What is classification of a mental disorder and how can it allow someone to be diagnosed with a mental disorder?
the process of organising symptoms into categories based on which symptoms often come together.
People can then be diagnosed by identifying their symptoms and deciding what mental disorder they have based on their cluster of symptoms.
what two systems are used for the classification of a mental disorder?
1) World Health’s Organisation: ICD-11:
2) DSM-5 (American Psychiatric Association)
- they do differ in some ways in their classification of schizophrenia.
What are positive symptoms and give the two examples (describe them)?
atypical symptoms experienced in addition to normal experiences.
1) Hallucinations: these are when an individua perceives something through their senses that isn’t actually there. They can either relate to the events in the environment (parts of their environment are distorted) or have no relation to the senses being picked up from the environment.
2) Delusions: fixed false beliefs that are not based in reality. Delusions of grandeur: believing they have exceptional power. Delusions of control: believe they are under external control. Delusions can make someone act in a bizarre way.
What are negative symptoms and give the two examples (describe them).
these are atypical experiences that represent the loss of a usual experience (e.g. loss of clear thinking).
1) speech poverty: reduction in frequency and quality of speech. Often there’s also a delay in verbal response.
2) Avolition: difficult to keep up or begin a goal-directed activity. Reduced motivation. Poor hygiene, lack of persistence in work, and a lack of energy.
Strengths of Diagnosis and Classification
Reliability: this is the extent to which a psychological test enables consistent findings. Inter-rater reliability: different clinicians reach the same diagnosis for an individual:
Test-retest reliability: same clinician reaches the same diagnosis for individual twice.
Osorio et al: used DSM-5 to test for sz in 180 ppl- found inter-rate reliability of +.97 and test-retest reliability of +.92. Therefore, sz diagnosed reliably.
Limitations of Diagnosis and Classification
1) Low validity: it has low criterion validity which refers to how accurately a test measures what it’s designed to measure. Cheniaux et al: 100 clients test twice, once using ICD-10 and the other using DSM-IV criteria. 68 diagnosed with ICD-10 and 39 under DSM- low criteria validity as different systems diagnose differently.
2) Gender Bias: Fischer and Buchanan: more men diagnosed than women in ratio 1.4:1. May be since women have closer relationships so get support so if had sz would function better.
3) Culture Bias: Pinto and Jones: British African Caribbean ppl, 9x more likely to be diagnosed with sz than white British ppl. May be since psychiatrist from different cultural background to patient so overinterpretation of symptoms e.g. hearing voices in some Afro-Caribbean societies may be communication from ancestors.
The genetic Basis of Schizophrenia: Family studies (biological explanation)
risk of sz increases in line with genetic similarity to relative with the condition.
Gottesman study: carried out family studies which focused on individuals with sz and determined likelihood of a relative developing it. e.g. someone with aunt has 2% chance, increasing to 9% if sibling, and 48% if identical twin.
Candidate genes in schizophrenia
- many genes code for sz so polygenic.
Ripke et al: genetic make up of 37000 people with sz was analysed and compared to 133000 control. found 108 genetic variation associated with increase risk of sz.
Role of mutations in developing sz.
if no family history of sz, could still have due to mutation in parental DNA, which could be caused by infection.
What is neural correlates (biological explanation)
patterns of brain structure or activity that are linked to specific symptoms or experiences of a disorder. In sz, it refers to changes in brain and structure and activity that are associated with positive and negative symptoms.
What is the original dopamine hypothesis in neural correlates (biological explanation)
sz caused by high levels of dopamine - hyperdopaminergia. It involves subcortex including Broca’s area which is linked to the mesolimbic system. It explains hallucinations and delusions. This is because they’ll have too many receptor sites on postsynaptic dendrites so make more dopamine so more dopamine is taken up. Only explains positive symptoms as if excess dopamine receptors so overactivity.
What is the updated dopamine hypothesis
sz caused by too much dopamine activities in some areas of the brain and too little in other areas- both hyperdopaminergia and hypodopaminergia.
Involves the brain regions: subcortex including Broca’s area which is linked to mesolimbic system and the prefrontal cortex.
Explains positive and negative symptoms.
Too few dopamine receptors means body makes too little in these areas of the brain. Leads to underactivity especially in frontal lobe- involved in thinking and so normal cognitive function reduced. Also leads to struggling with making decisions.
Evaluation of Biological Explanations for Sz
PEEL+: Strength is supporting research for dopamine involvement in symptoms of sz. Curran et al found when giving those without sz amphetamines, they induced symptoms of sz, and when they gave those with sz amphetamines it made their symptoms worse. shows dopamine is involved in symptoms of sz. However, Depatie and Lal challenged these findings when they found that other drugs that also increase dopamine levels such as apomorphine don’t cause sz symptoms like amphetamines do. therefore, perhaps not dopamine as doesn’t always cause symptoms.
PEEL+: Supporting research from Tienari et al study: studied 145 adopted children who’s biological mothers had been diagnosed with sz, and compared them to control group of 158 adopted children with no genetic risk of sz. Found that 11 from high risk developed sz, whilst only 3 from the low risk group. However, not all those in high-risk developed sz. Those who were adopted into healthy families, were less likely to develop sz, which suggests that perhaps there are other factors excluding genes that are involved in developing sz. However, Joseph found in twin studies that in monozygotic twins 40.4% both developed sz whilst only 7.4% in dizygotic indicating genes do play crucial role as more similar genes increases likelihood of developing it.
Psychological Explanations for sz: family dysfunction
schizophrenogenic mother: idea from Fromm-Reichman- developed from hearing about childhood stories from sz patients. Idea is that parent acts in a way that results in developing sz, e.g. cold, rejecting, controlling, but also over-protective. Creates secrecy and tension in family dynamic, leading to distrust in a child and paranoid delusions.
Double Bind Theory: from Bateson et al. When one receives two or more conflicting messages- child feels trapped as don’t want to do wrong thing but don’t know what the right thing is. When they do something wrong, punished by withdrawal of love. Leads to child viewing world as dangerous and confusing- fears reflected by paranoid delusion and disorganised thinking. Also won’t know what the correct way is to behave in the world.
Expressed Emotions: refers to the level of negative emotion expressed to the patient by the carer. Includes: verbal criticism, hostility, emotional overinvolvement. Results in high levels of stress in patient- can lead to relapse or result in development of sz in someone whose vulnerable.
Psychological explanations for sz: Cognitive explanations
this refers to abnormalities in cognitive function leading to development of sz.
Frith et al: two kind of dysfunctional thought processing:
1) central control dysfunction: this is the cognitive ability to suppress automatic responses while we perform deliberate actions. sz symptoms could be a result from inability to suppress their automatic thoughts.
2) Metarepresentation Dysfunction: the cognitive ability to reflect on thoughts and behaviours, helping us to understand ourselves and others. Sz is due to failure of mechanism that enables metarepresentation and so cannot recognise that their own actions were carried out by themselves leading to hallucinations.
Evaluation of Psychological Explanations for sz
PEEL+: Supporting research. Indicators of family dysfunction includes insecure attachment. Read et al found that adults with sz more likely to have insecure attachment to PCG, compared to matched grp without sz. Also found 69% of women and 59% of men with sz had reported some history of abuse. In addition to this, Morkved et al found that 67% of ppl with sz had reported at least one traumatic childhood memory, compared to matched grp where only 38% of ppl with non-psychotic mental health problems had experienced a childhood trauma.
PEEL+: Supporting research for cognitive explanations. Stirling et al found that 30 patients with sz took twice as long to complete the Stroop test compared to 18 non-patients who acted as controls. Shows that ppl with sz lack cognitive ability of central control as can’t restrain automatic response of reading the word rather than saying its colour. However, this research doesn’t explain origin of symptoms of sz, only that there’s a link between faulty cognitions and symptoms. Cognitive factors may be due to other things such as neural correlates which Stirling doesn’t address. therefore, limits usefulness of study.
Biological Therapy for Schizophrenia: Typical Antipsychotics
e.g. chlorpromazine
they work by reducing the action of the neurotransmitter dopamine. They block dopamine receptors in the synapses and so reduce the action of dopamine.
At first, dopamine levels increase but then production decreases. It normalises neurotransmission in the brain and helps reduce symptoms such as hallucinations.
Chlorpromazine also is an effective sedative to help calm patients.
Biological Therapy for Schizophrenia: Atypical antipsychotics
e.g. clozapine: binds to dopamine receptors (same as chlorpromazine) but also binds to serotonin and glutamate receptors. Helps improve mood and reduce depression and anxiety in patients. Has serious side effect of agranulocytosis where the number of white blood cells decreases- can be fatal.
e.g. risperidone: designed to be as effective as clozapine but with less serious side effects. Binds to dopamine and serotonin receptors.
Evaluation of biological therapy for schizophrenia
PEEL++: one strength is that there is supporting research for the effectiveness of both typical and atypical antipsychotics. Thornley et al completed a review study of 13 trials with 1121 participants which compared chlorpromazine (typical antipsychotic) to a placebo. They found that chlorpromazine was associated with significantly better overall functioning and a reduction in the severity of their symptoms compared to the placebo. This study can be generalised since it’s methodological. This is because it included a sample of both men and women, of all ages, who had become recently ill or had recently experienced a relapse. It also included patients taking a whole range of doses of chlorpromazine or placebos. This is important as it increases the internal validity of the study and so ensures that the results are more reliable. In addition to this, Melzer et al found that there are also benefits for atypical antipsychotics. Clozapine, an atypical antipsychotic has been found to be more effective then both typical antipsychotics and other atypical antipsychotics. It also reduces symptoms in 50% of trials where typical antipsychotics haven’t worked. Both of these findings are extremely significant as it highlights the effectiveness of antipsychotics and how they can help an individual suffering from schizophrenia.
PEEL: a limitation of antipsychotics is the side effects that it has which suggests that it lacks appropriateness. Both typical and atypical antipsychotics will often be accompanied by mild side effects such as dizziness and weight gain. However, typical antipsychotics can also results in TD which is a long-term effect causing involuntary facial movements such as grimacing and lip smacking. Furthermore, typical antipsychotics can cause NMS which is when the antipsychotic blocks dopamine action in the hypothalamus and so many regular body processes cannot occur. With atypical antipsychotics the side effect agranulocytosis could occur which is when there are less white blood cells and so the individual cannot fight off infections, which could be fatal.
Psychological Therapy: CBT
The aim is to help the client understand where their symptoms have come from, helping them to make sense of their irrational behaviour- provides alternative explanations to their feelings, and so they feel less stressed.
Steps:
1) Assessment: patient and therapist clarify the patient’s symptoms. Identify goals for therapy and a plan to achieve them.
2) Engagement: therapist builds relationship with the client emphasising that there are alternative explanations to their thoughts.
3) ABC model: patient gives the activating agent that results in the consequences and therapist disputes these beliefs and changes them.
Psychological Therapy: Family Therapy
This is based on the idea that the family is a complex social system where members interact and influence each other’s behaviour. It occurs with the whole family and the identified patient. Often family therapy used with drug therapy. By changing how communication is within the family, it reduces the risk of relapse.
Pharoah et al found strategies therapists can use to improve the functioning of a family that have a member with sz:
1) reduced levels of expressed emotions: by reducing these negative emotions e.g. anger/ guilt it leads to a reduction in stress- lowers likelihood of relapse.
2) Improves the family’s ability to help: therapist encourages family to agree on same aims for therapy. Therapist tries to improve family’s behaviour towards patient. Teaches them to balance caring for the patient and also maintaining their own lives.
Management: Token Economies for SZ- what is it and what for
this is a method to modify the behaviour of patients with sz by encouraging desirable behaviours through reinforcing specific behaviours by rewarding them with tokens.
When sz patient in hospital for long time, may develop institutionalisation- live there for so long, lose regular routine so adopt maladaptive behaviours.
Evaluation of psychological therapy
PEEL+: limitation of CBT is may not be appropriate since doesn’t completely cure sz. Although it improves quality of life as can function more adequately, never fully cured when using CBT. In addition to this, not effective for all patients. Addington and Addington found that not appropriate to use CBT at initial psychosis stage as cannot properly engage in therapy, especially in self reflection section.
PEEL+: family therapy is appropriate as benefits whole family. Lobban and Barrowclough found when reviewing evidence that the effects of family therapy are important since majority of care for patient is from family. By family therapy strengthening the overall functioning of the family, it leads to reduction in negative impact of sz on family members and increases ability of family to support individual. In addition to this, family therapy strengthens economy so helps NHD. It reduces relapse rates so less likely to need further hospitalisation. Less money spent on sz so strengthens economy.
What types of institutional behaviour does token economy help and what are it’s benefits for the patient
it helps improve their personal care, condition-related behaviours, and their social behaviour.
It helps to improve their quality of life in the hospital environment also helps to normalise their behaviour to help them adjust to regular life.
