Schizophrenia Flashcards

1
Q

what is schizophrenia?

A

schizophrenia involves hallucinations and delusions and is a type of psychosis.

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2
Q

what are the positive symptoms of schizophrenia?

A

positive symptoms means excess of normal functions.
delusions: unrealistic beliefs that appear real. they can be paranoid, involve inflated beliefs about the individuals power and importance. the schizophrenic individual will believe that the behaviour and comments of others is directed solely at them.
hallucinations: these can be auditory, visual, olfactory (smelling things) or tactile (something crawling under their skin).

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3
Q

what are the negative symptoms of schizophrenia?

A

loss of normal functions
speech poverty (alogia): poor speech which is thought to reflect slow or blocked thoughts. individuals with this will produce fewer words on a verbal fluency task because they have difficulty spontaneously producing them. speech poverty is also shown through less complex syntax, fewer clauses etc.
avolition: a lack of focused behaviour, instead the individual will appear disinterested in doing things and may simply sit doing nothing for hours sat at a time. they show no initiation or persistence with tasks.

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4
Q

what are the social/occupational dysfunctions of schizophrenia?

A

work, personal, social relationships below the quality of what they were prior to onset.

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5
Q

duration of schizophrenia

A

continuous signs of disturbance for at least six months, including one month of symptoms that meet criterion A. during non-active periods, disturbance may be limited to negative symptoms or two or more symptoms in criterion A.

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6
Q

define reliability in schizophrenia

A

the consistency of the classification system such as the DSM or a measuring instrument to assess particular symptoms of schizophrenia.

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7
Q

define validity in schizophrenia

A

the extent that a diagnosis represents something that is real and distinct from other disorders and the extent that a classification system such as the DSM measures what it claims to.

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8
Q

reliability: cultural differences in diagnosis

A

research suggests that when it comes to diagnosing schizophrenia there are significant variations between culture so culture has an influence on the diagnostic process. Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed schizophrenia compared to only 2% of British psychiatrists. one of the main characteristics of hearing voices also appears to be influenced by cultural environment. Luhrmann (2015) interviewed 60 adults diagnosed with schizophrenia, 20 each in India, Ghana, and the US. each was asked about what voices they heard, many of the African and Indian subjects reported positive experiences with their voices, describing them as playful and offering advice. no US PPs reported positive experiences, they were more likely to report the voices they heard as violent and hateful. Luhrmann suggests that the harsh, violent voices that are so common in the West may not be an inevitable feature of schizophrenia.

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9
Q

Evaluation of reliability

A

inter-rater reliability and unreliable symptoms: despite claims for increased reliability in the DSM, there is still little evidence that the DSM is routinely used with high reliability by mental health clinicians. Whaley (2001) found inter-rater reliability correlations in the diagnosis of schizophrenia of 0.11. Rosenhan’s (1973) study demonstrated the unreliability of the diagnosis of schizophrenia. ‘normal’ people presented themselves at a psychiatric hospital in the US. they all claimed to hear voices and were subsequently diagnosed and admitted to the hospital. during their stay, no staff recognised that they were not symptomatic.
culture: research has established cultural and racial differences in the diagnosis of schizophrenia. however, the prognosis for members of ethnic minority groups may be actually 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 most ethnic minority cultures. Brekke and Berrio 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 2 non-white minority groups and a white majority group. they found that non-minority group members were consistently more symptomatic than members of the 2 ethnic minority groups, findings which were supported by the ethnic cultural hypothesis.

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10
Q

validity: gender bias in diagnosis

A

this occurs when the accuracy of diagnosis is dependent on the gender of the individual. the accuracy of the diagnostic judgements can vary for several reasons, including gender-biased diagnostic criteria or clinicians basing their judgements on stereotypical beliefs held about gender. for example, the critics of the DSM diagnostic argue that some diagnostic categories are biased towards pathologising one gender rather than the other. Broverman (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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11
Q

validity: gender bias in diagnosis evaluation

A

Loring and Powell (1988) randomly selected 290 male and female psychiatrists to read two case study of patient behaviour. they were then asked to give their judgement on these individuals, using the standard diagnostic criteria. when the patients were described as male 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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12
Q

validity: symptom overlap

A

it is believed that identifying positive and negative symptoms of schizophrenia would help to create a more valid diagnosis of schizophrenia. however, many of these symptoms are found in other disorders. Schneider (1959) listed 1st rank symptoms (the most common), which he believed distinguished schizophrenia from other psychotic disorders. these symptoms included delusions of being controlled by external forces, beliefs that the individuals thoughts are being broadcast to others, hearing hallucinatory voices commenting on their thoughts or actions. this made diagnosis more reliable.

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13
Q

validity: co-morbidity

A

this refers to the extent to which two or more symptoms can co-occur. psychiatric co-morbidities are common among patients with schizophrenia. these include substance abuse, anxiety, and symptoms of depression. for example, Buckley (2009) estimated 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 OCD are 2 distinct psychiatric conditions. roughly 1% of the population develop schizophrenia and roughly 2-3% develop OCD. s evidence suggests that the two conditions appear together more than chance would suggest. Swets (2014) conducted a meta-analysis and 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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14
Q

validity: co-morbidity evaluation

A

Several studies have examined single co-morbidities with schizophrenia. One example is Weber (2009) who studied just under 6 million hospital discharge records to calculate co-morbidity rates. pPsychiatricand behaviour-related diagnosis accounted for 45% of co-morbidity. However, the study also found evidence of many co-morbid non-psychiatric diagnoses. Many patients with a primary diagnosis of schizophrenia were also diagnosed with medical problems including asthma and type 2 diabetes. It was concluded that the nature of a diagnosis of a psychiatric disorder is that patients tend to receive a lower standard of care, which in turn adversely affects the prognosis for patients with schizophrenia.

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15
Q

validity: prognosis evaluation

A

just as people with schizophrenia may not share the same symptoms, there is no evidence to suggest that they share the same outcomes (prognosis). the prognosis for patients diagnosed with schizophrenia varies between 20% recovering their previous level of functioning, 10% achieving significant and lasting improvement and about 30% showing some improvement with intermittent relapse. a diagnosis of schizophrenia has little predictive validity, some people never appear to recover form the disorder but some do. what does appear to influence the outcome is more to do with gender and psycho-social factors such as social skills, academic achievements, and family tolerance of schizophrenic behaviour.

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16
Q

biological explanations: genetics - general studies

A

Ripke (2014) carried out a study which combined all previous data from genome-wide studies of schizophrenia. the genetic make-up of 37,000 patients was compared to that of 113,000 control group. 108 separate genetic variations were associated with the increased risk of schizophrenia. genes associated with increased risk included those coding for the functioning of a number of neurotransmitters including dopamine.

17
Q

biological explanations: genetics -family studies

A

such studies conducted by researchers such as Gottesman (1991) find individuals who have schizophrenia and determine whether biological relatives are similarly affected more often than their non-biological relatives. Such 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. in Gottesman’s study, children with 2 schizophrenic parents had a concordance rate of 46% and children with one schizophrenic parent had a concordance rate of 13%. children with a schizophrenic sibling had a concordance rate of 9%.

18
Q

biological explanations: genetics - evaluation

A

at face value there seems to be evidence to support the genetic influence on developing schizophrenia, however, it is now accepted that some evidence can be lacking as direct evidence for a genetic link as we now more commonly accept that it could be due to common rearing patterns or environmental stressors that families endure that could lead to the development of the condition, such as expressed emotion. this then opens up the nature vs nurture debate as environmental factors could also increase/decrease the chance of developing schizophrenia, therefore is it solely due to genetics?
89% of those with schizophrenia have no known relative with the disorder. therefore, other biological factors can cause the condition. one explanation looks at the mutation of parental DNA in sperm cells. this mutation can be caused by radiation, poison, or viral infection. a positive correlation was found between paternal age and the risk of schizophrenia. it increased from around 0.7% with fathers under 25, to over 2% in fathers over 50.

19
Q

biological explanations: the dopamine hypothesis

A

This hypothesis claims that an excess of dopamine (neurotransmitter) in certain regions of the brain is associated with positive symptoms of schizophrenia. Messages from the neurons that transmit dopamine fire too easily or too often which leads to hallucinations and delusions (positive symptoms). People with schizophrenia are believed to have abnormally high numbers of D2 receptors on the receiving neurons, which results in more dopamine binding to the receptors and more neurons firing. The traditional version of the dopamine hypothesis stated that higher dopamine levels occur in the subcortex.
Davis and Kahn proposed a revision of the dopamine hypothesis. They suggested that the positive symptoms of schizophrenia are caused by an excess of dopamine in the subcortical areas of the brain. The negative and cognitive symptoms are thought to come from a deficit of dopamine in regions of the prefrontal cortex. Evidence from the revised hypothesis comes from:
Neural imaging: Patel used PET scans to assess dopamine levels in the individuals and those without. They found lower levels of dopamine in the dorsolateral prefrontal cortex of people with schizophrenia compared to the other individuals.
Animal studies: Wang and Deutsch induced dopamine depletion in rats in their prefrontal cortex. This resulted in them having cognitive impairment. The researchers were able to reverse these symptoms by using olanzapine an atypical psychotic drug thought to benefit the effects of negative symptoms in humans.

20
Q

biological explanations: the dopamine hypothesis evaluation

A

+ There is significant evidence for the dopamine hypothesis from the use of drugs that successfully altered the levels of dopamine in the hypothesis. Leucht (2013) carried out a meta-analysis of 212 studies that analysed the effectiveness of different antipsychotic drugs compared to a placebo. They found that all the drugs tested were significantly more effective than placebo treatments for both positive and negative symptoms, the drugs normalised the levels of dopamine in the body.
- however, others such as Moncrieff claim that evidence is far from conclusive for the dopamine hypothesis. Stimulants such as cocaine and amphetamines have been shown to induce schizophrenic episodes, but they are known to affect other neurotransmitters other than dopamine. Therefore, other neurotransmitters could lead to schizophrenic symptoms. Also, post-mortem studies have shown negative or inconclusive symptoms for dopamine. It is also known that other sources such as stress and smoking can also be linked to dopamine release which could confound evidence for the role of dopamine in causing schizophrenia. Therefore, it is suggested that the idea that symptoms of schizophrenia are caused by the over-activation of dopamine isn’t supported by strong evidence.

21
Q

biological explanations: neural correlates

A

This is changes in neuronal events and mechanisms that result in the characteristic symptoms of a behaviour/mental disorder.
Negative symptoms: avolition - motivation involves the anticipation of a reward and the ventral striatum is part of the brain involved in this, so abnormality in the area of the ventral striatum could lead to the development of avolition.
Positive symptoms: it is believed that reduced activity in the superior temporal gyrus and anterior cingulate gyrus is a neural correlate of auditory hallucinations.

22
Q

biological explanations: neural correlates evaluation

A

negative symptoms: Juckell measured activity levels in the ventral striatum in people with schizophrenia, compared to controls, and found lower levels for schizophrenia. therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia.
positive symptoms: Allen scanned the brains of patients experiencing auditory hallucinations whilst they identified recorded speech as their voice or others. they compared the results to a control group. the hallucination group made more mistakes than the control group and had lower activation levels in the 2 specified areas of the brain.

23
Q

drug therapy: typical antipsychotics

A

conventional/1st gen
used to combat positive symptoms
typical antipsychotics reduce the effects of dopamine and therefore reduce the symptoms of schizophrenia. They are dopamine antagonists; they block the action of dopamine. they bind to the dopamine receptors, particularly the D2 receptors in the mesolimbic dopamine pathway which blocks their action, reducing the stimulation of the dopamine system in the mesolimbic pathway and will eliminate hallucinations and delusions usually within a few days of being on the medication. other symptoms may take longer, up to several weeks before a significant improvement is seen. the effectiveness of these dopamine antagonists in reducing symptoms led to the dopamine hypothesis being developed. Kapur estimates that between 60%-75% of the D2 receptors in the mesolimbic dopamine pathway must be blocked for the drugs to be effective. to achieve this, a similar number of D2 receptors in other areas of the brain must be blocked which can lead to undesirable side effects. this was worked on in the development of atypical antipsychotic medication.

24
Q

drug therapy: atypical anti psychotics

A

these carry a lower risk of movement problems. they have a beneficial effect on the negative symptoms of schizophrenia and cognitive impairment. these drugs act on the dopamine system by blocking the D2 receptors. however, they only temporarily occupy the D2 receptors, and then rapidly disassociate to allow normal dopamine transmission. it is the rapid dissociation that is thought to be responsible for the lower level risk of movement problems because atypical antipsychotics have little effect on the dopamine systems that control movement.

25
Q

drug therapy: evaluation

A

Effectiveness of antipsychotic medication: support for how effective these drugs are comes from studies that have compared relapse rates for individuals taking the drug and for those taking a placebo. Leucht carried out a meta-analysis of 65 studies published between 1959 and 2011, involving nearly 6000 patients. All patients had stabilized their symptoms by taking typical or atypical medication. Some of these patients were then taken off their medication and given a placebo, whilst others remained on their medication. Within 12 months, 64% of the patients who had been given the placebo had relapsed, compared to 27% who stayed on their regular medication.
Ethical issues: It is believed that if a cost-benefit analysis was conducted, taking into account side effects, deaths, and psychosocial consequences of taking medication, it would probably be negative. In recent years, in the USA, a patient received a large amount of money out of a court settlement for suffering tardive dyskinesia based on the Human Rights Act. It is also widely believed that anti-psychotic drug medication is used in hospitals to calm patients down to make them easier for staff to work with, rather than the drug being given solely for the patient’s benefit. This short-term use of psychotics is recommended by the National Institute and Clinical Excellence but many question its ethics.

26
Q

psychological explanations: family dysfunction - double bind theory

A

Bateson emphasised the importance of communication within a family and suggested there was a link between parents being contradictory toward their child and the development of schizophrenia. This child may receive conflicting messages about their relationship with their parent through different forms of communication e.g. verbal, and non-verbal cues. This makes it difficult for the child to respond to the parent as the messages invalidate each other. Consequently, the child will have no opportunity to construct a coherent reality about the relationship and this could lead to schizophrenic characteristics such as affective flattening and social withdrawal. Similar concepts have been put forward by people such as Laing who suggested schizophrenia is a result of stresses in the family and society which the individual finds intolerable.

27
Q

psychological explanations: family dysfunction - double bind theory evaluation

A

Berger supports this concept put forward by Bateson, by reporting that schizophrenic individuals did report higher incidences of double-bind statements from their mothers compared to a control group. However, Leim studied patterns of parental communications of families and found no difference between those of a schizophrenic individuals and those who were not schizophrenic. Hall and Levin found no difference in verbal and non-verbal communication between the families of a schizophrenic individual and a control group.

28
Q

psychological explanations: family dysfunction - expressed emotion

A

This is a form of family communication that is hostile, critical, and emotionally overevolved. The family members speak about the schizophrenic individual in a hostile/critical way, or they will indicate emotional over-involvement or over-concern with the patient and their behaviour. Kuipers found that expressed emotion relatives talk more and listen less and that high levels of expressed emotion are most likely to influence relapse rates, a patient returning to a family high in expressed emotion is 4x more likely to relapse than a patient whose family is low in expressed emotion. This suggests that people with schizophrenia have a lower tolerance for instance environmental stimuli such as emotional comments and interactions with family members. Such negative climates arouses the patient and leads to stress beyond their already impaired coping mechanisms thus triggering symptoms: hallucinations, social withdrawal, paranoia, and low self-esteem.

29
Q

psychological explanations: family dysfunction - expressed emotion evaluation

A

Not all people who live in high-expressed emotional families or those who live in low-expressed emotional families will avoid relapse, we have to account for individual differences for each person. Altorfer found that 1/4 of the patients studied showed no psychological response to stressful comments from their relatives. This brings into question how the individual receives their environment, if you don’t perceive highly expressed emotion environments as negative or stressful then such people can do well in these families even if such family environments, even if such family environments are objectively rated as negative or stressful. Therefore showing people are not equally vulnerable to high levels of expressed emotion within a family environment.