Paper 3 Psych

• Introduction to Schizophrenia: Diagnosis and Classification


  Schizophrenia is more common in men, city-dwellers and lower socio-economic groups. Medical approach: Classification - identify symptoms that occur together = classify this as 1 disorder. Diagnosis - identify the symptoms and decide what disorder a person has.

  2 major systems for the classification of mental disorder: ICD-10 and DSM-5. These differ slightly e.g in DSM-5 system, one of the positive symptoms must be present for diagnosis but 2+ negative symptoms must be present in ICD-10
• Positive symptoms

  Additional symptoms beyond normal experience, including: Hallucinations - sensory experiences that either have no basis in reality or are distorted perceptions of things that are there e.g voices heard commenting on a person, criticising them, seeing people or animals that are not there etc. Delusions - irrational beliefs e.g being an important figure like Jesus, another class of delusions concerns the body e.g a person may believe they are under external control. Makes people behave in ways that make sense to them but not to others
• Negative symptoms


  Loss of usual abilities, including: Speech poverty - reduced amount and poor quality of speech however nowadays there is more emphasis on speech disorganisation - e.g speaker changes topic mid-sentence - classified in DSM-5 as a positive symptom whilst speech poverty remains a negative symptom

  Avolition - loss of motivation to carry out tasks and results in lowered activity levels e.g Andreasen (1982) identified 3 signs of avolition - poor hygiene and grooming, lack of persistence in work + education and lack of energy
• Evaluation - Good reliability - Strength


  When different diagnosing clinicians reach the same diagnosis for the same individual (inter-rater reliability) + the same clinician reaches the same diagnosis for the same individual on 2 occasions (test-retest reliability). Osorio et al - report excellent reliability for the diagnosis of schizophrenia in 180 individuals using the DSM-5. Pairs of interviewers achieved inter-rater reliability of +.97 and test-retest reliability of +.92.
• Low validity - limitation


  One way to assess validity of a psychiatric diagnosis is criterion validity. Cheniaux et al - had two psychiatrists independently assess the same 100 clients using ICD-10 and DSM-5 criteria + found that 68 were diagnosed with schizophrenia under the ICD system and 39 under DSM. This suggests that schizophrenia is either over/underdiagnosed according to the diagnostic system - criterion validity is low
• Counterpoint - Strength


  Osorio et al - there was excellent agreement between clinicians when they used two measures to diagnose schozphrenia both derived from the DSM system. Criterion validity for diagnosing schizophrenia is actually good provided it takes place within a single diagnostic system
• Co-morbidity - limitation


  Someone who is diagnosed with schizophrenia could also be diagnosed with other conditions e.g one review found that half of those diagnosed with schizophrenia, also diagnosed with depression/substance abuse (Buckley et al) As a result, Schizophrenia may not exist as a distinct condition which is a problem for diagnosis
• Gender bias in diagnosis - limitation


  Since the 1980s men have been diagnosed with schizophrenia more commonly than women (Fischer and Buchanan - a ratio of 1.4:1) - women are less vulnerable than men genetically. However it seems more likely that women are underdiagnosed because they have closer relationships + get support (Cotton et al) - leads to women with schizoprehnia often functioning better than men
• Culture bias in diagnosis - limitation


  Symptoms of schizophrenia e.g hearing voices, have different meanings in different cultures. E.g in Haiti people believe that voices = communications from ancestors. British people of African-Caribbean origin are up to 9x as likely to recieve a diagnosis as white British people (Pinto and Jones), BUT people living in African-Caribbean countries are not, ruling out a genetic vulnerability - due to culture bias - leads to an overinterpretation of symptoms in black British people (Escobar)
• Symptom overlap - limitation


  Someone who shows symptoms of schizophrenia could also be showing symptoms of another condition e.g both schizophrenia and bipolar disorder involve positive symptoms e.g delusions and negative symptoms e.g avolition. As with co-morbidity, symptom overlap means schizophrenia may not exist as a distinct condition and even if it does it is hard to diagnose.
• The genetic basis of schizophrenia - Family studies


  Family studies have shown that there is a higher chance of someone getting schizophrenia if their genes are similar to a relative who has the disorder e.g someone with an aunt with schizophrenia has a 2% change of developing it, increasing to 9% if the individual is a sibling and 48% if they are an identical twin. Family members share environments as well as genes, so the correlation represents both
• Candidate genes


  A number of different genes are involved in schizophrenia occuring i.e schizophrenia = polygenic. The most likely genes would be those coding for neurotransmitters including dopamine. Ripke et al 2014 - the genetic make-up of 37,000 people with a diagnosis of schizophrenia was compared to 113,000 controls , 108 separate genetic variations were associated with a slightly increased risk of schizophrenia. Schizophrenia = aetiologically heterogeneous - different combination of factors, including genetic variation can lead to the condition
• The role of mutation


  Schizophrenia can also have a genetic origin in the absence of a family history of the disorder - due to mutation in parental DNA- caused by radiation, posion, viral infection. Evidence comes from positive correlations between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50 (Brown et al 2002)
• Neural correlates of schizophrenia


  Research has identified some neural correlates which could cause symptoms of schizophrenia e.g Dopamine - which is important in the functioning of several brain systems related to the symptoms of schizophrenia
• Updated versions of the dopamine hypothesis


  Davis et al 1991 - proposed the addition of cortical hypodopaminergia i.e abnormally low dopamine in the brain's cortex - can explain symptoms of schizophrenia. E.g low DA in the prefontal cortex (responsible for thinking) could explain cognitive problems i.e negative symptoms of schizophrenia - also suggested that cortical hypodopaminergia leads to subcortical hyperdopaminergia. Both genetic variations and early experiences of stress, psychological and physical, make some people more sensitive to cortical hypdopaminergia and hence subcortical hyperdopaminergia (Howes et al 2017)
• Evaluation - Research support - Strength


  Gottesman family studies show that risk increases with genetic similarity to a family member with schizophrenia. Tienari et al - show that biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family. Hilker et al - showed a concordance rate of 33% for identical twins + 7% for non-identical twins
• Environmental factors - Limitation


  Environmental factors also increase the risk of developing schizophrenia. These include both biological and psychological influences. Biological - birth complications (Morgan et al) + smoking THC-rich cannabis in teenage years (Di Forti et al). Psychological - childhood trauma. Morkved et al - 67% of people with schizophrenia and related psychotic disorders reported at least 1 childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues.
• Evaluation extra - Genetic counselling

  A child will have a higher risk of developing schizophrenia if their parents have a relative who has schizophrenia however the risk estimate provided by genetic counselling will not factor environments which could also increase the risk
• Evaluation - Evidence for dopamine - Strength


  Amphetamines increase dopamine and worsen schizophrenia symptoms and induce symptoms in people without Curran et al. Antipsychotic drugs reduce dopamine activity and also reduce intensity of symptoms (Tauscher et al). Some candidate genes act on the production of dopamine or dopamine receptors
• Evaluation Extra - Amphetamine Psychosis


  Tenn et al - induced schizophrenia-like symptoms in rats using amphetamines + relieved symptoms using drugs that reduce dopamine action - supports dopamine hypothesis however other drugs that also increase dopamine levels (e.g apomorphine) do not cause schizophrenia - like symptoms (Depatie and Lal) . Garson - has challenged the idea that amphetamine psychosis closely mimics schizophrenia
• Family dysfunction - the schizophrenogenic mother


  Reichmann 1948 - noted that many of her patients spoke of a particular type of parent - the schizophrenogenic mother (schizophrenia-causing) - mother is cold, rejecting, controlling, is tense and secret, leads to distrust that later develops into paranoid delusions and ultimately schizophrenia
• Expressed emotion


  The level of emotion, particularly negative emotion, expressed towards a person with schizophrenia by their carers (often family). Contains several elements: verbal criticism of the person + violence sometimes, hostility towards the person + anger and rejection, emotional overinvolvement in the life of the person + needless self-sacrifice - serious source of stress, could result in relapsing however stress could trigger schizophrenia if they are already vulnerable due to their genetic make-up for example.
• Metarepresentation dysfunction


  Frith et al 1992 - two kinds of dysfunctional thought processes, the 1st = metarepresentation - the cognitive ability to reflect on thoughts and behaviour - allows us insight into our own intentions and goals - also allows us to interpret the actions of others. Dysfunction in metarepresentation disrupts our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else - explains hallucinations of hearing voices and delusions like thought insertion (the experience of having thoughts projected into the mind by others).
• Central control dysfunction


  Frith et al also identified issues with the cognitive ability to suppress automatic responses while we perform deliberate actions. Speech poverty and thought disorder could result from the inability to suppress automatic thoughts and speech triggers by other thoughts. E.g people with schizophrenia tend to experience derailment of thoughts because each word triggers associations and the person cannot suppress automatic reponses to these
• Evaluation extra - parent blaming


  Although early explanations for the family-schizophrenia link have no research support, research in this area may be useful in showing that insecure attachment and experience of childhood trauma affect individual vulnerability to schizophrenia however could lead to parent-blaming especially mothers - can be sensitive topic
• Evaluation - Research support - Strength


  Stirling et al- compared performance on a range of cognitive tasks in 30 people with sz and a control group of 30 people without sz - including the stroop task - people with sz took over 2x as long on average to name the font-colours
• Evaluation extra - psychological/biological


  The cognitive approach provides an excellent explanation for symptoms of schizophrenia - there is therefore an argument for seeing schizophrenia primarily as a psychological condition however abnormal cognition associated with sz is partly genetic in origin and the result of abnormal brain development (Toulopoulou et al) - suggesting sz is a biological condition
• Biological therapy for sz - Drug therapy


  The most common treatment for sz = antipsychotic drugs (psychosis drugs - a person with psychosis experiences some loss of contact with reality e.g hallucinations/delusions) - taken in the short/long term. Some may need them in the short term only, then stop using them, without symptoms returning, others in long term for life or else face it returning. Antipsychotics - typical (traditional) and atypical (newer)
• Typical antipsychotics


  Been around since the 1950s and include chlorpromazine - taken as tablets, syrup, injection. If taken orally - given daily up to a max of 1000mg, although 1st doses are much smaller and for most people the dosage is gradually increased to a max of 400 to 800mg. Typical prescribed doses have declined over the last 50 years (Liu and de Haan 2009)
• Dopamine antagonists


  If I take a typical antipsychotic eg chlorpromazine, its acts as an antagonist in the dopamine system and blocks dopamine receptors in the synapses of the brain. When I take it dopamine levels build up, but production is reduced. This reduces symptoms like hallucinations
• Sedation effect


  Chlorpromazine is often used to calm individuals not only with sz but with other conditions - done often when patients are first admitted to hospitals and are very anxious. Syrup is absorbed faster than tablets so given when chlorpromazine is used for its sedative properties
• Atypical antipsychotics


  Used since the 1970s. Aim in newer antipsychotics was to improve upon the effectiveness of drugs in suppressing the symptoms of psychosis and minimise the side effects of the drugs used.
• More on Clozapine


  Clozapine binds to dopamine receptors in the same way chlopromazine does but it acts on serotonin and glutamate receptors too. This helps improve mood, reduce depression, anxiety in patients, may improve cognitive functioning. Sometimes prescribed when an individual is at high risk of suicide - important as 30-50% of people with sz attempt suicide at some point
• Risperidone


  been around since the 1990s - developed in an attempt to produce a drug as effective as effective as clozapine but without its serious side effects - can be taken in the form of tablets, syrup, injection that lasts for around 2 weeks. A small dose is initally given - built up to a daily dose of 4-8mg and a max of 12mg. Believed to bind to dopamine and serotonin receptors - binds more strongly to dopamine receptors than clozpine - more effective in much smaller doses than most antipsychotics - evidence it leads to fewer side effects than other antipsychotics
• Evaluation - Evidence for effectiveness - Strength

  Thornley et al - reviewed studies comparing the effects of chlorpromazine to control conditions. Data from 13 trials with a total of 1121 participants - chlorpromazine was associated with better overall functioning and reduced symptom severity as compared to placebo. Meltzer - clozapine is more effective than typical antipsychotics and other atypical antipsychotics - effective in 30-50% of treatment - resistant cases where typical antipsychotics have failed
• Counterpoint - Limitation


  Healy - serious flaws with evidence for effectiveness. Eg most studies are short-term effects only and some successful trials have had their data published multiple times, exaggerating the size of the evidence base for positive effects. since antipsychotics also have powerful calming effects - it's easy to show that they have positive effects on people experiencing symptoms of sz. Not the same as saying they reduce the severity of psychosis.
• Serious side effects - Limitation


  Typical antipsychotics - side effects include dizziness, agitation, sleepiness, stiff jaw, weight gain, itchy skin. Long term use - tardive dyskinesia - caused by dopamine supersensitivity - causes involuntary facial movements e.g grimacing, blinking, lip-smacking. Most serious side effect of antipsychotics = neuroleptic malignant syndrome caused when drug blocks dopamine action in the hypothalamus (an area in the brain associated with the regulation of a number of body systems) - results in high temperature, delirium and coma, can be fatal - Estimates of its frequency range from less than 0.1% to just over 2%
• Mechanism unclear - Limitation


  Our understanding of the idea that symptoms of sz are linked to high dopamine levels in the subcortex of the brain but the original dopamine hypothesis is not a complete explanation for sz since dopamine levels in other parts of the brain are too low rather than too high. If this is true then most antipsychotics shouldn't work. Adds to the argument that antipsychotics are ineffective
• Evaluation extra - The chemical cosh


  It's widely believed that antipsychotics had been used in hospitals to calm people with sz and make them easier for staff to work with, rather than for the beenefits to the people themselves Moncrieff, however calming people distressed by hallucinations and delusions almost certainly makes them feel better, allows them to engage with other treatments (e.g CBT) and services (e.g meeting with a social worker to organise accomodation)
• More on CBT


  can also teach them that voice-hearing is an extension of the orindary experience of thinking in words - normalisation. Delusions can also be challenged e.g by a process of REALITY TESTING in which the person with sz and their therapist jointly examine the likelihood that beliefs are true - where delusions are resistant to reality testing CBT can be used to tackle anxiety and depression that results from living with sz