Topic 10: Schizophrenia Flashcards
(44 cards)
Define schizophrenia
Schizophrenia is a type of psychosis characterised by a profound disruption of cognition and emotion.
Types of schizophrenia
- Paranoid Sz - feels extremely suspicious or grandiose.
- Catatonic Sz - person is withdrawn, mute, negative and often assumes very unusual body positions.
- Hebephrenic/disorganised Sz - primarily negative symptoms.
- Undifferentiated Sz - exhibits the characteristics of Sz but the overall picture is not one of catatonic type, paranoid type, or disorganised type Sz.
- Residual Sz - A subtype of schizophrenia in which the individual has suffered an episode of Sz but there are no longer any delusions, hallucinations, disorganized speech or behaviour.
Negative symptoms of schizophrenia
Negative symptoms appear to reflect a diminution or loss of normal functioning.
Examples:
- Speech poverty/alogia - The lessening of speech fluency & productivity, which reflects slowing or blocked thoughts.
- Avolition - The reuction, difficulty, or inability to initiate and persist in goal-directedbehaviour (lack of drive & motivation).
- Affected flattening - A reduction in the range & intensity of emotional expression, including facial expression, voice tone, eye contact & body language.
- Anhedonia - Loss of enjoymnet of activities that were previously pleasurable.
- Asociality - social withdrawal
Positive symptoms of schizophrenia
Positive symptoms appear to reflect an excess or distortion of normal function.
Examples:
- Hallucinations - Disotortions or exaggerations in any of the senses, most notably auditory hallucinations (A pereception of things that are not present).
- Delusions - fasle, sustained beliefs, which match reality. Delusions of grandeur = False, sustained beleif of importance or superiority. Delusions of persecution = False, sustained belief that others are trying to inflict suffering.
- Echolalia - Pathological repetition of the words of others.
- Disorganised thinking - can be speech, thinking or behaviour. Difficulties concentrating on things.
Diagnosing schizophrenia
Clinicians can use two diagnostic manuals: DSM and ICD
2 symptoms need to be present for 6 months or more & active for at least one month before a person can be diagnosed with scizophreniaa.
Measuring reliability of diagnosis
Reliability is measured by:
- Intra-rater reliability = How consistent one clinician is in diagnosing symptoms (test-retest).
- Inter-rater reliability = How similar diagnosis is between clinicians (measured by a statistic called a kappa score - 0.7 or above is considered good reliability.
Evaluation/discussion into reliability of diagnosis
- In 1962, Beck found that diagnosis between different doctors were 52% similar, however measures of inter-rater reliability made in 2005 found that the diagnosis of Sz were 81% similar, so reliability has increased over time.
- Whaley (2001) found inter-rater reliability correlations in the diagnostic of schizophrenia as low as 0.11.
- Cultural differences in diagnosis: Copeland gave 134 US & 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed Sz but only 2% of the British ones gave the same diagnosis. This suggests a lack of consistency between American and British clinicians in diagnosing SZ. It also shows low concurrent validity between the DSM-V (primarily used in thd US) and the ICD (primarily used in the UK), suggesting that either one, or both, of the manuals are incorrectly measuring schizophrenia.
- Gender bias: Loring and Powell: Gave male and female doctors identical descriptions of a patient but varied whether the pateint was described as male of female. When the patient was described as male 56% of doctors diagnosed the pateint with SZ, compared to only 20% when the patient was described as female. This indicates that there may be an alpha bias in diagnosing sz.
- Cochrane (1977) conducted a review comparing the number of people diagnosed with schizophrenia in Britian and the Caribbean. The overall rate of schizophrenia was similar in the Caribbean and Birtian (around 1%). However, afro-caribean people were 7x more likely to be diagnosed with schizophrenia when living in Britian than when living in the Caribbean. Cochrane concluded that this was because of culutral bias by British doctors.
Problems with the validity of diagnosis
- Symptom overlap refers to the fact that symptoms of a disorder may not be unique to that disorder but may also be found in other disorders (many symptoms of schizophrenia are also found in other disorders, such as depression or bipolar disorder), making accurate diagnosis difficult.
- co-morbidity refers to the extent that two (or more) conditions ot diseases occur simultaneously in a patient. Substance abuse, anxiety and depression are common psychiatric co-morbitities among patients with Sz. Comorbidity can make it difficult to tell the difference between schizophrenia and other conditions, such as depression.
Evaluation/discussion of validity in diagnosis
- Rosenhan: Got 8 healthy volunteers to pretend to have schizophrenia, by claiming they heard an unfamiliar voice in their head saying ‘empty’, ‘hollow’, and ‘thud’, in order to be admitted into a US psychiatric hospital. It took the doctors between 7 and 52 days to realise the diagnosis were wrong and that the volunteers were healthy. This indicates that the diagnosis of schizophrenia can lack validity.
- Gender bias: Loring and Powell randomly selected 290 M & F psyhciatrists to offer their judgements on an account of patients’ behaviour. When patients were described as ‘male’ or their gender wasn’t shared, 56% gave a diagnosis of Sz. When patients were described as ‘female’, only 20% were given a diagnosis - alpha bias.
- Symptom Overlap: Ellason and Ross compared the symptoms of patients with dissociative identitiy disorders and schizophrenia, and found that pateints with dissociative identity disorder displayed more schizophrenic symptons than people who had been diagnosed with schizophrenia. So the DSM’s diagnositic criterea might not be clear enough to provide a reliable or valid diagnosis.
- Co-morbidity: Buckley et al estimate that co-morbid depression occurs in 50% of Sz patients, and 47% of patients have a lifetime diagnosis of co-morbid substance abuse and 23% had OCD. Therefore the criteria used to diagnose schizophrenia may lack valaidity as sz may not be a distinct mental disorder at all. Weber looked at nearly 6 million hospital discharge records and found evidence of many co-morbid non-psychiatric diagnoses including asthma, hypertension & type 2 diabetes.
- Lacks predicitve validity - Variation in prognosis: Harrison (2001) found that 30% of patients showed improvement in some cases, but only 10% in others.
- Cultural Bias: Cochrane conducted a review comparing the number of people diagnosed with Sz in Britian and the Caribbean. The overall rate of Sz was similar in the Caribbean and in Britian. Afro-Caribbean people were 7x more likely to be diagnosed with Sz when living in Britian than when living in the Caribbean. Cochrane concluded that this was because of culture bias by British doctors.
Measuring validity of diagnosis
- The extent that a diagnosis actually reflects the actual disorder (how accurate the DSM/ICD is).
- The extent which different assessement systems arrive at the same diagnosis for the same patient.
Cheniaux (2006)
- 2 idependent psychiatrists diagnosede 100 patients using both DSM & ICD.
Number of diagnosed schizophrenia cases: - 26 & 13 DSM = Lack of consistency between psychiatrists & therefore inter-rater reliability
- 44 & 24 ICD
There’s a discrepency between the number of diagnosis by DSM compared to ICD challenging the validity of the manuels.
Biological Explanation for schizophrenia: Genetics outline and evaluate
AO1: The genetic explanation of schizophrenia suggests that schizophrenia is a result of genetic fault and thus if more genes are shared there should be a greater concordance rate for schizophrenia. Thus it is often described as a heritable disorder.
Twin Studies:
For severe schizophrenia (involving 2+ years in hospital),Gottesman and shields found:
- CR for Mz twins = 75%
- CR for Dz twins = 24%
- General population = 1% risk
Eval:
If your romantic partner has Sz, your risk is twice that of the general population (2%). This suggest environment plays a role as they’re not genetically related.
Assumes that Mz twins and Dz twins have a similar amount of shared environment, however Mz twins are often treated more similarly, encounter similar environments & experience more identity confusion that Dz twins. Differences in CR’s may reflect environmental differences between the two types of twins
Family Studies:
Gottesman
- Children with 2 parents with Sz = 46% CR
- Children with 1 parent with Sz = 13% CR
- Siblings (where one has Sz) = 9% CR
Adoption Study:
Tienari et al
Of the 164 adoptees whose biological mothers had Sz, 11 (6.7%) also received a Sz diagnosis, compared to just 4 (2%) of the 197 control adoptees. Shows genetic liability to Sz.
Eval:
-Since these children were adopted at birth, any similarities between the child and their biological mother must be due to genetics rather than the environment. However adopted children are often matched with parents who are similar to their adoptive parents, and so any simmilarty between the child and their biological parents, might be caused by shared enviornmental factors as well as genetics.
- Adoptees may be selectively placed. A large adoption study into Sz took place in Oregon (1966), where it was assumed that procreation by any person admitted to a mental hospital would produce offspring with an inherited tendency to ‘insanity’. Therefore it is unlikely that the children born to women with Sz would have been placed in the same type of adoptive families as children without such a background.
Polygenetic (Ripke 2014):
Evidence that Sz is polygenic (a characteristic that is influenced by two or more genes).
P: He found the genetic makeup (genomes) of 37,000 patients and 113,000 controls.
F: 108 separate genetic variations were associated with increased risk of Sz. Link with genes which associated with number of neurotransmitters including dopamine.
Dopamine hypotheisis
Claims that an excess of the nuerotransmitter dopamine in certain areas of the brain is associated with the positive symptoms of scizophrenia.
Individuals with positive symptoms of Sz are likely to have high levels of dopamine and more dopamine receptors on the post-synaptic cell, increasing dopaminergic activity.
Th Revised dopamine hypothesis - Davis et al (1991):
Excess of dopamine (Hyperdopaminergia) in the mesolimbic pathway = positive symptoms
Deficit of dopamine (Hypodopaminergia) in areas of prefrontal cortex (area responsible for thinking, decision making etc) = Negative symptoms
Neural correlates hypothesis
Genes can cause abnormalities in the brain and according to the neural correlates explanantion of schizophrenia, schizophrenia is caused by abnormal brain structure (e.g. larger ventricles and smaller frontal cortex than normal)
Patterns of strucutre or function in the brain that correlate with a Sz experience. As they occur simultaneously this could lead us to believe that the patients observed are implicated in causing Sz.
neural correlates explanation of schizophrenia: evaluation and discussion
-
Torrey et al: results from an MRI scan found that on average the ventricles patients with schitzophrenia were 15% larger than the control group.
This correlation doesn’t necessarily mean causation. The enlarges ventricles might be a side effect of taking medication to treat SZ. - There are individual differences in the brain abnormalities that patients with schizophrenia display and so studies suporting the role of large ventricles, haven’t always replicated.
- Reduced myelation of white matter pathways in Sz patients, compared to controls (Due et al). Particularly in the neural pathways between the hippocampus & PFC.
- Negative symptoms:Theventral striatumis involved with reward anticipation. Schizophrenia patients have been found to have less activity in this region- the lower the activity, the more severe the negative symptoms. This could explain avolition (loss of motivation).
- Positive symptoms:Allenet al(2007) scanned the brains of patients experiencing hallucinations whilst they completed an auditory processing task. Lower activation levels were found in thesuperior temporal gyrusandanterior cingulate gyrus, and they made more errors, compared to a control group. Auditory hallucinations are therefore correlated with reduced activity in these areas.
- Neural explanations have been criticised as reductionist, explaining schizophrenia at quite a simplistic level of explanation. The role of upbringing, learning and emotions is not considered, weakening this as a full explanation.
- A neural correlates explanation of schizophrenia isan example of biological determinism as it assumes that specific brain structures and/or dopaminergic activity in the brain play a key role in the onset of schizophrenia
Evaluation of dopamine hypothesis
Strengths:
- Support from drug studies: Drugs that increase dopamine, like amphetamines cause hallucinations and delusions in healthy people. and drugs that decrease dopamine reduce the likelihood that pateints with schizophrenia will experience hallucinations and delusions.
- Practical Applications: Antipsychotic drugs, such as chlorpromazine, which reduce the symptoms of Sz work by inhibiting dopamine transmission. CP: Antipsychotic drugs only reduce all of the symptoms in around 20% of patients.
- Post-mortem (after death) examinations show schizophrenia patients have more dopamine receptors in the left amygdala (Falkai et al., 1988) and the caudate nucleus (Owen et al., 1978).
Weaknesses:
- Noll found that for 1/3 of pateints with schizophrenia, drugs that decrease the level of dopamine didn’t prevent hallucinations and dellusions. This suggests that high levels of dopamine in the mesolimbic system can cause positive symptoms but they aren’t the only cause of positive symptoms.
- Moncrieff conducted a review and claimed that the evidence supporting the dopamine hypothesis is inconclusive for two reasons: first, drugs like amphetamines, which cause positive symptoms, effect other neurotransmitters as well as dopamine - so we cannot be sure that it is the increased dopamine that is causing these symptoms. Second, not all post mortem studies support significant differences in levels of dopamine in schizophrenic patients mesolimbic systems.
- There is some evidence to suggest that dopamine is not the only neurotransmitter involved. Moghaddam & Javitt found evidence for the role of an NT called glutamate in which it appeared that Sz patients have a deficiency in glutamate function. Supports biological/neural explanation but challenges the simplicity of dopamine hypothesis on its own.
- Antipsychotics gradually reduce positive symptoms over several weeks, despite immediately blocking dopamine receptors. Suggests it’s not a direct cause and effect and challenges the simplicity of the theory.
Anti-psychotics
- Drugs used for hyperdopaminergia to reduce positve Sz symptoms. Antipsychotic drugs bind to post synaptic dopamine receptors. This prevents dopamine from binding to receptors, reducing the overactivity of neurones in the mesolimbic system.
- Typical (traditional) antipsychotics bind to dopamine receptors for long periods of time and thus have more side effects.
- Atypical (newer) antipsychoticcs bind to dopamine receptors for shorter periods of time and sso have less side effects.
- Examples: Chlorpromazinwe, clozapine, risperidone
Chlorpromazine
- Typical antipsychotic (1950s)
- Can be taken as tablets, syrups (absorbed faster than tablets), or injection.
- Blocks dopamine receptors, reducing dopaminergic activity.
- Reduced positive symptoms
- Also an effective sedative, often used to calm patients with Sz and other mental disorders.
- Side effects: dizziness, agitation, sleepiness, stiff jaw, weight gain, tardive dyskinesia, neruoleptic maligant syndrome (which can be fatal).
Clozapine
- Atypical antipsychotic (1970s)
- Binds to dopamine receptors & acts on serotonine & glutamine receptors, providing mood-enhancing effects & improving cognition. Important as 30-50% of Sz patients attempt suicide.
- Requires regular blood tests due to risk of fatal condition - agranulocytosis
- Not available as an injection
Risperidone
- Atypical antipsychotic (1990s)
- Binds to dopamine and serotonine receptors. More effective and requires smaller dosage due to stronger binding.
- Tablets, syrup or injection
Evaluate/discuss drug therapy as a treatment for schizophrenia
- Typical antispychotics can have extra-pyramidal side effects (involuntary and uncontrollable movements), which can be distressing for patients and may cause them to stop taken the medication. They can also lead to an increased risk of heart problems, obesity and diabetes. However atypical antipsychotics are less likely to produce these extra-pyramidal effects and as a result patients are more likely to continue taking their medication & see a reduction in their symptoms.
- Typical antispsychotics don’t treat negative symptoms of Sz
- Leucht (2001) conducted a meta-analysis of 65 studies into the effectiveness of antipsychotic drugs. He found that antispsychotic drugs were more effective at treating Sz than placebo pills, and that patients taking the drugs were less likely to relapse and experience severe postitive symptoms.
- Crossley (2010): meta-analysis of 15 studies comparing the effectiveness of typical and atypical antipsychotics. He found no difference in their overall effectiveness at preventing symptoms, but atypical antipsychotics had significantly fewer side effects than typical antipsychotics.
- Patients are likely to relapse if they stop taking the drugs. - Schooler et al (2005) randomly allocated 555 patients in first episode of Sz, to either treatment with haloperidol or risperidone. In both groups 75% showed a reduction in symptoms. However he found a 55% relapse rate. Drug therapy is a short-term fix only because it only manages symptoms and doesn’t deal with the cause (Schooler’s relapse %). However it is possible to be used in combination with another treatment that may be longer term.
- Drop out rates are high likely due to side effects like tardive dyskinesia and neuroleptic malignant syndrome, which can be fatal.
- Antipsychotics are expensive: Globally, around $14.5bn is estimated to be spent on antipsychotics each year. This can lead to an problem of inequality. While wealthy individuals can afford acces to treatment, less fortunate individuals may be forced to suffer.
- They help carers to look after patients with Sz. Mental Health nurses may rely on anti-psychotics to sedate & calm patients so that they are easier to work with. This can raise ethical issues of consent but also who the drugs are for. Are they being used to benefit the patients or the staff? While they can protect and help patients and nurses, it could also be unethical if misused. If given too high dosages too often patients may become zombie-like and withdrawn from reality, which doesn’t improve their lives and counteracts the purpose of treatment.
- Barlow & Durand (1955) chlorpromazine is effective in reducing Sz symptoms in about 60% of cases. Most impact on positive symptoms; treated patients may still suffer from severe negative symptoms.
- Emsley (2008) found that patients who were injected with risperidone early in the course of disorder has low relapse rates and high remission rates; 84% of patients showed at least a 50% reduction in both +ve and -ve symptoms and 64% went into remission.
Double bind theory
- Bateson (1956) suggests that children who frequently receive contradictory messages from their parents are more likely to develop Sz.
- e.g. a mother saying ‘I love you’ but turning away in disgust.
- These mixed & ambiguous messages cause confusion & mistrust - the child begins to question their own feelings and emotions as they cannot trust what their parent is telling them. These interactions prevent the development of an internally coherent construction of reality.
- As a result the child grows up mistrusting all communication (paranoia) & withdrawing from society (asociality) which explains many of the symptoms of Sz.
What are the psychological explanations for schizophrenia?
- Family dysfunction: The presence of problems within a family that contribute to relapse rates in recovering schizophrenics, including lack of warmth between parents and child, dysfunctional communication patterns and parental overprotection.
- Cognitive Explanations of mental disorders propose that abnormalities in cognitive function are a key component of Sz.
The schizophrenic mother
Fomm-Reichmann (1948) suggested that a cold, rejecting, controlling mother causes tension and secrecy within the family and that this behaviour could lead to distrust and & later develops into paranoid delusions and ultimately schizophrenia.
Later revised into theories like double-blind and expressed emotion because of it’s social sensitivity & simplicity.