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46 Cards in this Set
- Front
- Back
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What is schizophrenia? |
a mental illness that affects the way someone thinks, speaks, or feels to such a degree that they lose focus on reality. |
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What examples of positive symptoms can you give? |
Hallucinations (seeing things that aren't there) Delusions (false beliefs) Thought disorders (speech hard to follow, muddled thinking) |
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What are some negative symptoms of schizophrenia? |
Lack of energy Social withdrawal Flatness of emotions Lack of self-care |
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What are the different types of schizophrenia? |
Paranoid (suspicious of others, delusional. often hallucinations as well) Disorganised (speech muddled, inappropriate moods, no hallucinations) Catatonic (withdrawn, isolated, little movement) Residual (low-level positive symptoms, psychotic symptoms present) Undifferentiated (doesn't fit in other categories)
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What is the biological explanation for schizophrenia? |
The Dopamine Hypothesis |
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Explain the Dopamine Hypothesis.
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Excess numbers of dopamine receptors at the synapse contributes to schizophrenia. An increase in dopamine in one site of the brain can cause positive symptoms, and in another site can cause the negative symptoms. There are many ways in which sensitivity to dopamine can arise; genetically inherited to brain lesioning. |
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What evidence is there for the dopamine hypothesis? |
Amphetamines which raise dopamine levels can give similar symptoms to schizophrenia. Phenothiazines block dopamine receptors and reduce schizophrenic symptoms. Schizophrenics are more sensitive to dopamine uptake. Drugs increasing dopamine production in sufferers from Parkinson's give psychotic symptoms. Some genes link with dopamine production and are found with greater frequency in those with schizophrenia. Brain differences might link with dopamine sensitivity - schizophrenic brains seem to be different.
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What evidence goes against the dopamine hypothesis?
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PET scans show blocking dopamine receptors doesn't always remove the symptoms. Blocking dopamine receptors takes a few days to work (when they block them immediately, perhaps something other than excess dopamine causes psychotic symptoms?) Amphetamines only produce positive symptoms. Different types of dopamine receptor in different brain areas give different results. Glutamate might also be implicated (another neurotransmitter; also thought to cause psychotic symptoms in excess.) Social and environmental factors involved too. |
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What is the second explanation for schizophrenia? |
The Environmental Breeder Hypothesis |
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What is the environmental breeder hypothesis? |
There's evidence that people in lower social classes have a higher incidence of schizophrenia. Suggests social class could be a cause of schizophrenia or at least be involved in its development. |
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What is social drift? |
Those with schizophrenia become lower class because of the difficulties schizophrenia brings. It is now widely accepted, but recent studies suggest there may be an environmental cause for schizophrenia. |
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What is social adversity? |
Schizophrenia is more associated with cities not rural areas, so it might be something in city life that leads to schizophrenia. |
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What strengths does the environmental breeder hypothesis have? |
Not everyone with certain environmental circumstances develops schizophrenia, other causes are possible (neurotransmitter, genetic). Could be a combination of both. It helps explain the fact that there are more people with schizophrenia in lower classes, they are concentrated in inner-city areas, and black immigrants are more likely to be diagnosed with schizophrenia than white lower-class groups. |
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What weaknesses does the EBH have? |
Those living alone, unemployed, in lower socio-economic groups might be more likely to be diagnosed with schizophrenia, suggesting a diagnosis problem not an environmental one. |
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What is the social treatment of schizophrenia? |
Assertive Community Therapy (ACT) Aimed at patients who have frequent relapses and bouts of hospitalisation. Used by community mental health service. Treats patients in real life settings, visiting them and helping rather than offering therapies. Works with professionals such as psychiatrists, nurses and social workers. A commitment to spend as much time as necessary to rehabilitate them. |
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What evidence is there for the effectiveness of ACT? (Bond et al.) |
Bond et al. (2001) summarised 25 controlled studies which looked at the effectiveness of ACT. They concluded that compared with standard community care, ACT was highly effective as it engaged clients, prevented re-hospitalisations and increased stability, improving their quality of life. |
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What did Gomory (2001) suggest about ACT? |
The client has no choice whether to undergo such treatment. 11% of clients feel forced into treatment. Bond argued that by reducing re-hospitalisation, the client has more freedom by helping them to live in the community. |
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What strengths does ACT have? |
Good for relapse-prone clients; may be problems living outside the hospital which trigger such episodes. |
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What weaknesses does ACT have? |
They seem to have no effect on actual functioning, such as reducing positive/negative symptoms. Works best in high-density populations, as you require adequate staffing. |
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What are the symptoms of unipolar depression? |
Lethargy, disturbed sleep, permanent anxiety, irritability, feelings of hopelessness, loss of interest in previously engaging hobbies, lack of sex drive, suicidal thoughts. |
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What are the features of unipolar depression (facts?) |
It is twice as common in women than in men. Men are more likely to commit suicide. Usually occurs from ages 30-40, peaks at 50-60. Tend to live a shorter life than non-depressed people.
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What is the biological explanation for unipolar depression? |
The monoamine hypothesis |
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Explain the Monoamine Hypothesis |
Monoamines = group of neurotransmitters including serotonin, norepinephrine and dopamine. Serotonin regulates the other NT's, without regulation, erratic brain functioning and thinking patterns can occur. Low serotonin levels can produce low levels of norepinephrine (which shows alertness, energy, anxiety). It can also increase dopamine levels (shows attention, motivation, feels pleasure and reward). The drug is matched to the symptoms of depression. Eg. if you were feeling particularly unmotivated, you would increase your dopamine levels. |
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What are the strengths of the monoamine hypothesis? |
If the explanation is that there are monoamine deficiencies, and the drugs replacing the deficiencies work, this is evidence. Different monoamines link to the symptoms differently and treatment reflects the differences. E.g lack of interests or lack of energy can be explained by a deficiency in monoamines. |
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What are the weaknesses of the monoamine hypothesis? |
There are drugs which affect depression but aren't related to monoamine neurotransmitters. Experiments where monoamines are depleted do not cause symptoms of depression. MRIs show some physical differences in the brain in depressed people; related to the cause rather than faulty monoamine NT functioning. E.g depressed people have a smaller hippocampus. The increase in mass of the hippocampus could be what lifts the mood and improves memory, so serotonin is still a factor, but its action affects brain mass not monoamine deficiency. |
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Explain the non-biological (cognitive) approach for the treatment of unipolar depression. |
Beck's Cognitive Model of Depression - he looked at faulty thinking patterns. 1) the cognitive triad; a negative view of self, the world and the future. 2) cognitive errors; faulty thinking, along with negative and unrealistic ideas. 3) schemata; patterns of maladaptive thoughts and beliefs. |
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What is the 'cycle' in Beck's cognitive model for depression? |
Thoughts ----> Feelings ----> Behaviour ----> Consequences ----> Thoughts.... |
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What evidence is there for the cognitive model or depression? |
Hollen et al. (2002) - CBT helps at least as long as drug treatment in controlled trials. Bothwell and Scott (1997) - faulty thinking linked with symptoms of depression continuing after hospital care. Teichman - self-concept (how people see themselves) is the most marked link with the severity of depression.
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What strengths are there for the cognitive model of depression? |
Depressed people have negative thoughts and the cognitive explanation for depression is backed up by self-report data and other measures. Ingram ; adverse early experiences relate to later depression.
Takes into account genes, early experiences and learning suggests developmental issues lead to faulty thinking patterns and could predispose someone to depression.
Alloy and Abramson ; college students identified as having a negative mental schemata. Found that students with negative thought patterns were more at risk from depression.
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What weaknesses are there for the cognitive model of depression? |
Hard to find evidence for "negative thinking causes depression". Perhaps negative thinking is a SYMPTOM of depression not a cause.
Similarly, brain chemistry may affect us so we develop depression, or perhaps brain chemistry changes due to developing depression. |
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Describe the biological treatment for UPD. |
Work on principle that low serotonin levels cause depression, and increasing them will help. Selective Serotonin Re-uptake Inhibitors (SSRIs) are drugs for depression, eg. Prozac, Fluvoxamine. Tricyclic anti-depressants = older drugs. Atypical anti-depressants target other neurotransmitters too such as norepinephrine, and include Trazodone.
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What are some side effects of antidepressants? |
SSRIs - nausea, insomnia, anxiety, dizziness, weight change, headaches, fatigue. Atypical antidepressants - nausea, fatigue, blurred vision. Tricyclic antidepressants have more severe side effects (used as last resort) |
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What are examples of withdrawal symptoms of antidepressants? |
Crying spells, insomnia, dizziness, fatigue, aches. |
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What evidence is there comparing drug treatment with CBT? |
Kuyken (2008) - group based form of CBT is at least as successful in treating depression as Prozac, even long term. It was better at preventing relapse, improving quality of life and more cost-effective. Looked at 123 people who had repeated episodes of clinical depression. Random placement into two groups (one continued anti-depressant treatment, one took part in a CBT course). The CBT group had the choice whether to continue their antidepressants as well. Over 15 months, 47% of the CBT group relapsed. But 60% of those who only continued antidepressant treatment relapsed. The researchers thought CBT gave them skills for life, unlike the drugs. |
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What strengths are there for drug treatment? |
They can boost the mood so other therapies like CBT can be used. They need a change in thinking. Newer anti-depressants tend to be having fewer severe side effects. Newer anti-depressants also consider levels of neurotransmitters such as norepinephrine. |
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What weaknesses does drug treatment have? |
Less than 50% of those with depression who use drug treatment are symptom free. Many relapse regardless of drugs.
They ease symptoms, but do not "cure" depression. Therapy is just as effective, especially in relapse rates (Kuyken 2008) |
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What is CBT? |
Associated with psychotherapy. Developed from Beck's Cognitive Model. |
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What does the cognitive model suggest are ways of thinking in depressed people? |
All or nothing - if something goes wrong, so will everything else. Catastrophising - a single negative event = disaster. Crystal Ball Thinking - predicting negatively what someone will say or do. Over-generalisation - eg. loneliness = disliked. Jumping to conclusions - if something happens, the individual concludes they're worthless or eq. rather than seeking an explanation. Mislabelling - breaking diet once and referring to oneself as a failure or a pig. |
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How does CBT work in practice? |
50 minute sessions Sets scene and topics to discuss Confidentiality and Privacy are discussed Try to uncover core beliefs from own words
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Explain Stiles et al. study. |
Looked at effectiveness of CBT compared to psychodynamic and person-centred therapies over 3 years in NHS settings in UK. Researchers used clinical outcomes in routine evaluations - outcome measure (CORE-OM) at the beginning and end of their treatment. Clients divided into 6 groups. 3 groups were treated with 1 of the 3 therapies each (CBT, person-centred, psychodynamic) and 3 groups received one of the 3 therapies plus an additional treatment. All 6 groups showed marked improvement. No one group stood out as being better. |
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Evaluate Stiles et al. study. |
No control group, some data missing, clients not randomly allocated, no supervision of actual treatment. |
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What are the strengths of Stiles et al.? |
Evidence based - Kuyken et al. (2008) suggested CBT was more effective for reducing relapse than antidepressants. Backed by government funding in UK; quick to show results and fairly cheap. |
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What are the weaknesses of Stiles et al.? |
CBT depends on depression's cause being faulty thinking. However some studies show that when depression is removed, so are negative thoughts. A causal relationship is hard to prove.
Stiles found despite different theories and methods, all psychotherapies have equal success rates.
Many data used is self-report; unreliable. Client may want to please researcher and say the therapy is working. |
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What was the aim of Rosenhan's experiment? |
To see if 8 sane people who gained admission into 12 different hospitals would be 'found out' as sane. To experience being in such an institution, and to see how it is to be viewed as 'insane'. |
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What was Rosenhan's 1st procedure? |
8 pseudo-patients. 12 hospitals in 5 states, all different (old/new, private/not etc.) The patients called the hospital for an appointment. Arrived saying they'd been hearing voices - ("empty, hollow or thud"). Once admitted, acted normally. Did not take their medication. Had to convince staff they were sane to leave.
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What were Rosenhan's results from his 1st procedure? |
Pseudo-patients never detected. All but one were admitted with a diagnosis of schizophrenia in remission. No records suggested staff doubted them. Between 7-52 days spent in hospital. Patients recognised frequently that they were sane. |
