Schizophrenia Flashcards

1
Q

Define schizophrenia.

A

Schizophrenia is a mental condition where contact with reality is impaired.

It’s more diagnosed in men than women and more common in working class citizens than middle class citizens. Occurs commonly between 15-45 year olds.

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2
Q

What are two major systems for the classification of mental disorders?

A

WHO Organisation’s International Classification of Disease (ICD-10)

American Psychriactric Association’s Diagnostic and Statsical Manual Editions (DSM 5/ DSM V)

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3
Q

What are the THREE types of schizophrenia recognised by ICD-10? Recognise at least two examples.

A

ICD-10 recognises a range of subtypes of schizophrenia.

Paranoid schizophrenia - Characterised by delusions and hallucinations.

Hebephrenic schizophrenia - Involves primarily negative symptoms.

Catatonic schizophrenia - Characterised by a disturbance in movement, leaving the sufferer immobile.

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4
Q

What are the two differences between the two classification systems of schizophrenia? (ICD-10 and DSM-V)

A
  • ICD-10 recognises subtypes of schizophrenia, whilst DSM-V does not.
  • ICD-10 requires symptons to be present for ONE MONTH, whilst DSM symptons for SIX MONTHS.
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5
Q

Describe the three levels of severity that suffers may have.

A

RARE SEVERITY- Some people may encounter only one episode in their life (rare).

PERSISTENT BUT RESPONSIVE TO MEDICATION SEVERITY - Others have persistent episodes, but live a relatively normal lives as they take medication.

PERSISTENT AND NON RESPONSIVE TO MEDICATION SEVERITY - Others are persistent and are non-responsive to medication and remain severely distributed. This happens when doctors are trying to figure out the type of medication / dosage to give to someone.

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6
Q

What is Type 1 Schizophrenia? Mention the symptom type and two examples.

A

Type 1 Schizophrenia is an acute type characterised by positive symptoms and has better prospects of recovery.

Positive symptoms involve loss of touch with reality. Examples include hallucinations and delusions. These occur in acute, short episodes with more normal periods inbetween.

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7
Q

What are hallucinations? (Positive symptoms of schizophrenia)

A

Hallucinations: These are unusual sensory experiences.
Some hallucinations are related to events in the environment whereas others are not related to the senses.
A sufferer may see distorted facial expressions or hear voices talking.

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8
Q

What are delusions/paranoias? (Positive symptoms of schizophrenia) Then define common delusions & primary delusions

A

Delusions: These are irrational beliefs. They take a range of forms:

Common delusions - Being persecuted by aliens or the government or having superpowers. Can lead to agressions as they feel they’re under external control.

Primary delusions - Sufferers experience delusions of grandeur, believing they’re someone important ie being Jesus.

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9
Q

What is Type 2 Schizophrenia? Mention the symptom type and two examples.

A

A chronic type charcterised by negative symptoms and poorer aspects for recovery.

Negative symptoms involve the loss of usual abilitieis and experiences. Examples include avolition and speech poverty.

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10
Q

What is avoiliton? (Negative symptom of schizophrenia) List the three signs of it.

A

Where one finds it difficult to begin or keep up with goal-directed activities. Sufferers often carry out a range of activities.
Researchers identified 3 signs of avolition:
- poor hygiene
- lack of persistence at work
- lack of energy.

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11
Q

What is speech poverty? (Negative symptom of schizophrenia)

A

Schizophrenia is characterised by changes in patterns of speech. There’s a reduction in the amount and quality of speech in sufferers. This is sometimes accompanied by a delay in the sufferer’s verbal responses during conversations.

These occur in chronic, longer-lasting episodes and are resistant to medication. Negative symptoms are sufferers not being able to function effectively in society ie work/school or in relationships.

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12
Q

What is acute onset schizophrenia?

A

Symptoms appear suddenly after a stressful incident.

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13
Q

What is chronic onset schizphrenia?

A

Sufferers become increasingly disturbed through gradual withdrawal and motivational loss over a prolonged period.

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14
Q

What is reliability?

A

Consistency of symptom measurement and diagnosis. Someone with the same symptoms will gather the same illness.

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15
Q

What is inter-rater reliability?

A

Occurs when different clinicians make identical, independent diagnoses of the same patient.

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16
Q

What is co concordance rates?

A

The % rates representing the likelihood of the something happening somewhere else. (similarity)

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17
Q

What two reserachers (not key) carried out research on the reliability of diagnosis? MUST REMEMBER DATES / TIME PERIODS

Discuss the 3 different researchers and compare their results essay style! (HINT; COMPARE FIRST TWO AND CONTRAST WITH LATER RESULTS)

A

In 1962, Beck reported a 54% concordance rate between experienced practitioners when they diagnosed 153 patients.

In 2005, Soderburg reported a concordance rate of 81% using the DSM V classification system.

This suggests that classifications systems have become more reliable overtime.

However, in 2009, Cheniaux had two psychiarists diagnose 100 patients using both DSM and ICD-10.
Inter-rater reliability was poor.
When using DSM V, one psychiatrist diagnosed 26 with schizophrenia, whilst the other diagnosed 13.
When using the ICD, the first psychiatrist diagnosed 44 with schizophrenia whist the second psychiatrist diagnosed 24.

This suggests reliability is poor when diagnosing schizophrenia and this has held back research into the causes and treatment of schizophrenia. Even if reliability of diagnosis isn’t perfect, they do provide practioners with a common language that allows communiation of research ideas and finding, leading to a better understanding of the disorder and the devlopment of treatment.

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18
Q

Talk about validity of diagnosis. What is criterion validity? What did Cheniaux results show?

A

Validity concerns how accurate diagnosis is. 

One way to assess validity of the diagnosis is criterion validity. This considers whether the different assessment systems arrive at the same diagnosis for the same patient.

Cheniaux’s results show that schizophrenia is more likely to be diagnosed using ICD than DSM, suggesting schizophrenia is over-diagnosed in ICD or underdiagonosed in DSM, highlighting poor validity in diagnosing schizophrenia.

Additionally, being labelled a schizophrenic has a long-lasting negative effect on their social relationships, work prospects and self-esteem, highlighting the importance of making valid judgement.

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19
Q

What is comorbidity? 

A

Morbidity in itself refers to how common a medical condition is.
So comorbidity refers to 2 or more medical conditions that occur together.
In schizophrenia, it’s when we look at one or more additional disorders occurring simultaneously with schizophrenia.

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20
Q
State the two pieces of research for comorbidity with schizophrenia.  Must remember figures!
Evaluation included (2❌)
A

Buckley - Around half of patients with a diagnosis of schizophrenia also have a diagnosis of depression(50%), substance abuse(47%), PTSD (29%) and OCD (23%).

Jeste - Stated that schizophrenics with comorbid conditions are often excluded from research and yet before the majority of patients. This suggests that research findings into the causes of schizophrenia cannot be generalised to most sufferers. This also has a knock-on effect in regards to the course of treatment patients should receive.

❌ If half the schizophrenic patients are also diagnosed with depression, this suggests that clinicians might find it difficult to tell the difference between the two conditions.
❌ In classification, if schizophrenia and depression look similar maybe it should be considered as a single condition. This reduces the chance of a valid and reliable diagnosis regarding schizophrenia.

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21
Q

2❌ - Evaluate symptom overlap with schizophrenia and bipolar depression.

A

❌ Both schizophrenia and bipolar depression involve positive symptoms like delusions and negative symptoms like avolition.
This again raises doubts about the validity of both the classification and diagnosis of schizophrenia.

❌ Under the ICD classification, a patient might be diagnosed as a schizophrenic. However, many of the same patients have received a diagnosis of bipolar disorder according to the DSM criteria. This could even suggest schizophrenia and bipolar disorder may be one condition rather than two separate ones.

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22
Q

Discuss culture bias in schizophrenia.

A

There’s a tendency to over diagnose members of other cultures as suffering from schizophrenia.
> In Britain, people of Afro-Caribbean descent are more likely to be diagnosed as schizophrenic than white people.
> Afro-Caribbean schizophrenics in Britain are more likely to be confined in mental hospitals than white schizophrenics.
> Rates of schizophrenia in Africa and the West Indies aren’t particularly high so it’s likely this imbalance in diagnosis is due to issues of culture bias.

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23
Q

Discuss gender bias in schizophrenia.

A
  • Longenecker concluded that since the 1980s, men have been diagnosed with schizophrenia more than women. This may be because men are genetically vulnerable to developing schizophrenia.
  • Cotton et al in 2009 found that female patients are more likely to work and have a better family relationship than males. This suggests why they may have a higher level of functioning than males as they’re better at hiding their symptoms.
  • The fact that males and females develop schizophrenia at different ages suggest that there is different types of schizophrenia to which each gender is vulnerable to, questioning the validity of diagnosis.
  • Hafner reported that males are more likely to suffer with the negative symptoms of schizophrenia and have higher levels of substance abuse than females.
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24
Q

What is the biological explanation for schizophrenia?

A

GENETIC explanation - suggests that schizophrenia is hereditary. There is NOT a single schizophrenia gene, but several genes that increase an individual’s vulnerability to developing schizophrenia.

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25
Q

What studies are taken place for the genetic explanation of schizophrenia? Mention concordance rates and gene mapping.

A

At first, it was co cordance rates between twins, famillies and adoptees. Gottesman focused on the rates of developing schizophrenia between people with different levels of genetic relativeness. He suggested that the more genetically similar someone is to a schizophrenic, the higher the risk of schizophrenia. (high as 48% in twins)

More recently, gene mapping studies have been used to look for genetic material commonly found among sufferers. This has helped researchers identify a number of genes influencing the development of schizophrenia. Shields reviewed 5 twin studies and reported a concordance rate of between 71-91% for monozygotic twins with severe forms of schizophrenia, suggesting that genetics play a large role with severe form of schizophrenia.

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26
Q

Talk about the candidate genes and schizophrenia study.

A

Ripke carried out a study combining various previous data from the wide genome studies of schizophrenia rather than genes.
The genetic makeup of 37,000 patients was compared to 113,000 controls. 108 separate genetic variations were associated with increased risk of schizophrenia. Genes associated with increased risk included those coding for neurotransmitters including dopamine.
Gurling says evidence from fsmily studies found that schixpzophrenka was asociated with BLANK

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27
Q

Evaluate genetic explanations.

A
There is very strong evidence for genetic vulnerability to schizophrenia from a variety of sources. 	
However these studies do not consider the influence of social class and socio-psychological factors between twins. Twin and family studies also fail to consider shared environmental influences. 
Sorri carried out a longitudinal study over 21 years on Finnish adoptees with biological mothers with schizophrenia, comparing them with adoptees whose biological mothers did not have schizophrenia, but also considered family rearing styles among adoptive families. Adoptees with a high genetic risk of developing schizophrenia were more sensitive to non-healthy rearing patterns, suggesting that environmental factors are important too. Because if genes caused schizophrenia on their own, concordance rates between MZ (monozygotic twins) would be 100%, which they are not. 
Inconsistency is another issue with twin studies results – MZ concordance rates vary e.g. some studies have even suggested low concordance rates of 11% whilst others found 48%. This highlights that there are inconsistencies in producing similar findings which raises doubts about the overall influence genetics play in the development of schizophrenia. 
28
Q

What is the dopamine hypothesis?

A

Dopamine is one of the neurotransmitters in the brain which is responsible for transmitting signals between neurones in the brain.

The original hypothesis stated that schizophrenia is responsible for an excessive activity of dopamine, causing neurons that respond to dopamine to fire too often. Researchers says if too much dopamine is released it can lead to the onset of schizophrenia.

29
Q

What is the link between schizophrenia and dopamine? What is L-dopa?

A

Psychologists believed there was a link between schizophrenia and dopamine after it was discovered that antipsychotic drugs that lessen the symptoms of schizophrenia seem to work by decreasing dopamine activity.
• Also L-dopa a drug that leads to an increase activity of dopamine creates schizophrenic symptoms in non- schizophrenic patients

30
Q

Evaluate the link with schizophrenia and high dopamine results

A

✅Support for the dopamine theory comes from Iversen. He reported that post-mortems of schizophrenic patients showed an excess dopamine level in the limbic system.

✅Additional support comes from Munkvad created schizophrenic- like behaviour in rats by giving them amphetamines (drug)this activates dopamine production and then reversed the effects by giving them neuroleptic drugs (drugs used to manage psychosis) which inhibit the release of dopamine.
• This is important because it supports the idea that dopamine is a potential cause in schizophrenia.

❌ however neuroleptic drugs have an instant effect on dopamine levels and yet the recovery rate is slow when sufferers are given neuroleptic drugs. This is something the dopamine theory cannot account for.

There is some evidence against the schizophrenia being linked with high levels of dopamine.
• Firstly Davis found that not all schizophrenic patients have high levels of dopamine, and he also noted that newer anti-schizophrenic drugs such as Clozapine which work effectively at treating schizophrenia have very little impact on blocking dopamine activity (which older drugs do).
• This questions how important dopamine is in relation to schizphrenia (IMPORTANT POINTS

❌ Results for the role of dopamine seem inconclusive as several neurotransmitters may be involved in the development of schizophrenia.
• For instance newer anti-psychotic drugs implicate serotonin as also being involved. This is important as it suggests that the dopamine hypothesis is over simplistic as many other neurotransmitters may be involved in the development of schizophrenia.

31
Q

What are neural correlates? the two studies alongside it?

A

The idea of neural correlates is that abnormalities within specific brain areas may be associated with the development schizophrenia.
• Originally evidence was limited to post-mortems conducted upon the brains of dead schizophrenic patients. However research is now non-invasive scanning techniques such as fMRI which gives a picture of the brain in action through the use of magnetic fields and radio waves.
• This allows researchers to compare brain activity of schizophrenic patients within non-sufferers to identify areas that might be link to schizophrenia.
• Participants are often given tasks to participate in which are related to functions that are effected by schizophrenia, such as thought processing tasks and working memory task.
• Johnstone found that schizophrenics had enlarged ventricles (the fluid filled gaps between brain areas) while non-sufferers did not, which suggests that schizophrenia is related to a loss of brain tissue.
• However Weydant reported that enlarged ventricles are only associated with negative symptoms, which implies enlarged ventricles cannot explain all symptoms and incidences of schizophrenia.

32
Q

neural correlates of negative symptoms

A

one negative symptom avolition involves the loss of motivation.
• Motivation involves the anticipation of a reward, and certain regions of the brain e.g. the ventral striatum, are believed to be particularly involved in feeling this anticipation.
• It therefore follows that abnormality of areas like the ventral striatum may be involved in the development of avolition.
• Juckel measured activity levels in the ventral striatum (by using fMRI scans). He presented participants with reward- indicating and loss-indicating stimuli.
• He found that the schizophrenics showed reduced ventral striatal activity during the presentation of reward-indicating cues.
• It was found that decreased activation of the left ventral striatum was inversely (reverse) correlated with the severity of negative symptoms (means as the activation went down the severity of the symptom went up). Thus activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia.

33
Q

neural correlates to positive symptoms. talk about allen’s study

A

Positive symptoms also have neural correlates.

Allen scanned the brains of patients experiencing auditory hallucinations and compared them to a control group.
While scans were being carried out, participants had to identify if pre-recorded words they were being played were their voice or the voice of others.
Lower activation levels in the superior temporal gyrus (responsible for processing sounds) and anterior cingulated gyrus (one function is deals with attention) were found in the hallucination group, who also made more errors than the control group.
We can thus say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.

34
Q

evidence against neural correlate EVALUATION

A

there we have considered evidence that supports neural correlates being involved with Schizophrenia. However there is evidence against these links.
• There is evidence against the idea that schizophrenic patients have larger ventricles, for instance not all sufferers show this and in fact some non-schizophrenics have enlarged ventricles.
• This means that schizophrenia might not be due to a loss of brain tissue and also questions the overall validity of that link.
• In fact some psychologists have suggested that the large ventricles are an effect of suffering from schizophrenia after a long period and that this eventually leads to physical brain damage rather than the actual brain damage leading to schizophrenia.

Evidence against neural correlates
• There is an issue in determining cause and effect in neural correlates. For example the correlation between levels of activity in the ventral striatum and negative symptoms.
• It may be that something wrong in the ventral striatum is causing these negative symptoms.
• However, it is also possible that the negative symptoms themselves mean that less information passes through the striatum, resulting in the reduced activity.
• Alternatively another factor could influence both the negative symptoms and ventral striatum activity. Therefore the existence of neural correlates in schizophrenia tells us relatively little in itself.
• Finally it is also important to consider the role that environmental factors may play in brain abnormalities. For instance factors such as substance abuse and stress levels may also have a damaging influence upon brain tissue.

35
Q

What are the two psychological explanations for schizophrenia?

A
  • Family dysfunction

- Cognitive explanations i.e. dysfunctional thought processing.

36
Q

What is the family dysfunction model?

A

This model sees maladaptive relationships and poor patterns of communications within families as a source of stress which can potentially cause or influence the development of schizophrenia.

37
Q

What are 3 explanations for the family dysfunction model?

A
  1. The schizophrenic mother
  2. Difficulty communicating – double bind theory
  3. Expressed emotion
38
Q

Explain ‘the schizophrenic mother’

A

Frieda Fromm-Reichmann proposed a psychodynamic explanation for schizophrenia based on accounts she heard from her patients about their childhoods.
Fromm-Reichmann noted that many of her patients spoke of a particular type of parent, which she called the schizophrenic mother.
According to Fromm-Reichmann the schizophrenic mother is cold, rejecting and controlling and tends to create a family climate that is often tense and has an element of secrecy.
This leads to distrust that later develops into paranoid delusions (i.e. the belief that one is being persecuted by another person) and ultimately schizophrenia.

39
Q

Evaluate the schizophrenic mother.

A

X Little evidence - As most of the schizophrenia mother theory was based on clinical observations of patients there is very little evidence to support this theory and the idea that mothers should be assessed for ‘crazy-making characteristics’ was to awkward to investigate.

40
Q

double bind theoru

A
  • Bateson emphasised the importance of communication styles within a family.
    He suggested that issues arise when a developing child regularly finds themselves in fear of doing the wrong thing, but received mixed messages about what that is and they often feel unable to comment on the unfairness they feel or even to seek clarification.
    When they get it wrong such children tend to be punished by withdrawal of love.
    This leaves the child understanding the world as a confusing and dangerous and this is reflected in symptoms like disorganised thinking and paranoid delusions.
    Bateson created the term double bind theory to explain the contradictory situations children could be placed in by such parents, where a verbal message is given but opposite behaviour is exhibited.
    For example, if a mother tells her son that she loves him, while at the same time turning her head away in disgust, the child receives two conflicting messages about their relationship on different communicative levels, one of affection on the verbal level, and one of animosity (hostility) on the nonverbal level.
    It is argued that this contradiction makes a child’s unable to respond to the mother because one message invalidates the other – making it difficult to communicate
41
Q

eva.luate the double bind theory

A

Bateson reported on a case where a recovering schizophrenic was visited in hospital by his mother.
He embraced her warmly (hugged) but she stiffened, and when he withdrew his arms she said ‘Don’t you love me anymore?’ to which he blushed.
Then she commented, ‘Dear, you must not be so easily embarrassed and afraid of your feelings’.
She then left, and he went onto assault a worker and had to be restrained. This gives support to the double bind theory.

However the fact that Bateson recorded this data it is possible that he was bias in his observations and in fact the only support for double bind theories have come from such clinical cases, which would question the overall validity of his claims and theory.

42
Q

expressed emotion and schizophrenia

A

This refers to level of emotion, in particular negative emotion that is expressed towards a patient by their carers.
Expressed emotion contains several elements:
1. Verbal criticism of the patient, occasionally accompanied by violence.
2. Hostility towards the patient, including anger and rejection.
3. Emotional over-involvement in the life of the patient, including needless self-sacrifice.
These high levels of expressed emotions in carers directed towards the patient are a serious source of stress for the patient.
This is primarily an explanation for relapse in patients with schizophrenia. However, it is also been suggested that it may be a source of stress that can trigger the onset of schizophrenia in a person who is already vulnerable, for example, due to their genetic make-up

43
Q

evaluate expressed emotion.

A

Kavanagh reviewed 26 studies of expressed emotion; he found that the mean relapse rate for schizophrenics who returned to live with high expressed emotion families was 48% compared with 21% for those who went to live with families that were rated low on expressed emotions.
This supports that idea that expressed emotions can increase the risk of relapse in recovering patients.

Butzlaff who carried out a Meta analysis of 26 studies and found that patients returning to family environments of high expressed emotions were twice as likely to relapse as the average relapse rates.

44
Q

evaluate family dysfunction

A

There is support for the claim that dysfunctional family relationships might be linked to schizophrenia.
For example Read et al reviewed 46 studies of child abuse and schizophrenia, and found that 69% of the female patients that had been diagnosed with schizophrenia had a history of physical, sexual abuse or both in childhood. For men the figure was 59%.
Also adults with insecure attachments during childhood with their primary caregiver were more likely to have schizophrenia.

However most of the studies that have linked dysfunctional families to schizophrenia have a weakness. This is regarding the fact that most of the information collected about childhood experiences was gathered after the development of symptoms, and the schizophrenia may have distorted the patient’s recall of their childhood.
This creates a serious problem of validity. A small number of studies have been carried out prospectively (i.e. they followed a sample of children to see if their childhood experiences could predict adult behaviours). There is still evidence that links family dysfunction to schizophrenia but not a huge amount and results have been inconsistent.

 Another major issue with the dysfunctional family explanations for schizophrenia is that they have led historically to parent-blaming.

Parents, who have already suffered at seeing their children, develop schizophrenia and who are likely to bear a lifelong responsibility for their care – now have to deal with further trauma by receiving the blame for the condition.
This is literally adding insult to injury. In fact the shift in the 1980s from hospital to community care, often involving parental care, may be one of the factors leading to the decline of schizophrenic mother and double bind theories – parents no longer tolerated them.

45
Q

cognitive explanations of schizophernia

A

The cognitive explanation focuses on the role of mental processes. Schizophrenia is associated with several types of ‘abnormal information processing’ and as a result it can be presented as an explanation of schizophrenia.
Beck proposed that a cognitive model combines a complex interaction of neurological, environmental, behavioural and cognitive factors to explain the disorder.
It is thought that abnormalities within brain functioning increase the vulnerability to stressful life experiences, which in turn can lead to dysfunctional beliefs and behaviours.
Schizophrenia is characterized by disruptions to normal though processing and this is reflected in the symptoms of schizophrenia.
For instance, reduced processing in the ventral striatum is associated with negative symptoms of schizophrenia

46
Q

what are the two dysfunctional thought processing

A
  • Frith identified two types of dysfunctional thought processing that could underlie some symptoms:
    1. Meta-cognition
    1. Central control
47
Q

what is metacognition in dysfunctional thoughts (10 mins)

A

Meta-cognition is the cognitive ability to reflect on thoughts (cognitive monitoring) and behaviour (reactions triggered by thoughts and feelings).
• Meta-cognition allows individuals to ‘view’ their own mental states and the wishes and intentions of others, allowing them to make sense of their lives and deal with their ever-changing environments.
• However Schizophrenics are seen as experiencing meta-cognitive dysfunction. Dysfunction in meta-cognition would disrupt our ability to recognise our own thoughts and actions, and sufferers may believe these reflect the views and action of someone else. This would explain hallucinations of voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others).

48
Q

what is central control in dysfunctional thoughts? explain how it’s different in schizophrenia sufferers (HINT: white lies)

A

Central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead.

  • Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts.
  • For example, sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these.
49
Q

a03 cognitive explanation

A

SUPPORT FOR METACOGNITION
• Brunet reviewed 20 years of evidence to report that many symptoms of schizophrenia and the consequent impairments in social functioning result from poor meta-cognition, especially the ability to self-reflect and empathise with others, supporting the idea that meta-cognition dysfunction is an important part of schizophrenia.
• SUPPORT FOR CENTRAL CONTROL (Stroop effect results)
• There is strong support for the idea that information is processed differently
in the mind of the schizophrenia sufferer.
• In one study Stirling compared 30 patients with a diagnosis of schizophrenia with 18 non-patient controls on a range of cognitive tasks including the Stroop test, in which participants have to state the colour of the ink a set of words are written in and not the colour stated in written form; thus the task requires participants to suppress the impulse to read the words.
• It was found that Schizophrenic patients took over twice as long to name the ink colours than the control group. This is therefore in line with Frith’s theory of ‘Central control dysfunctio

☺Another key strength of the cognitive explanation is that it can account for both positive and negative symptoms. Also the fact that the cognitive explanation can be combined with other explanations, such as biological ones gives a fuller understanding of the causes and maintenance of the disorder.
• Also there are practical applications associated with the meta- cognition factor in the development of schizophrenia, as it indicates that therapies for the disorder will need to concentrate on improving meta-cognitive abilities in sufferers in order to be effective.
• Indeed therapies could be targeted at specific areas of meta-cognitive impairment. Woodward (2007) conducted a pilot study offering meta- cognition therapy for schizophrenic patients and it offered promising results and patients stated that they enjoyed their sessions (also reflected by high attendance rates) more than their usual therapy sessions.

Although there is a mass of evidence that suggests that information processing is different in the mind of schizophrenic patients, there is a problem with the cognitive explanations.
• Links between symptoms and faulty cognitive are clear; however, this link does not tell us anything about the origins of those cognitions or of schizophrenia.
• Cognitive theories can explain the proximal (closet) causes of schizophrenia i.e. what causes current symptoms but not the origins of the condition.
• Also as these are only links we cannot determine whether cognitive factors are a cause or a result of neural correlates and abnormal neurotransmitter levels seen in schizophreni

50
Q

what are biological treatments?

A

Drug therapy: typical and atypical antipsychotics.

51
Q

what are psychological treatments

A
  • cbt
  • family therapy
  • token economies
52
Q

what is drug therapy?

A

chemical treatment of abnormality

53
Q

what are antipsychotic drugs:? how does the effect occur within a few days, a few weeks and exactly 6 weekss?

A

Antipsychotic drugs can be taken in tablet form, as syrup or by injection (intravenous – through the veins by injection).
After a few days – Tends to reduce symptoms such as hallucinations and feelings of anxiety.
After a few weeks - Delusions start to reduce.
After 6 weeks – Patients see a lot of improvement, but there are wide individual differences in the types of responses to taking antipsychotic drugs.
Patients often have to take several types of antipsychotic drugs before they find the best one for them.
Some patients’ may require a short term course of antipsychotics then stop their use without the return of symptoms.
Other patients may require antipsychotics for life or face the likelihood of a recurrence of schizophrenia.

54
Q

what two catergories are antipsychotic drugs divided into?

A

Typical antipsychotics

Atypical antipsychotics

55
Q

what are typical antipsychotics? (chloropromazine)

A

The first antipsychotic drug was Chlorpromazine this can be taken as tablets, syrup or by injection.
If taken orally, doses often start small e.g. 400-800mg, with a maximum of 1000mg daily.
There is a strong association between the use of typical antipsychotics drugs like Chlorpromazine and the dopamine hypothesis.
Antipsychotic drugs are likely to lead to movement side effects (similar to Parkinson’s disease).

56
Q

how does chlopromazine work?

A

Typical antipsychotics like Chlorpromazine work by acting as antagonists in the dopamine system.
Antagonists are chemical which reduce the action of a neurotransmitter.
Therefore Dopamine antagonists work by blocking dopamine receptors in the synapse of the brain, reducing the action of dopamine.
This has been found to reduce positive symptoms of the disorder e.g. auditory hallucinations and delusions.
Chlorpromazine is also an effective sedative. This is believed to be related to its effect on histamine receptors (to do with allergies) but it is not fully understood how this leads to sedation.
Chlorpromazine is often used to calm patients not only with schizophrenia but with other conditions.

57
Q

what are atypical antipsychotics? (clozapine)

A

Atypical drugs were introduced as they were supposedly more effective than typical ones and incurred fewer side effects, although the validity of this claim has been questioned. Also found to be more effective with negative symptoms of schizophrenia.
Clozapine
Clozapine was developed in the1960s and first trialled in 1970s.
However Clozapine was withdrawn for a while in the 70s following the deaths of some patients from a blood condition called Agranulocytosis. Resold in the 1980s.
It is still used today, and people taking it have regular blood tests to ensure they are not developing agranulocytosis. Because of its potentially fatal side effects Clozapine is not available as an injection and daily dosages are less than Chlorpromazine, typically 300-450mg a day.

58
Q

how does clozapine work?

A

Clozapine binds to dopamine receptors in the same way that Chlorpromazine does, but in addition it acts on serotonin and glutamate receptors.
It is believed that this action helps improve mood and reduce depression and anxiety in patients, and that it may improve cognitive functioning.
The mood-enhancing effects of Clozapine mean that it is sometimes prescribed when a patient is considered at high risk of suicide.

59
Q

what is risperidone and how does it work/.

A

Risperidone
Risperidone is a more recently developed atypical antipsychotic, since the 1990s. It was developed in an attempt to produce a drug as effective as Clozapine but without its serious side effects. Risperidone can be taken in the form of tablets, syrup or an injection (like Chlorpromazine). Also a small dose is initially given and this is built up to a typical daily dose of 4-8mg and a maximum of 12mg.

How Risperidone works
It binds to dopamine and serotonin receptors (like Clozapine). However Risperidone binds more strongly to dopamine receptors than Clozapine and is therefore effective in much smaller doses than most antipsychotic drugs. There is also evidence that this drug also leads to fewer side effects than is typical for antipsychotics.

60
Q

evaluate drug treatment

A

Strengths
There is a large body of evidence to support the idea that antipsychotic drugs are effective in tackling the symptoms of schizophrenia. For instance Davis carried out a meta-analysis of more than 100 studies that compared antipsychotics with placebos. Davis found that the antipsychotic drugs were more effective at treating the symptoms of schizophrenia, 70% of sufferers started to show improvements in condition after 6 weeks. This is important as it shows that antipsychotics have a beneficial medical effect. Further support comes from Marder, he reported that the atypical antipsychotic drug Clozapine is as effective as typical antipsychotics in relieving the positive symptoms of schizophrenia, and is effective in approximately 30-61% of patients who are resistant to typical antipsychotics. This suggests that atypical drugs might be a superior form of treatment.

There is some evidence that suggests that atypical antipsychotics are more effective than typical antipsychotics for treating schizophrenia. For instance Schooler compared both types of drugs and although he found 75% of patients experienced at least a 20% reduction in symptoms. He found that 55% of those receiving typical antipsychotic suffered relapses (that is when you suffer from the same condition again), compared to only 42% of the atypical treatment. This could be due to the fact that atypical drugs have fewer side effects. However Kahn found no major difference in the effects of typical and atypical antipsychotic drugs, which casts doubts on the claim that atypical drugs are superior.

weakness

A major problem with antipsychotic drugs is the likelihood of side effects, ranging from the mild to the serious and even fatal.
Typical antipsychotics are associated with a range of side effects including dizziness, agitation (anxiety), sleepiness, stiff jaw and weight gain.
Long term use can result in tardive dyskinesia which leads to involuntary facial movements such as grimacing (e.g. facial expression for pain/disapproval) or blinking. https://www.youtube.com/watch?v=FUr8ltXh1Pc. The most serious side effect of typical antipsychotics is neuroleptic malignant syndrome (NMS). This results in high temperature and coma which can be fatal, however as doses of typical drugs have declined, NMS cases have become rarer.
Atypical drugs were developed to reduce the frequency of side effects and generally this has succeeded. However, side effects still exist and patients taking Clozapine have to have regular blood tests to help doctors detect early signs of agranulocytosis. This is important as it shows that side effects are still a significant weakness of antipsychotic drugs.

There is a theoretical issue with the use of antipsychotic drugs. Antipsychotic drugs work by reducing the activity of dopamine by blocking dopamine receptors which is concordance with the dopamine hypothesis .
However it has been found that there are very low levels of dopamine (rather than high) in other parts of the sub cortex in schizophrenic patients.
This then raises doubts about how useful it would be to reduce levels of dopamine in sufferers. In fact some psychologist’s modern views suggest that antipsychotic drugs should not work.

61
Q

what is cbt? an example of a question asked (PASTE DEPRESSION NOTES!)

A

This is the main psychological treatment used with schizophrenia.
The aim of CBT involves helping patients identify irrational thoughts and trying to change them.
This may involve an argument/discussion of how likely it is that the patient’s beliefs are true and consider other less threatening possibilities.
If a patient believes the mafia wants to kill them think of 3 questions the therapist could ask the client to make them doubt their thoughts?
For instance if a patient states that the mafia wants to kill them, the therapist might say ‘there must be a good reason for this?’ and a client may then start to doubt their thoughts, for instance the client may then ask, ‘Do you think it is the Mafia?’. At this point the therapist could state ‘that is a possibility, but there could be other explanations. How do you know it is the Mafia?’
This will not be able to block symptoms of schizophrenia but it can make patients better able to cope with them.

CBT can help the person understand that they have a condition, and make them believe that it is something that can be managed. It can help them recognise triggers for their schizophrenia.
CBT can help patients make sense of how their delusions and hallucinations impact their feelings and behaviours. The therapist will help the patient recognise hallucinations which can help filter out such beliefs.
https://www.youtube.com/watch?v=cqLb9hNWd8c

Antipsychotic drugs are usually given first to reduce psychotic thought processes, so that CBT can be more effective. CBT usually takes place once every 10 days for between 5 to 20 sessions either in groups or an individual basis.

62
Q

EVALUATE CBT

A

There is evidence which supports CBT as an effective treatment for schizophrenic patients. For instance Tarrier conducted a study where schizophrenic patients were given 20 sessions of CBT, along with drug therapy (including 4 booster sessions during the next year); experienced a greater reduction in symptoms than sufferers that received drug therapy alone or supportive counselling. However Jauhar performed a meta-analysis of 50 studies of CBT for schizophrenia conducted over the last 20 years, and found only a small therapeutic effect on symptoms, including positive symptoms which CBT is mainly thought to target.

There an issue that CBT is not suitable for all patients, especially those too paranoid to form trusting alliances with practitioners. It may be more suitable for those refusing drug treatments, though such patients are often highly disturbed and would therefore find it difficult to effectively undertake CBT.
Another issue with CBT results is that when studies have used blind testing (researcher does not know which patients received CBT) the impact that CBT has on helping patients manage their symptoms is very small. This strongly questions whether CBT should be used as a treatment for schizophrenia.

63
Q

FAMILY THERAPY

A

This form of therapy is based on the idea that a dysfunctional family can play a role in the development of schizophrenia. Therefore altering relationships and communication patterns and lowering levels of expressed emotion should help schizophrenics recover.
This therapy takes place with families rather than individual patients.
It aims to improve the quality of communication and interaction between family members. The therapy wants to improve positive and reduce negative forms of communication. Increase tolerance levels and decrease anger and criticism levels between family members. Also decrease feelings of guilt for causing the illness among family members. Also reduce levels of expressed emotion (EE).

Therapists meet regularly with the patient and family members, who are encouraged to talk openly about the patient’s symptoms, behaviour and progress with their treatment and how the patient’s illness affects them. Family members are taught to support each other and be caregivers, with each person given a specific role in the rehabilitation of the patient. There is an overall emphasis on ‘openness’. Family therapy like CBT is given a set amount of time, usually between 9 months to a year, with a focus on reducing symptoms, allowing families to develop skills that can be continued after the therapy has ended.
Family therapy is thought to increase the chances of the patients complying with medication; and this combination often helps reduce the chances of a relapse and re-admission back to hospital.

64
Q

EVALUATE FAMILY THERAPY

A

 There is a vast amount of evidence that family therapy is effective. For instance Xiong randomly allocated 63 Chinese schizophrenics to either standard drug care or standard drug care plus family therapy.
He found that after one year 61% of the standard care patients had relapsed compared with 33% of the standard care plus family therapy patients.
This suggests that family therapy is effective in combination with drug treatments and can help significantly reduce the chances of relapse.
 There is an issue with family therapy regarding the need for ‘openness’ in some families there is a reluctance to share sensitive information, as it may reopen family tensions. In some cases families are reluctance to admit their problems, and this can lower the overall effectiveness of this therapy.

65
Q

WHAT IS TOKEN ECONOMY

A

Token economies are a behaviouristic therapy approach to the management of schizophrenia, where tokens are awarded for demonstrations of desired behavioural change. This technique is mainly used with long term hospitalised patients, as such patients have often developed maladaptive behaviours e.g. developed bad hygiene or a tendency to remain in pyjamas all day. Therefore token economy can help enable them to leave hospital and live relatively independently within the community.
Tokens
The idea is that patients are given tokens (in the form of coloured discs) when they have carried out a desired behaviour – this acts as a reinforcement. Desired behaviours can be things like examples of self-care, adherence to medication and social interaction.
Rewards
The tokens can then later be exchanged for goods or privileges. Tokens economies are based on operant conditioning. The rewards can be in the form of materials such as sweets, cigarettes or magazines or rather in the form of services e.g. having their room cleaned or privileges such as a walk outside the hospital.

66
Q

EVALUATE TOKEN ECONOMY

A

 There is evidence that token economy does work at getting patients to complete certain tasks. For instance Arzin found that when patients were offered rewards for behaviours such as making their beds, the average number of daily chores completed rose from 5 to 42, illustrating the success of the token economy in getting patients to take responsibility for themselves.
 Token economy is good in that it offers a chance for patients to become more independent and active especially when they have been institutionalised for a long time, and in such patients often lack motivation.
 A major issue with token economies is desirable behaviour becomes dependent on being reinforced (rewarded) but when they are released in the community such reinforcements cease, which often leads to high re-admittance rates. This even has implications in jobs; if a patient gets a job and they are paid monthly this could cause problems as they are use to instant rewards. This could mean schizophrenics should go for jobs where they are paid on a short term basis.