schizo Flashcards

1
Q

THE NATURE OF SCHIZOPHRENIA

A

Schizophrenia is a type of psychosis, a severe mental disorder in which thoughts and emotions are so impaired that contact is lost with external reality.
Schizophrenia is the most common psychotic disorder, affecting about 1% of the population at some point in their lifetime, although many continue to lead normal lives after diagnosis and subsequent treatment.
Schizophrenia is most often diagnosed between the ages of 15 and 35, with men and women affected equally.
Someone diagnosed with schizophrenia would characteristically experience delusions (a belief in something that is not, nor could be, true) and hallucinations (experiencing stimuli that are not present).
There are many symptoms of the disorder, although not every patient displays all the symptoms.

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2
Q

Diagnosis & classification of schizophrenia (these two things are interlinked)

A

To diagnose a disorder, we must be able to distinguish between disorders
Diagnosis means identifying clusters of symptoms that occur together
We then classify these symptoms as one disorder
A disorder can then be diagnosed by identifying the symptoms
There are two major systems for classification of mental disorders
World Health Organisation’sinternational classification of diseases (ICD-10, version 11 currently,) and
American Psychiatric Association’s Diagnostic & Statistical Manual (DSM-5)
There are some differences between them egin DSM, one positive symptom (see next slide)must be present for diagnosis whereas in ICD, two or more negative symptoms are sufficient
NB Previously recognised subtypes of schizophrenia have now been dropped eg paranoid schizophrenia, because it has been found that individuals will not necessarily display the exact same symptoms a few years on

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3
Q

Positive symptoms:

A

The symptoms of schizophrenia are typically divided into positive symptoms and negative symptoms.
Positive symptoms are those that appear to reflect an excess or distortion of normal functions. They include the following:

  • Hallucinations
  • Delusions
    Disorganised speech
  • Grossly disorganised or catatonic behaviour
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4
Q

Hallucinations

A

bizarre, unreal perceptions of the environment that are usually auditory (hearing voices that other people can’t hear) but may also be visual (seeing lights, objects or faces that other people can’t see), olfactory (smelling things that other people cannot smell) or tactile (e.g. feeling that bugs are crawling on or under the skin or something touching the skin).
Many schizophrenics report hearing a voice or several voices, telling them to do something (such as harm themselves or someone else) or commenting on their behaviour.

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5
Q

Delusions

A

bizarre beliefs that seem real to the person with schizophrenia, but they are not real.
Sometimes these delusions can be paranoid (i.e. persecutory) in nature.
This often involves a belief that the person is being followed or spied upon by someone.
They may believe that their phone is tapped or that there are video cameras hidden in their home.
Delusions may also involve inflated beliefs about the person’s power and importance (delusions of grandeur).
For example, the individual may believe they are famous or have special powers or abilities.
An individual may also experience delusions of reference, when events in the environment appear to be directly related to them - for example, special personal messages are being communicated through the TV or radio.

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6
Q

Disorganised speech

A

is the result of abnormal thought processes, where the individual has problems organising his or her thoughts and this shows up in their speech.
They may slip from one topic to another (derailment), even in mid-sentence, and in extreme cases their speech may be so incoherent that it sounds like complete gibberish - something that is often referred to as “word salad’”

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7
Q
  • Grossly disorganised or catatonic behaviour
A

includes the inability or motivation to initiate a task, or to complete it once it is started, which leads to difficulties in daily living and can result in decreased interest in personal hygiene.
The individual may dress or act in ways that appear bizarre to other people, such as wearing heavy clothes on a hot summer’s day.
Catatonic behaviours are characterised by a reduced reaction to the immediate environment, rigid postures or aimless motor activity.

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8
Q

Negative symptoms:

A

Involve the loss of usual abilities & experience

  • Speech poverty (alogia)
  • Avolition
    Anhedonia
  • Affective flattening
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9
Q

Speech poverty (alogia)

A

characterised by the lessening of speech fluency and productivity.
this is thought to reflect slowing or blocked thoughts.
Patients who display speech poverty display a number of characteristic signs.
They may produce fewer words in a given time on a task of verbal fluency (e.g. name as many animals as you can in one minute).
This is not a matter of not knowing as many words as non-schizophrenics, but more a difficulty of spontaneously producing them.
Speech poverty may also be reflected in less complex syntax, e.g. fewer clauses, shorter utterances, etc.
This type of speech appears to be associated with long illness and earlier onset of the illness.

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10
Q
  • Avolition
A

a reduction of interests and desires as well as an inability to initiate and persist in goal-directed behaviour (e.g. sitting in the house for hours every day, doing nothing).
Avolition is distinct from poor social function or disinterest, which can be the result of other circumstances.
For example, an individual may have no social contact with family or friends because they have none, or communication with them is difficult.
This would not, however, be considered avolition, which is specified as a reduction in self-initiated involvement in activities that are available to the patient.

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11
Q
  • Affective flattening
A

a reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language.
Compared to controls without this symptom, individuals show fewer body and facial movements and smiles, and less co-verbal behaviour, i.e. those movements of the hands, head and face that usually accompany speech.
When speaking, patients may also show a deficit in prosody, ie paralinguistic features (such as intonation, tempo, loudness and pausing) that provide extra information that is not explicitly contained in a sentence, and which gives cues to the listener as to emotional or attitudinal content and turn-taking.

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12
Q
  • Anhedonia
A

a loss of interest or pleasure in all or almost all activities, or a lack of reactivity to normally pleasurable stimuli.
It may be pervasive (ie, all-embracing) or it may be confined to a certain aspect of experience.
Physical anhedonia is the inability to experience physical pleasures such as pleasure from food, bodily contact and so on.
Social anhedonia is the inability to experience pleasure from interpersonal situations such as interacting with other people.
Because social anhedonia overlaps with other disorders (such as depression), whereas physical anhedonia does not, the latter is considered a more reliable symptom of schizophrenia (Sarkar et al, 2010).

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13
Q

RELIABILITY

A

Diagnostic reliability means that a diagnosis of schizophrenia must be repeatable, i.e. clinicians must be able to reach the same conclusions at two different points in time (test-retest reliability), or different clinicians must reach the same conclusions (inter-rater reliability).
Inter-rater reliability is measured by a statistic called a kappa score.
A score of 1 indicates perfect inter-rater agreement; a score of 0 indicates zero agreement.
A kappa score of 0.7 or above is generally considered good.
In the DSM-V field trials (Regier et al., 2013), the diagnosis of schizophrenia had a kappa score of only 0.46.

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14
Q

Cultural differences in diagnosis:

A

Research suggests there is a significant variation between countries when it comes to diagnosing schizophrenia, i.e. culture has an influence on the diagnostic process.
Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient.
Sixty-nine per cent of the US psychiatrists diagnosed schizophrenia, but only 2% of the British ones gave the same diagnosis.
One of the main characteristics of schizophrenia, ‘hearing voices, also appears to be influenced by cultural environment.
Luhrmann et al. (2015) interviewed 60 adults diagnosed with schizophrenia - 20 each in Ghana, India and the US.
Each was asked about the voices they heard.
Strikingly, while many of the African and Indian subjects reported positive experiences with their voices, describing them as playful or as offering advice, not one American did.
Rather, the US subjects were more likely to report the voices they heard as violent and hateful - and indicative of being ‘sick’
Luhrmann suggests that the “harsh, violent voices so common in the West may not be an inevitable feature of schizophrenia.

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15
Q

Rosenhans study of the unreliability of the diagnosis of mental disorder:

A

The unreliability of diagnosis was highlighted by Rosenhan’s famous study in which ‘normal’ people presented themselves to psychiatric hospitals in the US claiming they heard an unfamiliar voice in their head saying the words ‘empty, ‘hollow’ and ‘thud’ (Rosenhan, 1973).
They were all diagnosed as having schizophrenia and admitted.
Throughout their stay, none of the staff recognised that they were not actually displaying symptoms of schizophrenia.
In a follow-up study, Rosenhan warned hospitals of his intention to send out more ‘pseudopatients.
This resulted in a 21% detection rate, although none actually presented themselves!

Within the study Rosenhan ran a small field experiment in four of the hospitals.
Either a pseudopatient or a young lady approached a staff member and asked questions such as: ‘Pardon me, Mr/Mrs/Dr X, could you tell me when I will be eligible for grounds privileges?’
The pseudopatient did this as normally as possible and avoided asking any particular person more than once in a day.
Only 4% of the psychiatrists and 0.5% of the nurses stopped; 2% in each group paused and chatted
When the young lady approached staff members and asked them the same questions, they all stopped and answered her questions, maintaining eye contact.

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16
Q

VALIDITY:
Gender bias in diagnosis:

A

Gender bias in the diagnosis of schizophrenia is said to occur when accuracy of diagnosis is dependent on the gender of an individual.
The accuracy of diagnostic judgements can vary for a number of reasons, including gender-biased diagnostic criteria or clinicians basing their judgements on stereotypical beliefs held about gender.
For example, critics of the DSM diagnostic criteria argue that some diagnostic categories are biased towards pathologising one gender rather than the other.
Broverman et al. (1970) found that clinicians in the US equated mentally healthy ‘adult’ behaviour with mentally healthy ‘male’ behaviour.
As a result, there was a tendency for women to be perceived as less mentally healthy.

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17
Q

Symptom overlap:

A

Despite the claim that the classification of positive and negative symptoms would make for more valid diagnoses of schizophrenia, many of these symptoms are also found in many other disorders, such as depression and bipolar disorder.
This problem is referred to as symptom overlap.
For example, Ellason and Ross (1995) point out that people with dissociative identity disorder (DID) actually have more schizophrenic symptoms than people diagnosed as being schizophrenic!
Most people who are diagnosed with schizophrenia have sufficient symptoms of other disorders that they could also receive at least one other diagnosis (Read, 2004).

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18
Q

Co-morbidity:

A

It refers to the extent that two (or more) conditions co-occur.
Psychiatric co-morbidities are common among patients with schizophrenia.
These include substance abuse, anxiety and symptoms of depression. For example, Buckley et al. (2009) estimate that co-morbid depression occurs in 50% of patients, and 47% of patients also have a lifetime diagnosis of co-morbid substance abuse.
Schizophrenia and obsessive-compulsive disorder (OCD) are two distinct psychiatric conditions.
Roughly 1% of the population develop schizophrenia, and roughly 2-3% develop OCD.
Since both are fairly uncommon, we would expect that only a few people with schizophrenia would develop OCD and vice versa.
However, evidence suggests that the two conditions appear together more often than chance would suggest. A meta-analysis by Swets et al. (2014) found that at least 12% of patients with schizophrenia also fulfilled the diagnostic criteria for OCD and about 25% displayed significant obsessive-compulsive symptoms.

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19
Q

EVALUATION/DISCUSSION OF RELIABILITY:

A

Lack of inter-rater reliability:
Unreliable symptoms:
A comment on cultural differences in the diagnosis of schizophrenia:

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20
Q

Lack of inter-rater reliability:

A

Despite the claims for increased reliability in DSM Ill (and later revisions), over 30 years later there is still little evidence that DSM is routinely used with high reliability by mental health clinicians.
For example, Whaley (2001) found inter-rater reliability correlations in the diagnosis of Scizophrenia as low as 0. 11.
Further problems with the inter-rater reliability of the diagnosis of schizophrenia are illustrated in the Rosenhan study
This suggests that, because psychiatric diagnosis lacks some of the more objective measures enjoyed by other branches of medicine, it inevitably faces additional challenges with inter-rater reliability.

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21
Q

Unreliable symptoms:

A

For a diagnosis of ‘schizophrenia’, only one of the characteristic symptoms is required ‘if delusions are bizarre’
However, this creates problems for reliability of diagnosis.
When 50 senior psychiatrists in the US were asked to differentiate between ‘bizarre’ and ‘non-bizarre’ delusions, they produced inter-rater reliability correlations of only around 0.40 (Mojabi and Nicholson, 1995).
The researchers concluded that even this central diagnostic requirement lacks sufficient reliability for it to be a reliable method of distinguishing between schizophrenic and non-schizophrenic patients.

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22
Q

A comment on cultural differences in the diagnosis of schizophrenia:

A

Research (e.g. Barnes, 2004) has established cultural, and racial, differences in the diagnosis of schizophrenia.
However, the prognosis for members of ethnic minority groups may be more positive than for majority group members.
The ethnic culture hypothesis predicts that ethnic minority groups experience less distress associated with mental disorders because of the protective characteristics and social structures that exist in these cultures.
Brekke and Barrio (1997) found evidence to support this hypothesis in a study of 184 individuals diagnosed with schizophrenia or a schizophrenia-spectrum disorder.
This sample was drawn from two non-white minority groups (African Americans and Latinos) and a majority group (white Americans).
Consistent with the predictions of the ethnic culture hypothesis, they found that non-minority group members were consistently more symptomatic than members of the two ethnic minority groups.

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23
Q

EVALUATION/DISCUSSION OF VALIDITY:

A

Research support for gender bias in diagnosis
The consequences of co-morbidity:
Differences in prognosis

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24
Q

Research support for gender bias in diagnosis

A

Loring and Powell (1988) found evidence of gender bias among psychiatrists in the diagnosis of schizophrenia.
They randomly selected 290 male and female psychiatrists to read two case vignettes of patients’ behaviour.
These psychiatrists were asked to offer their judgement using standard diagnostic criteria.
When the patients were described as ‘males’ or no information was given about their gender, 56% of the psychiatrists gave a diagnosis of schizophrenia.
However, when the patients were described as ‘female’, only 20% were given a diagnosis of schizophrenia.
This gender bias was not as evident among the female psychiatrists, suggesting that diagnosis is influenced not only by the gender of the patient but also the gender of the clinician.

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25
Q

The consequences of co-morbidity:

A

A number of studies have examined single co-morbidities with schizophrenia, but these studies have usually involved only relatively small sample sizes.
By contrast, Weber et al. (2009) looked at nearly 6 million hospital discharge records, finding evidence of many co-morbid non-psychiatric diagnoses.
Many patients with a primary diagnosis of schizophrenia were also diagnosed with medical problems including asthma, hypertension and type 2 diabetes.
The authors concluded that the very nature of a diagnosis of a psychiatric disorder is that patients tend to receive a lower standard of medical care, which in turn adversely affects the prognosis for patients with schizophrenia.

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26
Q

Differences in prognosis:

A

In the same way that people diagnosed as schizophrenic rarely share the same symptoms, likewise there is no evidence that they share the same outcomes.
The prognosis for patients diagnosed with schizophrenia varies with about 20% recovering their previous level of functioning, 10% achieving significant and lasting improvement, and about 30% showing some improvement with intermittent relapses.
A diagnosis of schizophrenia, therefore, has little predictive validity - some people never appear to recover from the disorder, but many do.
What does appear to influence outcome, therefore, is more to do with gender (Malmberg et al., 1998) and psychosocial factors such as social skills, academic achievement and family tolerance of schizophrenic behaviour (Harrison et al., 2001).

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27
Q

Biological explanations:

A

emphasise the role of inherited factors and dysfunction of brain activity the development of a behaviour or mental disorder

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28
Q

Neural correlates:

A

Changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour or mental disorder.

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29
Q

GENETIC FACTORS:

A

Family studies:
Twin studies:
Adoption studies:

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30
Q

Family studies:

A

Family studies have established that schizophrenia is more common among biological relatives of a person with schizophrenia, and that the closer the degree of genetic relatedness, the greater the risk.
For example, in Gottesman’s study, children with two schizophrenic parents had a concordance rate of 46%, children with one schizophrenic parent a rate of 13%, and siblings (where a brother or sister had schizophrenia) a concordance rate of 9%.

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31
Q

Twin studies:

A

If monozygotic (MZ - genetically identical) twins are more concordant (similar) than dizygotic (DZ - who share only 50% of their genes), then this suggests that the greater similarity is due to genetic factors.
Joseph (2004) calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.

32
Q

Adoption studies:

A

Because of the difficulties of disentangling genetic and environmental influences for individuals who share genes and environment, studies of genetically related individuals who have been reared apart are used.
Probably the most methodologically sound study of this type was carried out by Tienari et al. (2000) in Finland.
Of the 164 adoptees whose biological mothers had been diagnosed with schizophrenia, 11 (6.7%) also received a diagnosis of schizophrenia, compared to just four (2%) of the 197 control adoptees (those born to non-schizophrenic mothers).
The investigators concluded that these findings showed that the genetic liability to schizophrenia had been ‘decisively confirmed.

33
Q

The dopamine hypothesis:

A

claims that an excess of dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia.
Schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing.

34
Q

The key role played by dopamine was highlighted in two sources of evidence:

A

Drugs that increase dopaminergic activity:
Amphetamine is a dopamine agonist, i.e. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter.
‘Normal’ individuals exposed to large doses of dopamine releasing drugs such as amphetamines can develop the characteristic symptoms of a schizophrenic episode, which generally disappear with abstinence from the drug.

Drugs that decrease dopaminergic activity
Although there are many different types of antipsychotic drugs, they all block the activity of dopamine in the brain.
By reducing activity in the neural pathways of the brain that use dopamine as the neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions.
The fact that these drugs (known as dopamine antagonists because they block its action) alleviated many of the symptoms of schizophrenia strengthened the case for the important role of dopamine in this disorder.

35
Q

The revised dopamine hypothesis:

A

Davis and Kahn (1991) proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway.
The negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway).
For example, Patel et al. (2010), using PET scans to assess dopamine levels in schizophrenic and normal individuals, found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls.

36
Q

Specific brain areas involved in schizophrenia:

A

The prefrontal cortex - (PFC)
The hippocampus:
Grey matter:
White matter

37
Q

The prefrontal cortex - (PFC)

A

the main area of the brain involved in executive control (i.e. planning, reasoning, and judgement), and research has shown that this is impaired in schizophrenia patients (Weinberger and Gallhofer, 1997).
It has been hypothesised that the cognitive symptoms of schizophrenia result from deficits within the PFC and its connections with other areas of the brain, particularly the hippocampus.

38
Q

The hippocampus:

A

The hippocampus is an area of the brain in the temporal lobe.
Several studies have reported anatomical changes in the hippocampus in schizophrenia patients (Conrad et al., 1991).
Deficits in the nerve connections between the hippocampus and the prefrontal cortex have been found to correlate with the degree of working memory impairments, a central cognitive impairment in schizophrenia (Mukai et al., 2015).
Goto and Grace (2008) suggest that hippocampal dysfunction might also influence levels of dopamine release in the basal ganglia, indirectly affecting the processing of information in the prefrontal cortex.

39
Q

Grey matter:

A

Individuals with schizophrenia have a reduced volume of grey matter (mostly cell bodies and unmyelinated axons) in their brain, especially in the temporal and frontal lobes.
Hartberg et al. have also found that many people with schizophrenia, particularly those displaying negative symptoms, have enlarged ventricles (brain cavities filled with cerebrospinal fluid).
Enlarged ventricles are thought to be a consequence of nearby parts of the brain not developing properly or being damaged.
Cannon et al. (2014) found that individuals at high clinical risk who developed schizophrenia showed a steeper rate of grey matter loss and a greater rate of expansion of brain ventricles compared to those who did not develop schizophrenia.

40
Q

White matter

A

White matter is found in the brain and spinal cord and is made up of nerve fibres covered in myelin.
Myelin creates an insulating sheath around nerve fibres and helps to conduct information quickly through the central nervous system, enabling efficient information processing.
Du et al, has found reduced myelination of white matter pathways in schizophrenic patients, compared to healthy controls. This is particularly the case in the neural pathways between the PFC and the hippocampus.

41
Q

EVALUATION/DISCUSSION OF GENETIC FACTORS:

A

MZ twins encounter more similar environments
Adoptees may be selectively placed:

42
Q

MZ twins encounter more similar environments

A

A crucial assumption underlying all twin studies is that the environments of monozygotic (MZ) twins and dizygotic (DZ) twins are equivalent.
However, as Joseph (2004) points out, MZ twins are treated more similarly, encounter more similar environments and experience more ‘identity confusion’ (i.e. frequently being treated as ‘the twins’ rather than as two distinct individuals) than DZ twins.
This suggests that differences in concordance rates between MZ and DZ twins reflect nothing more than environmental differences that distinguish the two types of twin.

43
Q

Adoptees may be selectively placed:

A

An assumption of adoption studies is that adoptees are not ‘selectively placed, i.e. adoptive parents who adopt children with a schizophrenic biological parent are no different to adoptive parents who adopt children whose background is normal.
One of the largest adoption studies of schizophrenia took place in Oregon (Heston, 1966), where it was assumed that procreation by any person admitted to a mental hospital would produce offspring with an inherited tendency to ‘feeble-mindedness, insanity and degeneracy’
It is extremely unlikely that the children born to women with schizophrenia would have been placed into the same type of adoptive families as children without such a background (Joseph, 2004).
This, coupled with other problems with twin and adoption studies, suggests we cannot accept their conclusions about the role of genetics in schizophrenia.

44
Q

EVALUATION/DISCUSSION OF NEURAL CORRELATES:

A

The dopamine hypothesis: Evidence from treatment
Challenges to the dopamine hypothesis:
Support for the influence of grey matter deficits:

Implications for treatment:

45
Q

The dopamine hypothesis: Evidence from treatment

A

Much of the evidence supporting the dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain.
Leucht et al. (2013) carried out a meta-analysis of 212 studies.
They concluded that all the antipsychotic drugs tested in these studies were significantly more effective than placebo in the treatment of positive and negative symptoms, achieved by reducing the effects of dopamine.
These findings also challenge the classification of antipsychotics into typical and atypical groupings because differences in their effectiveness were only small.

46
Q

Challenges to the dopamine hypothesis

A

Noll (2009) claims there is strong evidence against both the original dopamine hypothesis and the revised dopamine hypothesis.
He argues that antipsychotic drugs do not alleviate hallucinations and delusions in about one-third of people experiencing these symptoms.
Noll also points out that, in some people, hallucinations and delusions are present despite levels of dopamine being normal.
This suggests that, rather than dopamine being the sole cause of positive symptoms, other neurotransmitter systems, acting independently of the dopaminergic system, may also produce the positive symptoms associated with schizophrenia.

47
Q

Support for the influence of grey matter deficits:

A

Support for the significance of grey matter deficits in schizophrenia comes from a meta-analysis by Vita et al. (2012).
They analysed the results of 19 studies.
Patients with schizophrenia, compared with healthy controls, showed a higher reduction in cortical grey matter volume over time.
This pattern of grey matter reduction was specific to discrete cortical areas in the frontal, temporal and parietal lobes.
This loss of grey matter was especially active in the first stages of the disease, consistent with the relatively early onset of schizophrenia (late teens/early 20s).

48
Q

Implications for treatment:

A

The importance of neural correlates for schizophrenia is that early intervention might prevent development of the later stages of this disorder.
This concept of’ treatment as prevention’ is seen in the North American Prodrome Longitudinal Study (Addington et al., 2015), which uses a number of different assessments, including neuroimaging, to predict who will develop psychoses such as schizophrenia.
With a better understanding of how schizophrenia develops, researchers can detect loss of brain tissue early and treat at-risk patients before psychosis develops.

49
Q

Family dysfunction:

A

The presence of problems within a family that contribute to relapse rates in recovering schizophrenics, including lack of warmth between parents and child, dysfunctional communication patterns and parental overprotection.

Double bind theory:
Expressed emotion:

50
Q

Double bind theory:

A

Gregory Bateson et al. (1956) suggest that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia.
For example, if a mother tells her son that she loves him, yet at the same time turns 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 on the non-verbal level.
The child’s ability to respond to the mother is incapacitated by such contradictions because one message invalidates the other.
These interactions prevent the development of an internally coherent construction of reality, and in the long run this manifests itself as schizophrenic symptoms (e.g. flattened affect and withdrawal).
These ideas were echoed in the work of psychiatrist R.D. Laing, who argued that what we call schizophrenia is actually a reasonable response to an insane world

51
Q

Expressed emotion:

A

Another family variable associated with schizophrenia is a negative emotional climate or, more generally, a high degree of expressed emotions.
Expressed emotion (EE) is a family communication style in which members of the family of a psychiatric patient talk about that patient in a critical or hostile manner or in a way that indicates emotional over-involvement or over-concern with the patient or their behaviour.
For example, research by Kuipers et al. (1983) found that high EE relatives talk more and listen less.
High levels of EE are most likely to influence relapse rates (i.e. an increase in symptoms).
A patient returning to a family with high EE is about four times more likely to relapse than a patient whose family is low in EE (Linszen et al., 1997).
This suggests that people with schizophrenia have a lower tolerance for intense environmental stimuli, particularly intense emotional comments and interactions with family members.
It appears that the negative emotional climate in these families arouses the patient and leads to stress beyond his or her already impaired coping mechanisms, thus triggering a schizophrenic episode.
In contrast, a family environment that is relatively supportive and emotionally undemanding may help the person with schizophrenia to reduce their dependence on antipsychotic medication and help reduce the likelihood of relapse (Noll, 2009)

52
Q

COGNITIVE EXPLANATIONS:

A

Compared to normal controls, research has found evidence of dysfunctional thought processing in people with schizophrenia, i.e. they process information differently to those without the disorder.
Cognitive explanations of schizophrenia emphasise the role of dysfunctional thought processing particularly evident in those who display the characteristic positive symptoms of schizophrenia such as delusions and hallucinations.

53
Q

Cognitive explanations of delusions:

A

During the formation of delusions, the patient’s interpretations of their experiences are controlled by inadequate information processing.
A critical characteristic of delusional thinking is the degree to which the individual perceives him or herself as the central component in events (egocentric bias) and so jumps to conclusions about external events.
This is manifested in the patient’s tendency to relate irrelevant events to themselves and consequently arrive at false conclusions.
Muffled voices are interpreted as people criticising them, and flashes of light are a signal from God.
Delusions in schizophrenia are relatively impervious to reality testing, in that patients are unwilling or unable to consider that they may be wrong (Beck and Rector, 2005).
They are considered to have impaired insight, an inability to recognise cognitive distortions and substitute more realistic explanations for events.

54
Q

Cognitive explanations of hallucinations:

A

Why are patients with schizophrenia predisposed to experience some thoughts as external ‘voices’?
Hallucinating individuals focus excessive attention on auditory stimuli (hypervigilance) and so have a higher expectancy for the occurrence of a voice than normal individuals.
Aleman (2001) suggests that hallucination-prone individuals find it difficult to distinguish between imagery and sensory-based perception
For these individuals, the inner representation of an idea (e.g. ‘What other people think of me) can override the actual sensory stimulus and produce an auditory image (‘ He is not a good person’) that is every bit as real as the transmission of actual sound.
Hallucinating patients with schizophrenia are significantly more likely to misattribute the source of a self-generated auditory experience to an external source than are non-hallucinating patients with schizophrenia (Baker and Morrison, 1998).
These errors are not corrected by disconfirming evidence because patients with schizophrenia do not go through the same processes of reality testing (such as checking external sources) that others would do.

55
Q

EVALUATION/DISCUSSION OF FAMILY DYSFUNCTION

A

Family relationships:
Double bind theory:
Individual differences in vulnerability to EE:

56
Q

Family relationships:

A

The importance of family relationships in schizophrenia was demonstrated in an adoption study by Tienari et al. (1994).
In this study, adopted children who had schizophrenic biological parents were more likely to become ill themselves than were children with non-schizophrenic biological parents.
However, this difference emerged only in situations where the adopted family itself was rated as disturbed.
This suggests that the illness only manifests itself under appropriate environmental conditions, therefore genetic vulnerability alone is not sufficient.

57
Q

Double bind theory:

A

There is some evidence to support this particular account of how family relationships may lead to schizophrenia.
For example, Berger (1965) found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. However, other studies are less supportive.
Liem (1974) measured patterns of parental communication in families with a schizophrenic child and found no difference when compared to normal families.
Despite these inconsistencies in research support, Gibney (2006) claims that the real value of double bind theory is that it led to the development of family therapy.
If interactions could be problematic and pathology producing, then they might also be organised more constructively and so become health producing.

58
Q

Individual differences in vulnerability to EE:

A

Not all patients who live in high EE families relapse, and not all patients who live in low EE homes avoid relapse.
Research has found individual differences in stress response to high EE-like behaviours.
Altorfer et al. (1998) found that one-quarter of the patients they studied showed no physiological responses to stressful comments from their relatives.
Vulnerability to the influences of high EE may also be psychologically based.
Lebell et al. (1993) claims that how patients appraise the behaviour of their relatives is important.
In cases where high EE behaviours are not perceived as being negative or stressful, patients can do well regardless of how the family environment is objectively rated.
This shows that not all patients are equally vulnerable to high levels of expressed emotion within the family environment.

59
Q

EVALUATION/DISCUSSION OF COGNITIVE EXPLANATIONS:

A

Supporting evidence for the cognitive model of schizophrenia:

Support from the success of cognitive therapies:

An integrated model of schizophrenia:

60
Q

Supporting evidence for the cognitive model of schizophrenia:

A

Sarin and Wallin (2014) found supporting evidence for the claim that the positive symptoms of schizophrenia have their origins in faulty cognition.
For example, delusional patients were found to show various biases in their information processing, such as jumping to conclusions and lack of reality testing.
Likewise, schizophrenic individuals with hallucinations were found to have impaired self-monitoring and also tended to experience their own thoughts as voices.
A consequence of this is that a therapist can use this information when he or she chooses techniques for the treatment of patients.

61
Q

Support from the success of cognitive therapies:

A

The claim that the symptoms of schizophrenia have their origin in faulty cognition is reinforced by the success of cognitive-based therapies for schizophrenia.
The effectiveness of cognitive behavioural therapy for psychosis (CBTp) was demonstrated in the National Institute for Health and Care Excellence (NICE) review of treatments for schizophrenia (NICE, 2014).
This review found consistent evidence that, when compared with treatment by antipsychotic medication, cognitive behavioural therapy was more effective in reducing symptom severity and improving levels of social functioning.
This supports the view that faulty cognitions have an important causal influence in the development of schizophrenia.

62
Q

An integrated model of schizophrenia:

A

A problem with the cognitive model of schizophrenia is that it deals adequately with one aspect of the disorder (e.g. cognitive impairment) but fails to explain, or ignores, other aspects (e.g. social adversity).
Howes and Murray (2014) addressed this problem with an integrated model of schizophrenia.
Early vulnerability factors (e.g. genes, birth complications, etc.), together with exposure to significant social stressors (e.g. social adversity), sensitises the dopamine system, causing it to increase the release of dopamine.
Biased cognitive processing of this increased dopamine activity results in paranoia and hallucinations and eventually the development of a psychosis.
By putting the impact of life events at the centre of the process leading to schizophrenia, this model fits in with more recent research showing that exposure to significant social stressors is associated with a considerable increase in risk of developing this disorder.

63
Q

Interactionist approach:

A

A way to explain the development of behaviour in terms of a range of factors, including both biological and psychological ones.
Most importantly such factors don’t simply add together but combine in a way that can be predicted by each one separately i.e. they interact.

64
Q

Diathesis-stress model:

A

An interactionist approach to explaining behaviour.
For example schizophrenia is explained as the result of both an underlying vulnerability (diathesis) and a trigger (stressor), both of which are necessary for the onset of schizophrenia.
In early versions of the diathesis-stress model, vulnerability was genetic and triggers were psychological.
Nowadays both genes and trauma are seen as diathesis, and stress can be psychological or biological in nature.

65
Q

The interactionist approach

A

Put simply the interactionist approach (also sometimes called the ‘biosocial approach’) is an approach that acknowledges that there are biological, psychological and social factors in the development of schizophrenia.
Biological factors include: genetic vulnerability and neurochemical and neurological abnormality.
Psychological factors include stress, for example, resulting from life events and daily hassles including social factors such as poor quality interactions in the family.

66
Q

The diathesis-stress model:

A

The diathesis-stress model is one way to present an interactionist approach.
Diathesis means vulnerability.
In this context stress simply means a negative experience.
The diathesis-stress model says that both a vulnerability to schizophrenia and a stress-trigger are necessary in order to develop the condition.
One or more underlying factors make a person particularly vulnerable to developing schizophrenia but the onset of the condition is triggered by stress.

67
Q

Meehl’s model:

A

In the original diathesis-stress model (Meehl 1962) diathesis (vulnerability) was entirely genetic, the result of a single ‘schizogene’.
This led to. the idea of a biologically based schizotypic personality, one characteristic of which is sensitivity to stress.
According to Paul Meehl, if a person does not have the schizogene then no amount of stress would lead to schizophrenia.
However, in carriers of the gene, chronic stress through childhood and adolescence, in particularly the presence of a schizophrenogenic mother could result in the development of the condition.

68
Q

Modern understanding of diathesis:

A

One way in which our understanding of diathesis has changed is that it is now clear that many genes each appear to increase genetic vulnerability only slightly, there is no single ‘schizogene’ (Ripke et al. 2014).
Modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma (Ingram and Luxton 2005) - so trauma becomes the diathesis rather than the stressor.
John Read et al. (2001) proposed neurodevelopmental model in which early trauma alters the developing brain.
Early and severe enough trauma, such as child abuse, can seriously affect many aspects of brain development.
For example the hypothalamic-pituitary-adrenal (HPA) system can become overactive, making a person much more vulnerable to later stress.

69
Q

Modern understanding of stress:

A

In the original diathesis-stress model of schizophrenia, stress was seen as psychological in nature, in particular related to parenting.
Although psychological stress, including that resulting from parenting may still be considered important, a modern definition of stress (in relation to the diathesis-stress model) includes anything that risks triggering schizophrenia (Houston et al. 2008).
Much of the recent research into factors triggering an episode of schizophrenia has concerned cannabis use.
In terms of the diathesis-stress more cannabis is a stressor because it increases the risk of schizophrenia by up to seven times according to dose.
This may be because cannabis interferes with the dopamine system.
However, most people do not develop schizophrenia after smoking cannabis
presumably because they lack the requisite vulnerability factors.

70
Q

Treatment according to the interactionist model:

A

The interactionist model of schizophrenia acknowledges both biological and psychological factors in schizophrenia and is therefore compatible with both biological and psychological treatments.
In particular the model is associated with combining; antipsychotic medication and psychological therapies, most commonly CBT.
Douglas Turkington et al. (2006) point out that it is perfectly possible to believe: in biological causes of schizophrenia and still practise CBT to relieve psychological symptoms.
However, this requires adopting an interactionist model - it is not possible to adopt a purely biological approach and tell people diagnosed with schizophrenia that their condition is purely biological and that there is no psychological significance to symptoms, and then to simultaneously treat them with CBT.
In Britain it is increasingly standard practice to treat people diagnosed with schizophrenia with a combination of antipsychotic drugs and CBT.
In the US there is more of a history of conflict between psychological and biological models of schizophrenia and this may have led to slower adoption of an interactionist approach
Thus medication without an accompanying psychological treatment is more com in the US than in the UK.

71
Q

Key study: Tienari et al. (2004):

A

This study tested the hypothesis that genetic factors moderate susceptibility to environmental risks associated with adoptive family functioning.

72
Q

Procedure:
Key study: Tienari et al. (2004):

A

Hospital records were reviewed for nearly 20,000 women admitted to Finnish psychiatric hospitals between 1960 and 1979, identifying those who had been diagnosed at least once with schizophrenic or paranoid psychosis.
The list was checked to find those mothers who had one or more of their offspring adopted away.
The resulting sample of 145 adopted-away offspring (the high-risk group) was then matched with a sample of 158 adoptees without this genetic risk (the low-risk group).
Both groups of adoptees were independently assessed after a median interval of 12 years, with a follow-up after 21 years.
Psychiatrists also assessed family functioning in the adoptive families using the OPAS (in English this translates to the ‘Oulu Family Rating Scale).
This scale measures families on various aspects of functioning such as parent-offspring conflict, lack of empathy and insecurity.
The interviewing psychiatrists were kept blind as to the status of the biological mother (i.e. schizophrenia or no schizophrenia).

73
Q

Findings:

A

Of the 303 adoptees, 14 had developed schizophrenia over the course of the study.
Of these 14, 11 were from the high-risk group (i.e. those with mothers previously diagnosed with schizophrenia or paranoid psychoses) and three were from the low-risk group (i.e. the control group adoptees).
However, being reared in a ‘healthy’ adoptive family (low OPAS ratings) appeared to have a protective effect even for those at high genetic risk for schizophrenia.
High-genetic-risk adoptees reared in families with low OPAS ratings were significantly less likely to have developed schizophrenia than high-genetic-risk adoptees reared in families with high OPAS ratings.
In adoptees at high genetic risk of schizophrenia, but not in those at low genetic risk, adoptive-family stress was a significant predictor of the development of schizophrenia.

74
Q

EVALUATION/DISCUSSION:

A

Diatheses may not be exclusively genetic:
Urban environments are not necessarily more stressful:
Limitations of the Tienari et al. study:

75
Q

Diatheses may not be exclusively genetic:

A

Most diathesis-stress models emphasise ‘vulnerability’ in terms of genetic influences alone, which are assumed to cause neurochemical abnormalities that, in turn, result in an increased risk for schizophrenia.
However, this increased risk can also result from brain damage caused by environmental factors.
Verdoux et al. (1998) estimated that the risk of developing schizophrenia later in life for individuals who have experienced obstetric complications at birth (e.g. prolonged labour, which can cause oxygen deprivation) is four times greater than those who experience no such complications.
These findings suggest that brain damage can play a role in the development of schizophrenia, although some researchers claim that birth complications and neurological abnormalities are caused by an already compromised foetus (Weinberger, 1995).

76
Q

Urban environments are not necessarily more stressful:

A

The Vassos et al. study on the previous page suggested that living in densely populated urban environments was a significant stress factor for schizophrenia.
However, not all research has agreed with this finding.
Romans-Clarkson et al. (1990) found no urban-rural differences in mental health among women in New Zealand.
Other studies (e.g. Paykel et al., 2000), although finding evidence of urban-rural differences, showed that these differences disappeared after adjusting for the socio-economic differences for the two groups.
This suggests that, although social adversity may well be a significant trigger for the onset of schizophrenia, the claim that social adversity and urbanisation are synonymous is likely to be an over-simplification.

77
Q

Limitations of the Tienari et al. study:

A

Researchers in the Tienari et al. study identified a number of limitations of their study, particularly in the assessment of adoptive family functioning.
For example, when psychiatrists assessed stress in the adoptive family using the OPAS scale, they were assessing family functioning only at one given point in time. Tienari et al. acknowledged that this fails to reflect developmental changes in family functioning over time.
Observing reciprocal interactions between the adoptive family and the adoptees makes it impossible to determine how much of the stress observed is assigned to the family and how much is actually caused by the adoptees themselves.