Schizophrenia

• The positive symptoms of schizophrenia are delusions (a false belief maintained despite being contradicted by rational argument) and hallucinations (the perception of something not present - can be auditory or visual).
• The negative symptoms of schizophrenia are avolition (the reduction or inability to start or continue goal-directed behaviour) and speech poverty (inability to respond to questions or speak fluently).
• According to the DSM, a person must have 2 or more of the following symptoms for a one month period to be diagnosed:

  • delusions
  • hallucinations
  • disorganised speech
  • grossly disorganised or catatonic behaviour
  • negative symptoms
  • Also, signs of the disturbance must have been present for at least 6 months, as well as a general decline in functioning
• The ICD definition of schizophrenia is different to the DSM as it does not specify a time-period for symptoms to be present but does include subtypes of schizophrenia. This causes reliability issues because of inconsistency across classifications - two different doctors might diagnose the same patient differently.
• There may be issues with test-re-test reliability in the diagnosis of schizophrenia because symptoms can be inconsistent due to treatment or the disorder worsening.
• RELIABILITY AO3: In the 1960s Beck et Al did research into inter-rater reliability of the diagnosis of schizophrenia. They asked psychiatrists to diagnose the same 153 patients and found only a 54% concordance rate. However, this research is subject to issues of temporal validity as the DSM has now become more specific and detailed - a similar study was done in 2005 using the DSM which found an 81% concordance rate.
• Signs of validity for a schizophrenia diagnosis would be: treatment working, symptoms matching the DSM, accurate prediction of the course of the illness e.g. a schizephrenic person would not develop mania - this is more likely bipolar disorder.
• An issue for validity of schizophrenia diagnosis is comorbidity - having multiple mental health problems at once. It is very common for schizophrenic patients to also struggle with depression or drug abuse. This makes it difficult to differentiate which symptoms are caused by which disorder.
• An issue for validity of schizophrenia diagnosis is symptom overlap. Many mental health conditions have similar symptoms, for example, schizophrenia and bipolar disorder both include delusions and reduced functioning. This can lead to a patient being diagnosed with the wrong disorder.
• An issue for validity of schizophrenia diagnosis is gender or culture bias. Definitions of psychological issues have mainly been devised by white men and therefore centre their experiences. Psychiatrists are also more likely to be white and male (in the west). This means misdiagnosis on the basis of bias, sterotypes, language difficulties or difference in moral/cultural values is more likely for a female and/or ethnic minority patient.
• VALIDITY AO3: In 1973 Rosenhan tested the validity of diagnosis via the DSM 2 by sending 8 mentally healthy volunteers into different mental health hospitals in the US, all with the same symptom of 'hearing voices'. 7 were diagnosed with schizophrenia and 1 with bipolar depression. Normal behaviours were seen as schizophrenic symptoms. It took 7-52 days for them to be released. This supports diagnosis lacking validity but also reliability because of the difference in diagnoses.
• VALIDITY AO3: Buckley et al concluded that half of patients with a diagnosis also have depression (50%) or substance abuse (47%).
• VALIDITY AO3: Serper et al assessed 3 groups of patients: one with schizophrenia, one with cocaine abuse and one with both. They found that despite symptom overlap, it was possible to make accurate diagnoses. However, symptom overlap may be more of an issue with more similar disorders like schizophrenia and bipolar.
• VALIDITY AO3: Loring and Powell asked randomly selected m and f psychiatrists to read the same patient case and diagnose them using the standard criteria. With m psychiatrists and m patients, 56% were given a schizophrenia diagnosis. However, f patients were only diagnosed in 20% of cases. When the psychiatrist was female no gender bias occured.
• According to the genetic explanation, people with schizophrenia have inherited mutated genes that make them vulneranbke to it. This is because genes determine the structure of the brain and level of neurotransmitters. The two components of the explanation are heredity - identifying those who are at risk - and candidate genes - identifying genes to correct them via gene therapy or engineering.
• Heredity AO1: Gottesman did a meta-analysis into the concordance rates of schizophrenia for different family members. The general chance of developing it is 1%, but with an identical twin it is 48%, a fraternal twin 17% and one parent 6%. This suggests that the more genes you share with a schizophrenic person, the greater the likelihood is of you also developing it.
• AO3 Heredity: the Gottesman meta-analysis also suggests that environment must factor into the development of schizophrenia, not just genes. For fraternal twins the concordance rate is 17%, whereas for a sibling it is 9%. Both have the same number of shared genes - the difference is that fraternal twins share a more similar environment than normal siblings.
• AO3 Heredity: Tienari did an adoption study (a quasi experiment) which found 155 schizophrenic mothers and compared them to 155 adopted children without a schizophrenic parent. 10% of those in the first category developed the disease but only 1% in the second category. This removed environment as a factor.
• AO3 Heredity: In a follow-up to Tienari's study it was found that both a genetic disposition to the disorder and an 'unhealthy' family environment were necessary for someone to develop schiophrenia, suggesting a diathesis stress model.
• Candidate Genes AO1: Schizophrenia is 'aetiologically heterogenous' meaning different combinations of genes are implicated in the disorder. Gene mapping shows multiple genes are affected and these are different for each person which is known as polygenic inheritance.
• Candidate Genes AO3: In 2016 McCarroll et al compared around 29000 people with schizophrenia and 36000 without and found that people had a higher risk of developing it when they had higher levels of C4 activity (excess of synaptic pruning).
• AO3 Genetics overall:

  • Treatment is positive as it means those who know they are high risk can take measures to avoid being triggered
  • Gene mapping is scientific and produces empirical data however concordance studies less so
  • May be socially sensitive as it might encourage people who have schizophrenia not to have children
• Another biological explanation for schizophrenia is neural correlates, specifically the dopamine hypothesis. An imbalance in neurotransmitters in the brain such as dopamine and serotonin play a role in schizophrenia.
• The original dopamine hypothesis from the 1970s stated that schizophrenia was caused by high density and sensitivity of serotonin receptors in the subcortex. This causes neurons that respond to dopamine to fire too often - hyperdopaminergia - which results in the positive symptoms.
• The newer dopamine hypothesis explains both positive and negative symptoms. It states that low levels of dopamine in the pre-frontal cortex are associated with negative symptoms - this area is responsible for thinking and planning so causes avolition and attention difficulties. This is known as hypodopaminergia.
• Kessler et Al used PET and MRI scans to compare schizophrenics and control groups. Schizophrenics were found to have a higher number of dopamine receptor (C2) levels in central brain areas.
• A strength of research into the dopamine hypothesis is that it has practical applications as it has led to the development of treatments that block the correct neurotransmitters. Cole et al found that 75% of schizophrenics were judged to have reduced symptoms when on antipsychotic medication which blocks dopamine receptor sites, compared to only 25% on a placebo. This supports the theory that increased receptor sensitivity is related to schizophrenic symptoms.
• The development of new atypical drugs such as clozapine block other receptor sites such as serotonin - this suggests a limitation to the dopamine hypothesis as other neurotransmitters are implicated in schizophrenia.
• cognitive explanation for schizophrenia:

  • Biological factors CAUSE the initial sensory experiences. Patients experience these faulty neural messages in the same way as ‘normal ones’ and so their brain assigns them meaning.
  • This faulty thinking then causes and worsens the symptoms as the patient attempts to incorrectly understand their biological experiences. Although adopting delusions is irrational, it is inevitable and excusable, given the intensity of the patient’s anomalous biological experience.
• cognitive explanation for schizophrenia part 2:

  • Impaired attention processing occurs; schizophrenics cannot filter out irrelevant sensory information and so become overwhelmed with data they cannot interpret meaningfully.
  • Cognitive impairments accompany schizophrenia in 75% of cases. Affected cognitive functions can include memory, attention and motor skills. Cognitive deficits have been suggested as possible explanations for a range of behaviours associated with schizophrenia such as reduced levels of emotional expression.
• One type of dysfunctional thought processing that is part of the cognitive approach is lacking metarepresentation. This is the cognitive

  ability to reflect on thoughts, behaviour, intentions and goals. This disrupts our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else. This would explain auditory hallucinations (mistaking our own inner voice for the voice of someone else) and delusions like thought insertion (the false belief that thoughts are being projected into the mind by others).
• One type of dysfunctional thought processing that is part of the cognitive approach is lacking central control. This is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts. Sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers associations and the patient cannot suppress automatic responses to these.
• McGuire et al studied 12 male schizophrenics and found increased activity via PET scans in Broca's area (responsible for producing speech), at the same point as the patients heard auditory hallucinations. They were then re-scanned when their hallucinations had resolved and there was no additional activation. This supports the cognitive explanation as it indicates that they are mis-interpreting their own inner voice for an external source due to a lack of meta-representation.
• Stirling et al. compared 30 patients with a diagnosis of schizophrenia with 18 healthy controls on the Stroop Test, in which participants have to name the ink colours of colour words, without reading the words. Patients took over twice as long to name the ink colours as the control group. This supports the cognitive explanation because it suggests they lack the central control to pay attention to the correct feature of the task. However, the researchers make a leap from the results to their conclusions. There might be other reasons the patients take longer and find it difficult.
• The cognitive explanation has practical application through CBT, which has been found to reduce both positive and negative symptoms of schizophrenia by training schizophrenics to recognise and change their dysfunctional thoughts. Therefore, the cognitive approach is likely to be valid, as treatments based on cognitive assumptions are effective in improving symptoms of schizophrenia.
• The cognitive approach is not reductionist as it combines both biological problems with cognitive ones – the idea is that both cumulate together to result in symptoms. So far cognitive psychologists have identified attention deficits and working memory deficits in people with schizophrenia that are shared by their first-degree non-schizophrenic relatives, which could link the cognitive factors with the genetic causes. This is a positive for the future of schizophrenia as it may lead to more accurate diagnosis and more holistic treatments that are more effective.
• Bateson’s ‘Double Bind’ theory was first proposed in the 1950s. It suggests that a child is put into a bind by two conflicting messages, e.g. the mother may communicate verbally that she loves the child but be giving off hostile body language so that the child does not know if they should respond with love or caution - the response will be wrong either way!
• The double bind may lead to schizophrenia because it results in the child feeling confused and unloved. In turn this makes them feel that the world is confusing and dangerous and this outlook could explain symptoms such as delusions of paranoia and disorganised thinking. This is not a cause in itself, but a risk factor for triggering the disorder.
• Expressed Emotion is a measure of the family environment. Expressed emotion refers to levels of criticism, over-involvement, lack of trust and hostility. Theoretically, a high level of EE in the home can worsen the prognosis or act as a risk factor for development of schizophrenia.
• It is determined whether a family has high EE through the Camberwell Family Interview. It rates the patient's view of how their family feels about them and also the actual views of the family toward the patient. If this is negative it may cause the patient stress and lead to relapse and mean they have a harder time coping with their illness if too much time is spent with the EE family.