenia (AO1)

• diathesis-stress model

• diathesis= vulnerability

• originally Meehl argued that diathesis was entirely the result of a single schizogene

• someone without this gene shouldn't develop schizophrenia no matter how much they're exposed to

• but a person who does have the gene is vulnerable to the effects of chronic stress (e.g. a schizophrenogenic mother)

• it's now believed that diathesis isn’t due to a single schizogene but rather it's thought that many genes increase vulnerability

• e.g. COMT gene which if abnormally expressed depletes frontal lobe of dopamine+ has been linked to problems regarding perception of reality (psychosis)

• stress= negative psychological experiences that risk triggering schizophrenia

• e.g. cannabis use can increase risk of schizophrenia up to seven times depending on dose, probably because it interferes with the dopamine system

• other examples of stress include family dysfunction for example a schizophrenogenic mother leads to distrust that later develops into paranoid delusions

• interactionist approach argues that schizophrenia is result of combination of biological predisposition/ diathesis (e.g. genes + brain abnormality) + an environmental trigger (e.g. family dysfunction+ faulty cognitions)

evaluation of the interactionist approach to explaining schizophrenia (AO3)

• evidence to support dual role of biological predisposition + environmental trigger: Tiernari conducted an adoption comparing 155 children adopted from schizophrenic mothers to 155 children given up for adoption by non-schizophrenic mothers. 10% of children from schizophrenic mothers went on to develop schizophrenia compared to only 1% in the non-schizophrenic group. evidence for schizophrenia being passed on to children in DNA inherited from their mothers

• results were further analysed- Tiernari looked into parenting styles of the adoptive parents + found parenting sytles characterised by high levels of criticism, conflict + low levels of empathy were implicated in the development of schizophrenia but only for children with an increased genetic risk. This is evidence for interactionist approach, showing interaction between genes (diathesis) + upbringing (stress)

• evidence from Gottesmans twin studies provides support: reviewed over 40 twin studies + found concordance rates of 48% for monozygotic twins + 17% for zygotic twins for schiziophrenia. Higher concordance rates for monozygotic twins provides support for genetic explanantion, however they’re not 100% so there must be environmental influence on development of schizophrenia

• Cannon found evidence linking birth complications to an increased risk of developing schizophrenia. Damage to hormone + neurotransmitter systems increased later vulnerability to schziophrenia. Birth complications are environmental, so this supports interaction bewteen environment + biological vulnerability

• approach is outdated- newer versions acknowledge difficulties in seperating effects from biology + environment. childhood abuse would originally have been thought of as an environmental trigger (stress), however it’s now considered a diathesis by many researchers. Read put forward a neurodevelopmental model in which ealry trauma physically alters the developing brain. early + severe enough trauma (e.g. child abuse) can seriously affect many areas of the brain (e.g. stress response becomes overactive making the person hypersensitive to stressors + increasing their vulnerability to triggers)

• overall, interactionist approach is well supported, however we can’t predict who will or won’t develop schizophrenia as causes differ wildly between individuals. Approach has useful applications: lead to widespread adoption of a combined approach to treatment (e.g. in Britain, antipsychotic medication- biological- is often combined with CBT-psychological) which provides better outcomes for patients than having any of the treatments alone, leading to better quality of life for patients + families

outline the interactionist approach to treating schizophrenia (AO1)

• acknowledges biological + psychological factors in cause of schizophrenia so is compatile with combining both biological + psychological treatments

• combining antipsychotic medication (biological treatment) with psychological therapies like CBT

• typical antipsychotic drugs (e.g. chlorpromazine) are dopamine antagonists which means they bind to dopamine receptors but don’t stimulate them

• they reduce dopamine transmission which is linked to reduction is positive symptoms

• they also work on histamine receptors + help people feel more calm

• although research clearly shows that schizophrenia symptoms are linked to a biochemical imbalance in the brain, many of the symptoms are psychoogical in nature + so also benefit from psychological therapy

• e.g. delusions are fixed, faulty beliefs which are strongly held despite contradictory evidence

• CBT aims to identify faulty beliefs + challenge them using techniques like reality testing

• other psychological therapies like family therapy helps to provide psychoeducation for family members + help families + patients with practical problem-solving strategies

• this helps patients to regain a more normal level of social + occupational functioning

• in Britain it’s increasingly standard practice to treat patients with a combination of anti-psychotic drugs + CBT

evaluation of interactionist approach to treating schizophrenia (AO3)

• Support: Tarrier randomly allocated 315 schizophrenia patients to either medication + CBT group, medication + counselling group or a medication alone group. Patients in the combination groups showed lower levels of symptoms than those in the medication alone group, which shows a clear practical advantage to adopting an interactionist approach in the form of superior treatment outcomes

• Support: research shows when on antipschotic medication alone, up to 75% of patients discontinue + stop taking their medication (Lieberman). Pharoah found patients who were also receiving family therapy were significantly more likely to comply with taking their medication, leading to a greater reduction in symptoms

• combining therapies makes treatment much more expensive which means potentially fewer people can access treatment. However due to higher success rates + relapse rates, a combined approach saves money in the long term because fewer patients are re-hospitalised

• limitation: combined treatments don’t work for all patients. around 20-30% of people diagnosed with schizophrenia don’t make a recovery. if schizophrenia has gone undetected for many years, the person often becomes unresponsive to treatments. for patients who don’t respond to drugs + psychological therapy there is a last resort to use ECT + this has been successful but only for a small number of patients. overall, this reduces the strength of combined treatments, as they don’t help all people with schizophrenia