Schizophrenia Flashcards
(47 cards)
1
Q
Psychosis
A
A term used to describe a Sever health problem where the individual loses contact with reality.
2
Q
Stirling and Hellwell (1999)
A
25% of sufferers will ‘get better’ after one episode; 50,65% will improve but have bouts of illness. The remainder will have persistent difficulties
3
Q
Classification of schizophrenia
A
ICD-10: recognises a range of subtypes
DSM-V: used to also recognise the subtypes but the most recent DSM-V have dropped these
4
Q
Disorganised schizophrenia
A
The persons behaviour is generally disorganised and not goal directed. Symptoms include thought disturbances, and absence of expressed emotion, large mood swings, incoherent speech and a loss of interest in life (social withdrawal
- usually diagnosed in adolescence / young childhood
5
Q
Catatonic schizophrenia
A
Diagnosed if the patient has severe motor abnormalities. Patients gesture repeatedly. Often involves doing the opposite of what is required of them. Main feature is immobility for hours at a time.
6
Q
Echolalia
A
The involuntary parrot-like repetition of a word or phrase spoken by another person
7
Q
Echopraxia
A
The involuntary imitation of repetition of the body movements of another person, sometimes practiced by catatonic patients
8
Q
Paranoid schizophrenia
A
Involves delusions of various kinds: however, the patent remains emotionally responsive. They are more alert than patient with other types of schizophrenia, people who are diagnosed with this schizophrenia tend to be argumentative.
9
Q
Undifferentiated schizophrenia
A
Broad, ‘catch all’ category which includes patients who do not clearly belong within any other category. They show symptoms of schizophrenia but do not fit into other types.
10
Q
Residual schizophrenia
A
Describes people who have symptoms not strong enough to merit putting them in other categories, consist of patients who are experiencing mild symptoms
11
Q
Positive symptoms
A
+ hallucinations
+ delusions
+ disorganised speech / behaviour
12
Q
Negative symptoms
A
- avolition
- speech poverty
- anhedonia
13
Q
Secondary symptoms
A
- depression
- employment loss
- relationship breakdown
14
Q
Evaluation of types of schizophrenia
A
- lacks validity- Rosenhan ‘on being sane in insane places’. Psychiatrists struggle to distinguish between real and pseudo patients. Difficult to remove the label of schizophrenia.
- reliability- consistency of diagnosis. An important measure of reliability is inter rated reliability. In relation to diagnosis, this means that different clinicians make identical, independent diagnosis of the same patient. Cheniaux (2009) had 2 psychiatrists independently diagnose 100 patients using DSM and ICD criteria
+ reliability- consistency of diagnosis. Does private common language to practitioners which leads to a better understanding of the disorder. Generally suggests that reliability diagnosis had improved as classic actions systems have been updated - co-morbidity affects reliability and validity. The occurrence of 2 illnesses or conditions occurring simultaneously can create a problem with reliability of diagnosis. Symptoms can overlap
- gender bias in diagnosis. Longnecker (2010) men have been diagnosed more than women. Men are more genetically vulnerable to developing disorders. Many other studies
- cultural bias in diagnosis. The tendency to diagnose people from other cultures as suffering from schizophrenia. 69% American psychiatrists have diagnosed a patient whereas 2% in Britain
15
Q
Genetic vulnerability
A
Has been proposed that there is a genetic component to schizophrenia which predisposes some individuals to illness. Whether a person develops schizophrenia is at least partly due to their genes. May explain why patients often have other family members with schizophrenia.
16
Q
Family studies
A
One very large scale family study was carried out by Gottesman. Findings showed greater degree of genetic relatedness, greater risk of schizophrenia.
17
Q
Twin studies
A
Gottesman and Shields (1962) found concordance rate for schizophrenia in MZ twins was 48% compared to 17% for DZ twins. Suggested schizophrenia is inherited through shared genes, Joseph (2004) showed concordance rate of 40.4% MZ and 7.4% DZ
18
Q
Adoption studies
A
Heston (1966) compared 47 adopted children whose biological mother had schizophrenia with a control group of adopted children with no history of schizophrenia in their biological family. None of the control group was diagnosed with illness: 16% of offspring of mothers with schizophrenia were diagnosed.
- Tienari (2000) adoption study-11% of 164 adoptees whose mothers have schizophrenia
19
Q
Candidate gene
A
- schizophrenia is thought to be polygenic
- Ripke (2014) completed a study combining all data from a genome wide study of schizophrenia. 37,000 patients were compared to 113,000 controls; 108 separate genetic variations were associated with an increased schizophrenia risk
20
Q
The dopamine hypothesis
A
- an excess of the neurotransmitter dopamine has been implicated in the symptoms of schizophrenia.
- older hypothesis- hyperdopaminergia in the sub cortex. High dopamine in sub cortex. Express receptors in Broca’s area. Poverty of speech. Auditory hallucinations
- newer hypothesis-hypodopaminergia in the sub cortex. Abnormal dopamine systems. Goldman- Rakic (2004) identified the role for low levels of dopamine in prefrontal cortex. Negative symptoms
21
Q
Evaluation of dopamine hypothesis
A
- amphetamines: stimulates nerve cells containing dopamine causing the synapse to be ‘flooded’ - large dieses of the drug can cause hallucinations and delusions of schizophrenic episode
- cocaine also increases the levels of dopamine in the brain an con cause the positive symptoms of schizophrenia and exaggerate them in people who already have the disorder
22
Q
Neural correlates of schizophrenia negative schizophrenia
A
- activity in the Ventura striatum has been linked to the development of avolition
- the ventral striatum are believe to be particularly involved in the anticipation of a reward for certain actions
- Juckel (2006) found grey matter was smaller in schizophrenia compared to controls
- negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms
23
Q
Neural correlates of positive symptoms
A
- Allen (2007)
- reduced activity in the superior temporal gyrus and anterior cingulate gyrus have been linked to the development of auditory hallucinations
- patients experiencing auditory hallucinations showed lower activation levels in these areas than controls
- therefore reduced activity in these areas of the brain is a neural correlates of auditory hallucinations
24
Q
Evaluation of neural correlates of schizophrenia
A
- people with schizophrenia have abnormally large ventricles in the brain. Ventricles are fluid filled cavities. This means the brains of people with schizophrenia are lighter than normal
+ multiple sources of evidence for genetic susceptibility. Genetic links, adoption studies, genetic variation: - mixed evidence for the dopamine hypothesis. Curran (2004) found that dopamine agonists increase the levels of dopamine and can make the symptoms of schizophrenia worse
- Tauscher (2014) found antipsychotic drugs reduce the levels of dopamine
- Lindsroroem (1999) found the chemicals needed to produce dopamine are taken up faster in the brains of people with schizophrenia- suggesting they produce more dopamine
- Moghadam and Javitt ( 2012) have found the evidence for the roles of a neurotransmitter called glutonate
- findings are inconsistent therefore inconclusive
+ the role of mutation. Evidence of mutation causes by radiation, poison etc. - role of psychological environment is important but unclear
25
Typical antipsychotics
The first generation of antipsychotics. They work as dopamine antagonists
26
Atypical antipsychotics
Second generation of antipsychotics. Typically target a range of neurotransmitters such as dopamine and serotonin
27
Typical antipsychotic - Chlorpromazine
- taken daily with a dose up to 1000mg typical does are 400-800mg and this has decreased over the last 50 years
- strong association with dopamine hypothesis
- is a sedative. Used to calm patients especially when added to the body
28
Atypical antipsychotics - Clozapine
- Developed in 1960s and have trialed in 1970s
- daily dosage of 300-450mg
- used when other treatments have failed to help mood and reduce depression and anxiety
- binds to dopamine receptors, similarly to chlorpromazine however it also acts in serotonin and glutonate receptors
29
Atypical antipsychotics- Risperidone
- Developed in 1990s as an attempt to reduce side effects of clozapine
- smaller doses are given from 4-8mg up to 12mg per day
- binds to dopamine and serotonin receptors. However it has a stronger binding effect on dopamine than clozapine and is effective in smaller doses
30
Serious side effects
- some side effects are mild but they can be fatal - dizziness, agitation, sleepiness, etc
- neuroleptic malignant syndrome: where the drugs block dopamine in the hypothalamus - high temp, coma, etc
- typical antipsychotics produce- Tardive dyskinesia (uncontrollable movements of the face, lips, tounge etc
31
Evaluation of drug therapies
- data from trials showed chlorpromazine was associated with better overall functioning and reduced symptom severity
- use of antipsychotics depends on the dopamine hypothesis. Much higher levels of dopamine activity in the sub cortex. However not a complete explanation for schizophrenia. Léveles were too low rather than too high
- problems with the evidence. Healy (2012) has suggested over publication has lead to misleading positive
- they help patients with schizophrenia, due to the calming effects
32
Family relationships
- The impact of family relationships has been put forward as a possible explanation for schizophrenia
- psychologists have attempted to link schizophrenia to childhood and adulthood experiences in a dysfunctional family
33
Schizophrenogenic mother
- early theorist influenced by Freudian ideas, thought a ‘schizophrenogenic mother’, who was cold, dominant and created conflict, caused schizophrenia to emerge in the child
- these mothers were said to be rejecting overprotective, self sacrificing, moralistic about sex
- the distrust, resentful ness and instability caused by such a parent leads to distrust, turning into paranoid delusions and then schizophrenia
34
Double bind theory
- Bateson (1972) agreed family climate is important in development of schizophrenia but communication style within the family is just as important
- children who receive contradictory messages ‘double binds’ are more likely to get schizophrenia. Prevents the development of coherent constructional reality, manifesting itself into a symptom of schizophrenia
35
Expressed emotion (EE)
- explanation for relapse in patients with schizophrenia although it’s been suggested it may be a source of stress that can trigger the onset of schizophrenia
- family variable associated with schizophrenia is a negative emotional climate, or more generally a high degree of EE. EE is a family communication style where members talk about the patient in a hostile manner
- involves: critical comments, hostility, over emotional involvement. If these are high relapse risk is high
36
Cognitive explanation
- schizophrenia is characterised by disturbance in language, attention, thought and perception
- this had led cognitive psychologists to explain the disorder as a result of dysfunctional thought processing
- lower than usual levels of processing suggest that cognition is likely to be impaired
37
Dysfunction in meta-representation Frith (1992)
- Frith suggested that people with schizophrenia fail to monitor their own thoughts correctly, misattributing them to the outside world
- when a person hears voices it is actually their own inner speech being misinterpreted, however, sufferers may believe that someone or something in the external world is communicating with them
- such processing problems in people with schizophrenia are sometimes referred to as alien control symptoms because the suffer feels as if the external forces are influencing their thoughts and actions and they have no personal control
38
Dysfunction in central control
- the cognitive ability to suppress automatic responses while we perform deliberate actions
- disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by others
- derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these
39
Sociocultural theory
- Harrison (2001) people born in the deprived areas were more likely to develop schizophrenia. Poverty unemployment and crowding
- correlational results that doesn’t show cause and effect
- the social drift hypothesis is more likely to be in deprived areas because having schizophrenia gives them a lower social status
40
Family dysfunction as a risk factor (support and weaknesses)
+ read (2005) reviews 46 studies of child abuse and schizophrenia and concluded 69% of adult women - in patients with a diagnosis of schizophrenia had a history of physical or sexual abuse or both. 54% of men
+ Berry (2008) adults with insecure attachments are more likely to have schizophrenia
- information was gathered after the development of symptoms and the diagnosis of schizophrenic may have distorted parents recall
- Tiernari (2004) investigated children following a childhood experience to see if these experiences predicted any adult characteristics
41
Psychological explanations evaluation
- schizophrenogenic mother. Only a small percentage of people who fit the schizophrenic mother had schizophrenic children. Also many schizophrenic people had mothers who didn’t fit the criteria
- double bind theory. Evidence may not be reliable as parents recall may be affected by their schizophrenia. Liem (1994) and Hall + Levin (1980) found no difference in the patterns of parental communication in families with a child with schizophrenia in comparison to normal families
+ Family dysfunction theory. Brown (1966) EE: families where communications are commonly to do with criticism, hospitality and disapproval are said to have high EE. In families where EE levels were higher, people with schizophrenia were more likely to refute for treatment (58%) compared to only 10% in low EE families
- however unclear whether EE is a casual agent in the relapse rates or just a reaction to patients behaviour. More evident in western families
- weak evidence for family based explanations
+ strong evidence for dysfunctional information processing. Stirling (2006) compared 30 patients with schizophrenia to 18 controls on a range of cognitive tasks. Indicated patients took over twice as long as controls to name colours
- cognitive approach. Does describe how information proffering is affected in schizophrenia but doesn’t provide a distal cause explanation
- biological factors are not adequately considered. Biological and psychological factors can make sane symptoms. Realises question weather both are actually schizophrenia
42
Psychological therapies for schizophrenia
- token economy
- family therapy
- CBT
43
Evaluation of psychological therapies
- Jauhar (2014) reviewed the results of 34 studies of CBT. Concluded that CBT had a small but significant effect on positive and negative symptoms
- Pharoah (2010) reviewed family therapy. Moderate evidence that it significantly reduces hospital readmission and improved quality of life
- token economy. Mcmonagle and Sultana (2009) found only three studies where patients were randomly allocated to conditions with a total of 110 patients. Only 1/3 studies showed improvement in symptoms. Schizophrenia remains one of the harder mental health problems to treat
- ethical issues. CBT may involve challenging a persons paranoia, but at what point does this interfere with an individuals freedom of thought. These issues are weaknesses of psychological treatments
+ alternative psychological treatments. NICE recommends therapy, particularly for negative symptoms. Explore the patients inner world in a non threatening way. Compliance was high but not enough evidence of effectiveness
44
Meehl’s model
- Believed diathesis was entirely genetic, the result of a single ‘schizogene’
- this led to the development of a biologically based schizotypic personality, one characteristic is sensitivity to stress
- If a person doesn’t have the schizogene then no amount of stress would lead to schizophrenia, however in carriers, it could result in schizophrenia
45
Modern understanding of día their
- now clear that many genes increase generic vulnerability, there is no single schizogene
- modern views of diathesis also includes a range of factors beyond the genetic, including psychological trauma- trauma becomes the diathesis rather than the stressor
- read (2001) proposed a neurodevelopmental model in which early trauma alters the developing brain
46
Modern understanding of stress
- originally stress was seen as psycho in nature in particular related to parenting
- psychological stress is still seen as important. A modern definition of stress includes anything that risks triggering schizophrenia
- cannabis is a stressor because ir increases the risk of schizophrenia x7 as it interferes with the dopamine system
- however most don’t develop schizophrenia after smoking cannabis so there must also be other vulnerability factors
47
Interaction isn’t approach evaluation
+ Tienari (2004) investigated a combination of genetic vulnerability and parenting styles. Children adopted from 19000 finish mothers found rates of schizophrenia when adopted behaviour was different to controls
- original diathesis stress model was over simplistic as there are multiple genes which increase vulnerability not a single gene and stress comes in many forms
+ tarrier (2004) 315 patients were given medication and Cbt, medication and counselling and a control group. Patients with a combination showed lower symptom levels than control
- we do not yet fully understand how symptoms for schizophrenia are produced
