Chapter 10- Schizophrenia Flashcards
Describe the clinical characteristics of SZ:
According to DSM-V 5, there are 2 main types of symptoms, positive (excess of normal functioning) and negative (loss of normal function)
- Positive Symptoms:
1. Delusions - irrational beliefs that seem real to SZ person, but in actualality are not real. 2 types of delusions: delusions of persecution (false belief that they are being attacked/followed, paranoid in nature) and delusions of grandeur (false belief that they are powerful/important/famous/have special abilities).
- Hallucinations - unusual and unreal perceptions of the environment that can be auditory (hearing), visual (seeing), olfactory (smell), tactile (touch). These feel real only to SZ person.
- Negative Symptoms:
1. Poverty of Speech (alogia) - reduction in amount and quality of speech, produce fewer words, difficulty spontaneously producing words.
2. Avolition - reduction of interests and desires and inability to initiate + persist in goal directed behaviour. Reduction in self-initiated involvement in activities available to patient.
Under DSM-V 5 criteria, diagnosis of SZ needs 2 or more +ve or -ve symptoms to persist for at least 6 months.
What are some issues with validity of classification and diagnosis of SZ:
Validity = extent to which diagnosis of SZ is accurate diagnosis, and is distinct from other disorders, and the extent to which classification systems like ICD and DSM measure what they intend to measure.
A number of issues make it difficult for classification sys. and diagnosis to be valid:
1. Gender Bias - accuracy of SZ diagnosis dependent on individual’s gender; diagnostic criteria may be more biased towards one gender rather than the other; also, clinicians may base judgements on stereotypical beliefs held about gender (freud believed women had hysteria)
2. Symptom Overlap - symptoms of SZ found in other disorders like depression and BPD (BPD and SZ both have positive symptoms like delusions and negative symptoms like avolition). Therefore, difficult to distinguish accurately SZ from related disorders during diagnosis.
3. Co-morbidity - extent to which 2 or more conditions occur, e.g. people with SZ may also experience depression. This makes it difficult to separate different conditions and deciding which treatments to administer.
What are the evaluations for the issues of validity in the classification and diagnosis of SZ?
- Evidence for gender bias in diagnosis, Loring + Powell ‘95: when group of randomly selected male and female psychiatrists were given a case described as male, 56% gave diagnosis of SZ, and when given a case described as female, ony 20% gave diagnosis of SZ. It was also found that the gender bias wasn’t evident amongst the female psychiatrists, this suggets that diagnosis of SZ is unfairly influenced by gender of patient and this is prevelant amongst male psychiatrists.
- Evidence for Symptom Overlap issues in diagnosis, Ellason + Ross ‘95: found great amount of overlap between SZ and BPD, and also another disorder called Dissociative Identity Disorder (DID), with people with DID having more symptoms of SZ than people diagnosed with SZ. This is an issue as it questions whether SZ, BPD, DID are separate disorders or all part of the same spectrum.
- Evidence for Co-morbidity, Buckley et al 2009: found comorbid depression occurs in 50% of SZ patients, which suggests that there is significant overlap between disorders making SZ diagnosis as a distinct disorder difficult.
- HOWEVER: criterion validity is whether or not different diagnostic tools like DSM-V 5 and ICD 11 arrive at the same assessment of condition of individual. Cheniaux et al found lack of truth in these supposedly objective measures, as each diagnostic tool was found to diagnose different symptoms. BUT, nowadays, DSM-V 5 has been refined and has evolved with evidence, so diagnosis today is more consistent with ICD.
What are the issues with reliability of classification and diagnosis of SZ?
Reliability = consistency of diagnosis when two independent assessors use same classification system given same diagnosis (inter-observer reliability) or whether diagnostic tests are consistent of different occassions, (test-retest reliability).
There seems to be a **culture bias **- this may lead to problems with both reliability and validity of SZ diagnosis, as this is when psychiatrists are influenced by their own culture’s values and expectations when diagnosing patients. If what is seen as unusuale in one culture is not viewed as unusual in another culture, this leads to inconsistent therefore unreliable diagnosis.
Evaluate the issues with reliability of classification and diagnosis of SZ:
- Evidence for cultural bias in diagnosis comes from Copeland 1971, found when UK and USA psychiatrists given description of patient and asked for diagnosis, 69% of USA psychiatrists diagnosed SZ, but only 2% of UK ones did. Suggests diagnosis has low inter-observer reliability between cultures.
- Some patients are more likely to being diagnosed with SZ than others, suggesting reliability and validity issues; Harrison et al ‘97 reported that African-Caribbean groups were 8x more likely to be diagnosed with SZ than white groups in UK. This suggests psychiatrists may be misinterpreting cultural differences in behaviour as SZ symptoms when they are simply differences in culture. This ethnocentric bias reduces validity of diagnosis. HOWEVER, it could indeed be that genuine differences between cultures is caused by genetic inheritance of SZ. It could represent effects of poorer housing, more unemployment and social isolation commonly experienced by minority groups that may lead them to have SZ.
- Cheniaux et al 2009 has 2 psychiatrists independently diagnose 100 patients using DSM and ICD. Using DSM, psychiatrist 1 diagnosed 26 people with SZ whereas psychiatrist 2 diagnosed 13. Using ICD, psychiatrist 1 diagnosed 44 people with SZ, whereas psychiatrist 2 diagnosed 24. There is a disparity between diagnosis, ICD diagnoses more people with SZ, and psychiatrist 1 had higher perception of diagnosis.
What is the genetic explanation for SZ?
- Family Studies: confirmed risk of SZ is directly proportional to genetic similarity to relative with SZ. Gottesman ‘91 reviewed 40 twin studies and found 48% concordance for SZ in MZ twins, and 17% concordance for DZ twins. Gottesman also found found that if you have parents with SZ, you are at 47% risk, and if you have sibling with SZ, you are 8% risk. He found that if you have first degree relative with SZ, you are 18x more likely to have SZ. Problems with this research? MZ twins may be treated the same by environment, DZ twins may be treated differently. Also, if both parents have SZ, why not 100% risk? Shows there is some role of environment, maybe using SLT?
- Candidate Genes: number of different genes trigger SZ, = polygenic. These genes likely code for NTs like dopamine. Ripke et al combined previous data from genome-wide studies of SZ, compared genome of 37,000 SZ poeple with 113,000 controls with no SZ, and found 108 genetic variations that were associated with increased risk of SZ. This also proves that SZ is **aetiologically heterogenous ** as different combinations of genes and factors lead to condition.
What is the Neural Correlates explanation of SZ?
Neural Correlate = brain function associated with SZ. Dopamine is related to symptoms of SZ.
The original dopamine hypothesis:
Based on discovery that antipsychotics caused symptoms similar to people with Parkinson’s disease, a condition associated with low dopamine levels (hypodopaminergia). Therefore, it was concluded that SZ is caused by high levels of dopamine (hyperdopaminergia) in subcortical regions of the brain. Excess of dopamine D2 receptors in pathways from subcortex to Broca’s area may explain SZ symptom of speech poverty.
Updated version of dopamine hypothesis:
Davis et al proposed addition of cortical hypodopamingeria (abnormally low dopamine in brain’s cortex) can also explain SZ symptoms, like cognitive problems. Cortical hypodopaminergia leads to subcortical hyperdopamingeria, both high and low levels of dopamine in different regions may lead to SZ.
Evaluate the genetic explanation for SZ:
- Research Support: strong evidence base; family studies like Gottesman show increased risk with genetic similarity to family member with SZ. Adoption studies like Tienari et al show that biological children of parents with SZ have more SZ risk even if they grow up in adoptive family. This shows that some people are more vulnerable to SZ due to their genetic make-up.
- LIMITATION: clear evidence for environmental factors increasing risk of SZ too; this includes biological and psychological influences, like birth complications and smoking THC rich cannabis in teen years, and childhood trauma, leaving people vulnerable to mental health problems, and perhaps SZ. Morkved at al found that 67% people with SZ had at least one childhood trauma, opposed to 38% to matched control group with no psychotic mental health issues. Therefore, genetic factors alone may not provide complete explanation for SZ.
Evaluate Neural Correlates explanation for SZ:
- Evidence for dopamine: amohetamines increase dopamine and worsen symptoms in SZ people and induce symptoms in non-SZ people (Curran et al). Antipsychotic drugs reduce dopamine activity and reduce intensity of symptoms (Tauscher et al). This strongly suggests dopamine is involved in symptoms of SZ.
- Limitation of dopamine hypothesis is that there is evidence for central role of glutamate; post-mortem and live-scanning show raised levels of NT glutamate in several regions of brain in people with SZ (McCutcheon et al). This means that many other NTs may also be involved in SZ symptoms, not just dopamine.
What is the biological therapy for SZ?
Drug Therapy:
Using ‘antipsychotic drugs’, either for short or long term basis. 2 types of antipsychotics:
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Typical Antipsychotics:
Chlorpromazine, taken as tablets, syrup, injection.. Maximum dosage of 800mg. Positive symptoms of SZ thought to be products of overactive dopamine system, the typical antipsychotic drugs like chlorpromazine are dopamine antagonists, work directly on reducing effects of dopamine, by binding to D2 dopamine receptors. This reduces dopamine’s influence on thought, cognition, behaviour therefore reduces positive symptoms of SZ, like hallucinations.
Chlorpromazine is an effective sedative as well.
**2. Atypical Antipsychotics: **
Clozapine have been developed with aim of more effective treatment of both positive and negative symptoms of SZ. Unlike typical antipsychotics, these drugs only temporarily block D2 receptors before dissociating to allow normal dopamine transmission. These drugs have lower risk of extreme side effects, have beneficial effect of negative + positive symptoms and suitable for treatment resistant patients.
Evaluate the biological therapy for SZ:
- Evidence for effectiveness of Chlorpromazine comes from placebo research: Thornley et al reviewed studies comparing effects of Chlorpromazine to control groups where patients receieved a placebo. Found that chlorpromazine was associated with reduced symptom severity and reduced relapse rates. Suggests that typical antipsychotics are medically effective at preventing relapse.
- Support for benefits of atypical antipsychotics; Meltzer concluded that Clozapine is more effective than typical antipsychotics and that it is effective in 30-50% pf treatment-resistant cases where typical antipsychotics failed. Suggests that atypical antipsychotics are much more effective than typical antipsychotics in treating SZ.
- Criticism of typical antipsychotics is they are less appropriate for their worrying side effects, about 30% of people taking it develop ‘tardive dyskinesia’, whihc causes patient to suffer uncontrollable, repetitive movements like grimacing, blinking and jaw clenching. It makes the patient’s life more difficult and also may increase costs.
- Issues with patient compliance, side effects may effect patient is willing to take drug, on average 50% of SZ patients stop taking their own medication after a year, 75% after 2 years. This causes something called ‘Revolving Door Syndrome’, where patient is reluctant to take their medication and regularly relapses before being admitted for care, treated with drugs again, and then only to avoid taking them when released. This raises doubts over how appropriate antipsychotic treatments are if they rarely lead to long term and stable recovery.
What is the Family Dysfunction explanation (psychological) for SZ?
- The schizophrenogenic mother; Fromm-Reichmann proposed psychodynamic explanation for SZ based on accounts from her patients. She noted that many patients spoke of a particular type of parent which she called schizophrenogenic mother, which is a cold, rejecting and controlling person, who tends to create a family climate of tension and secrecy - this leads to distrust that later turns into paranoia delusions, and ultimately SZ.
- Double-bind theory: Bateson et al agreed that family climate is important in development of SZ, but emphasised role of communication style within family, the developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed signals on what exactly is the wrong thing. They feel unable to comment on unfairness of situation or seek clarification. When they get things wrong, the child is punished by withdrawal of love. This leads them to understand the world as a confusing and dangerous place, and this is reflected in SZ symptoms like disorganised thinking, paranoid delusions. Bateson recognised that this was only a risk factor, not the only factor.
- Expressed emotion, EE : is the level of emotion, particularly negative, expressed towards patient by their carers (family). EE contains several elements:
1. Verbal Criticism of patient, with violence
2. Hostility towards patient, anger + rejection
3. Emotional overinvolvement in life of patient, including needless self-sacrifice
These high levels of EE directed towards patient are serious source of stress for patient, this is primarily explains relapse in patients with SZ. It has also been argued that EE may trigger onset of SZ in someone who is already vulnerable (diathesis-stress model).
What are is the cognitive explanations (psychological) for SZ:
- Dysfunctional thinking: a cognitive explanation focusses on mental processes, SZ is associated with dysfunctional thought processing. SZ characterised by disruption to normal thought processing; reduced thought processing in ventral straitum is associated with negative SZ symptoms, whilst reduced processing of info in temporal + cingulate gyri are associated with positive SZ symptoms (Simon et al). This shows that decrease in cognitive processes in certain areas provokes SZ symptoms.
- **Metarepresentation dysfunction: **Fritch et al identified two kinds of dysfunctional thought processes. Metarepresentation, the cognitive ability to reflect on thoughts and behaviour, allowing us to have insight into our own intentions and goals, and interpret other people’s actions. Dysfunction in metarepresentation disrupts our ability to recognise our own actions, thoughts as being a product of one’s own action, explaining hallucinations of hearing voices.
- Central Control Dysfunction: Frith et al also identified issues with cognitive ability to suppress automatic responses while perforiming deliberate actions. Speech poverty + thought disorder could result from inability to suppress automatic thoughts and speech triggered by other thoughts. People with SZ cannot suppress automatic responses so when speaking, their words jumble due to associations of the words.
Evaluate Family Dysfunction explanation (psychological) for SZ:
- Research Support: evidence linking family dysfunction to SZ; indicators of family dysfunction include insecure attachment and exposure to childhood trauma, like abuse. Read et al did a review and found that adults with SZ are disproportionately more likely to have insecure attachment, particularly type C or D. Read et al also reported 69% women and 59% men with SZ had history of physical and/or sexual abuse. This suggests that family dysfunction make people more vulnerable to SZ.
- Limitation; poor evidence base of any explanaton. Despite there being evidence for idea of childhood family stress associating with adulthood SZ, almost no support for importance of traditional family theories like schizophrenogenic mother and double bind theory. Both these theories are based on clinical observations from patients and informal assessment of personality of mothers of patients, but no systematic evidence.
Evaluate the cognitive explanations (psychological) for SZ:
- Research support; evidence for dysfunctional thought processing; Stirling et al compared performance on range of cognitive tasks in 30 people with SZ and control group of 30 people without SZ. Tasks included the Stroop task, where PPs had to name font colour of colour words and so had to suppress the tendency to read the words aloud. As predicted by Frith et al central control theory, SZ people took twice as long to name font colours. This shows that the cognitive processes of people with SZ is impaired.
- Limitation of cognitive explanations is that they only explain proximal origins of symptoms, so what is happening now to produce symptoms. A distal explanation focusses on what initially caused the condition. It is uncelar how genetic variation or childhood trauma might lead to issues in metarepresentation or central control. Therefore cognitive theories on their own only provide partial explanations for SZ.