Clinical Flashcards
Anorexia nervosa
An eating disorder characterised by persistent low body weight. There are three main criteria that must be met for a diagnosis to be given.
Anorexia nervosa - criterion A
Restriction of energy intake resulting in body weight being significantly below what would be expected based on the patients age and height (BMI under 17.5)
Anorexia nervosa - criterion B
An intense fear of gaining weight or participating in persistent behaviour that will interrupt the gaining of weight even though current body weight is very low. E.g. excessive exercise or purge-binge
Anorexia nervosa - criterion C
Distortion of body image where the body weight is hugely overestimated and the patient is unable to accept the severity of the low body weight. There is an emphasis on body weight in the patients view of themselves leading to poor body image.
Anorexia nervosa - features (onset)
Usually diagnosed in teenage years (13-18), often coinciding with stressors such as starting university or leaving home
Anorexia nervosa - features (prevalence)
1:10 Male to female ratio, 3.6% prevalence in females, 0.1% in males, high prevalence in high income countries
Anorexia nervosa - features (prognosis)
High mortality rate, six times as many deaths as expected for females, staying longer during the first hospitalisation predicted better outcomes
Anorexia nervosa - physical symptoms
Affects the whole body. Symptom include: thinning hair, low blood pressure, weak muscles, osteoporosis, kidney stones, intestinal problems, periods stopping and bruising easily.
Anorexia nervosa - subtypes - restrictive
Weight loss shown through dieting, excessive exercise or fasting in significant periods within the last three months
Anorexia nervosa - subtypes - binge eating/purging
Recurrent bouts of binge eating behaviours alternating with purging, such as self induced vomiting or laxatives, shown within the last three months
Anorexia nervosa - reliability of diagnosis
Strength - Sysko et al (2012)
Weakness - Thomas et al (2015)
Sysko et al (2012)
Measured test-retest reliability with patients being interviewed by telephone using the DSM-5 criteria, three to seven days later the interview was repeated using a different assessor. The extent of agreement was described as excellent
Thomas et al (2015)
Pointed out that many studies go beyond the DSM-5 criteria, for instance using the BMI cut off of 17.5, therefore reliability may be lower in real life.
Anorexia nervosa - validity of diagnosis
Weakness - Smith et al (2017)
Smith et al (2017)
Looked at the validity of four severity specifiers. In 109 adults diagnosed with anorexia nervosa, a higher BMI (indicating low severity) was linked to greater eating disorder psychopathology, the opposite of the expected outcome.
Co- morbidity
Anorexia nervosa is associated with comorbidity, where two or more medical conditions are simultaneously present in the patient
Classification system definition
A checklist of signs and symptoms which helps a clinician to reach a diagnosis of a specific disorder, often through a process of elimination
DSM-5 (Diagnostic and statistical manual)
Describes the symptoms, features and risk factors of over 300 mental and behavioural disorders
DSM-5 - section one
Offers guidance about using the new system
DSM-5 - section two
Details the disorders and is categorised according to our current understanding of the underlying causes and similarities between the symptoms, it is used to provide a diagnosis.
DSM-5 - section three
Includes suggestions for new disorders, which currently require further investigation. It also includes information on the effect of culture on the presentation of symptoms and how they are presented
Diagnosing using the DSM-5
Clinicians would gather information about an individual through observation and interviews (structured and unstructured).
Process of elimination, with a best-fit system
DSM-5 - inter-rater reliability
Two clinicians interview the same individual, strong reliability if they both reach the same diagnosis
DSM-5 - test-retest reliability
The diagnosis is repeated by the same clinician after a time period, strong reliability if the same diagnosis is reached
Descriptive validity
Individuals diagnosed with the same disorder show similar symptoms, a high DV if the symptoms are only accurate for that disorder.
Aetiological validity
Individuals with the same disorder have similar causes for their behaviour
Concurrent validity
Using more than one method or technique to diagnose
4D model of diagnosis
Used to help determine when a mental issue is considered a mental disorder, giving treatment implications. It involves deviance, dysfunction, distress and danger
4D model of diagnosis - deviance
Deviant behaviours are those that are unusual or undesirable, therefore an understanding of the social norms and context are required to evaluate it. The failure to conform to social norms may lead to negative attention so is a good indicator of psychological abnormality.
4D model of diagnosis - dysfunction
Symptoms which distract, confuse or interfere with a persons ability to carry out their usual roles and responsibilities (such as working or socialising). The WHODAS II is one of the main questionnaires used to measure dysfunction.
4D model of diagnosis - distress
Symptoms that cause emotional pain or anxiety, as well as physical symptoms such as always feeling tired. However distress can be normal in some scenarios so context is important before a diagnosis can be given. The Kessier psychological distress scale (a ten item questionnaire) is used to help determine the length and intensity of the distress.
4D model of diagnosis - danger
Careless, hostile or hazardous behaviour that jeopardises the safety of the individual or others.
4D model of diagnosis - strengths
High validity - the model is neither over or under inclusive, when all four Ds are used in the diagnosis. If only one was used (such as deviance an erratic person may be diagnosed yet somebody with depression may not be)
Objective measurements e.g the Kessier psychological scale are used, increasing reliability
4D model of diagnosis - weaknesses
Can be subjective - deviance is subjective as it is dependent on statistical and cultural norms, decreasing validity
Inconsistencies in the expression of the Ds - inconsistencies in how distress is displayed and is caused between people, clinicians need to know the context
Language may result in labelling - using danger as a criterion may lead to negative labelling and ultimately self-fulfilling prophecy.
DSM-5 - strengths
Good levels of agreement - Regier et al (2013)
High validity - Kim-Cohen et al (2005)
DSM-5 - weaknesses
Diagnosis says nothing about the causes of the disorder, the result of a diagnosis is simply a label that says nothing useful (such as how to treat it based on its causes)
Falling standards - Cooper et al (2014)
Regier et al (2013)
Reported that three disorders had kappa values from 0.6-0.79 (very good) and seven more had values from 0.4-0.59 (good). This is important as the criterion for these disorders have changed over time, shows that the DSM-5 is reliable due to high levels of agreement
Kim-Cohen et al (2005)
Demonstrated the concurrent validity of (CD) through interviewing children and mothers, observing the children’s behaviour and questionnaires from teachers. Specific risk factors showed aetiological validity and predictive validity was also shown as five year olds with CD were more likely to show behavioural difficulties at age seven. Shows high validity in some orders in the DSM.
Cooper et al (2014)
Showed that what counts as acceptable agreement has decreased over time. The DSM-5 taskforce classified levels as low as 0.2-0.4 as acceptable, therefore it may be less reliable than previous DSM editions, with some diagnoses being made in error or being missed
Schizophrenia
A psychotic disorder characterised by positive symptoms such as delusions, hallucinations and disorganised thinking. The DSM requires at least two of the four main symptoms for a diagnosis to be made and one month of active symptoms, with six months of disturbance to everyday functioning
Schizophrenia - four key symptoms
Though insertion
Hallucinations
Delusions
Disorganised thinking
Schizophrenia - thought insertion
When a person believes that their thoughts do not belong to them and have been planted by an external source, they experience a blurring of the boundaries between themselves and others believing it to be permeable.
Schizophrenia - hallucinations
Involuntary, vivid and clear perceptual experiences that occur in the absence of any external stimuli. They can be visual, olfactory, somatosensory or auditory (which are most common, with people hearing voices that are not their own inner voice).
Schizophrenia - delusions
Fixed beliefs that are not amenable to change even in the light of conflicting evidence. They may be related to everyday life (thinking the police are watching you) or be more bizarre (thinking an alien is trying to remove your brain).
Schizophrenia - disorganised thinking
Is inferred from a person’s speech, which may be characterised by derailment (having a series of unrelated ideas) or tangentiality (going off on a completely different topic). The person may switch from one topic to another or jumble seemingly unrelated ideas, word salad refers to apparently random and incoherent stringing together of words and neologism to the blending of words together to create new words. Mixing up words can be common so it is only symptomatic if it leads to dysfunctional communication.
Schizophrenia - features
Lifetime prevalence 0.3-0.7% (varies with ethnicity and nationality)
Onset - males (early to mid 20s), females (late 20s)
Prognosis - males poorer than females (a minority recover completely but positive symptoms tend to reduce over time with the negative symptoms remaining.)
Diagnosis of schizophrenia - reliability
Regier et al (2013) reported a kappa score of 0.46 (good) using the DSM-5 while Sartorius et al (1995) used the ICD-10 to quote a score of 0.86. Only 3.8% of clinicians said that they lacked confidence in their diagnoses using the ICD-10. However it is not easy to diagnose as many symptoms are shared e.g. hallucinations with drug withdrawal
Diagnosis of schizophrenia - validity
It can be difficult to diagnose if the client is from a different cultural background to the clinician. For example, Rastafarians often use neologisms that are a play on English words, however a clinician that was unaware of this may think that they showed disorganised thinking , reducing the accuracy of diagnosis.
Anorexia nervosa - biological explanations
Specific genes - EPHX2, ITPR3, DAT1, 5-HTR2A
Twin studies - Holland et al (1984)
Grice et al (2002)
Studied 192 families, where one family member had received an AN diagnosis and another had been diagnosed with an eating disorder. No significance until they looked at the sub-group of 37 families with two members diagnosed with restrictive AN.
Gorwood et al (2003)
Heritability of AN is 70%
Strober et al (2000)
Anorexia nervosa is rare in first-degree relatives of those that have never had an eating disorder, but is 11.3 times more likely in those that did.
EPHX2
Codes for the enzyme epoxide hydrolase, a mutation may lead to a change in the active site of the enzyme, disrupting the metabolism of cholesterol. People with anorexia likely to have high cholesterol (maybe less impulse to eat)
ITPR3
Codes for a taste receptor (sweet and bitter). Mutation may lead to faulty receptor, people with AN may have less motivation to eat because it tastes weird.
DAT1
Codes for a dopamine transporter protein (re-uptake channel), a mutation may lead unusually levels of dopamine desensitising the reward pathway and leading to down regulation. Less motivation to eat
5HTR2A
Codes for a serotonin receptor, a mutation may lead to less motivation to eat
Scott-Van Zeeland (2014)
EPHX2 gene was faulty in people with anorexia compared controls (1200 compared to 1900). However no cause and effect
Anorexia nervosa - biological explanations - weaknesses
Polygenic - not solely down to the influence of a single gene, AN is a complex disorder three different criterion
New science and technology (isolating genes), reductionist approach and needs to be developed
Holland et al (1984)
30 female pairs (16Mz, 14Dz), four male pairs and one set of male triplets, selected as one member was diagnosed with AN. High concordance (55%) for Mz female twins compared to 7% for Dz twins. Significant
Equal environment assumption decreases validity
Anorexia nervosa - cognitive explanation
Distorted body schemas
Irrational beliefs
Impaired global and enhanced local processing
Anorexia nervosa - cognitive explanation - distorted body schemas
Gadsby (2017). Our body schema is our mental image of what our body’s own shape and size, people with AN have a distorted one seeing themselves as bigger than they actually are
Anorexia nervosa - cognitive explanations - irrational beliefs
Steinglass (2007) suggests that people with AN have the dominant core belief of fearing gaining weight or becoming fat, for some this is so extreme that it is delusional. This can make them resistant to treatment
Anorexia nervosa - cognitive explanations - enhanced local and impaired global processing
Enhanced local processing - have an eye for detail, readily perceiving and focusing on tiny flaws
Impaired global processing - the ability to integrate details into a meaningful overall pattern, people with AN find it difficult to see the bigger picture and are unable to perceive their overall body shape accurately
Anorexia nervosa - cognitive explanations - strengths
Guardia et al (2012)
Sachdev et al (2008)
Sachdev et al (2008)
Tested brain activity levels using fMRI, finding a difference between activity levels in AN patients when looking at images of their own bodies.
Anorexia nervosa - cognitive explanations - weaknesses
Long et al (2016) - explanation lacks validity as it does not explain the causes of AN
Cornelissen et al (2013) - challenges the role of body image distortion
Long et al (2016)
No difference between recovered AN patients and non-AN control participants on the ROCFT, a measure of global and local processing. Concluded that weak central coherence could be due to starvation in AN rather than causing it, explaining why it may disappear after recovery.
Cornelissen et al (2013)
Compared AN and control participants on a morphing task, adjusting a computerised image of themselves until it matched their own estimate of body size. No significant difference between AN participants and controls.
Anorexia nervosa - cognitive treatment
CBTE - enhanced cognitive behavioural therapy
CBTE
Used to tackle behaviours associated with distorted behaviours towards food and eating
Usually 20 sessions with four defined stages (Murphy et al 2010)
Fairburn (2008) adjusted CBT to CBTE as a therapy for all eating disorders on an outpatient basis
CBTE - stage 1
Introduces a weekly weigh in (they cannot weigh anywhere else) and regular eating (by creating an eating plan, giving a daily routine).
Usually takes four weeks with two sessions a week
CBTE - stage 2
Reviewing progress over two sessions
Barriers identified and planning for stage 3
CBTE - stage 3
The main stage of treatment that will take approximately 8 sessions
Identify the ways that the clients self-evaluation is dependent on body weight and shape, learning how to focus on other parts of life
Dietary rules (current) are identified and the therapist helps the client to break them
CBTE - stage 4
Aims to maintain progress and prevent relapse
Weekly weigh ins continue at home and working together in a plan for the next twenty weeks, before a follow up session
The client continues with strategies such as rule breaking and avoiding body checking.
Anorexia nervosa - cognitive treatment - strengths
Fairburn et al (2015)
Cooper et al (2016)
Fairburn et al (2015)
Randomly allocated 130 participants with eating disorders to either CBT-E or IPT. After 20 weeks 65.5% of CBT-E patients and 33.3% of IPT patients were judged to be in remission. After 60 weeks 69.4% for CBT-E and 49% for IPT.
Cooper et al (2016)
The people with the longest duration of the disorder, as well as the people with the greatest pre-occupation for body shape had worse outcomes.
Anorexia nervosa - cognitive treatment - weaknesses
Soderston et al (2017)
High drop out rates - (Carter et al 2012) it is a demanding therapy that requires commitment from the client (homework and attending sessions) as well as making difficult changes to their thoughts and behaviours.
Not effective on everyone - NICE recommends it for use on adults, and all of Fairburn’s participants had a BMI of over 17.5
Soderston et al (2017)
Compared CBT and a ‘normalisation of eating’ procedure. They found a remission rate of 75% and relapse of 10% over five years compared to 45% and 30% for CBT.
Carter et al (2012)
Found a 45% dropout rate for a CBT-E programme. This decreases the effectiveness as only the participants that complete a course are included in the results
Anorexia nervosa - biological treatment
Drug treatments - biochemical mechanisms (such as neurotransmitters) are known to underly the disorder therefore altering or stabilising these mechanisms may benefit AN symptoms
Antipsychotics
Antidepressants
Second generation antipsychotics (SGAs)
Anorexia nervosa - biological treatment - antipsychotics
Dopamine antagonists as dopamine levels are thought to be abnormally high in people with AN.
They block some post-synaptic dopamine receptors reducing the activity of the dopamine symptom.
This helps to counter the distorted cognitions of fatness (similar to schizophrenic delusions) and reduced appetite
Anorexia nervosa - biological treatment - antidepressants
Reduce the uptake of serotonin at the synapse, increasing its availability in neurotransmission, extending the appetite enhancing effects of serotonin. This would help as low serotonin is thought to play a role in the disorder.
Anorexia nervosa - biological treatment - SGAs (second generation antipsychotics)
Affect the activities of several other neurotransmitters apart from dopamine and are a current, promising research focus. This includes the drug olazapine, which has the well known side effect of weight gain. It is a powerful antagonist of dopamine as well as a weak antagonist of serotonin
Anorexia nervosa - biological treatments - strengths
Boachie et al (2003)
Application to managing drug side effects - knowing about side effects means that they can be managed, increasing the likelihood of sufferers continuing treatment
Boachie et al (2003)
Used olanzapine to treat four children with AN, these children gained significant amounts of weight (a kilo a week) and experienced less anxiety at mealtimes when on the treatment
Anorexia nervosa - biological treatment - weaknesses
Kafantaris et al (2011)
Lebow et al (2013)
Drugs treat symptoms and not causes - they may treat the symptoms but not the causes, therefore it is only a temporary fix that could be reversed if they stop taking the drug
Kafantaris et al (2011)
Found that 15 adolescents given olanzapine gained weight and showed improved eating attitudes but so did the control group at the same rate
Lebow et al (2013)
People with AN that took SGAs showed increases in BMI and body satisfaction, however these were not significantly different from the placebo group. Drugs were also associated with greater anxiety and worse overall symptoms than controls
Rosenhan (1973) - aims
To reveal what he saw as flaws in the process of psychiatric diagnosis.
To provide evidence that mental health disorders did not lie within the individual but within the diagnosis
Rosenhan (1973) - procedure - initial study
Eight pseudo patients (5 male, 3 female including a psychology student, paediatrician, painter and three psychologists)
Each presented themselves at a psychiatric hospital complaining of the same symptoms (hearing a same sex, unfamiliar and unclear voice that said words such as ‘empty’, ‘hollow’ and ‘thud’ that are not normally associated with schizophrenia)
Pseudonyms used to protect the pseudo patients and those involved with psychology or medicine gave false professions to avoid suspicion, all other information provided was true and if asked they said the voices had stopped.
In total they approached twelve hospitals in five states
Once admitted they behaved normally, as in order to be released they had to convince staff that they were sane
They kept records of their observations, initially in private but later in public
Rosenhan (1973) - procedure - follow up study
After the initial study hospitals wanted to show that they couldn’t be tricked so Rosenhan agreed to send more pseudopatients to see if they would be identified (none were sent)
Staff had to rank all patients 1-10 where 1 was high confidence that the patient was fake
Rosenhan (1973) - procedure - mini experiment
Pseudopatients approached a staff member at a hospital and asked a courteous question about their release, compared to asking a member of staff a question at Stanford university campus
Rosenhan (1973) - findings - initial study
All pseudopatients were admitted to hospital (seven with schizophrenia and one with bipolar disorder)
When released they were said to have schizophrenia in remission
The length of stay ranged from 7-52 days with an average of 19
30% of patients in the wards voiced suspicions on the pseudopatients
Rosenhan (1973) - findings - follow up study
At least one member of staff (psychiatrist or nurse) reported with high confidence that 41/193 were fake, 23/193 were reported by at least one psychiatrist and a further 19 were reported by both
Rosenhan (1973) - findings - mini study
Only 4% received an answer from a psychiatrist and 0.5% from a nurse, compared to 100% on university campus
Rosenhan (1973) - conclusions
We cannot distinguish between the sane and insane in psychiatric hospitals, the hospital creates situational factors that led to the depersonalisation and segregation of patients.
Overdiagnosis was because clinicians avoided calling sick people healthy, however in the follow up they learnt that a more benign environment may lead to less distorted perceptions of participants
Rosenhan (1973) - strengths
High ecological validity - covert participant observation increased the validity of the findings.
Application to the DSM - the study led to changes being made to the DSM, through the defining of mental disorders.
Rosenhan (1973) - weaknesses
Demand characteristics - the psychiatrists would not expect anybody to pretend that they had symptoms, assuming that everyone that seeks admission would have a good reason to do so. This may challenge some of the conclusions.
Low generalisability - a limited sample of hospitals were used and only a small number of individuals were pseudo patients, limiting the generalisability as culture has been shown to affect diagnosis.
Schizophrenia - neurotransmitters explanation - dopamine hypothesis - hyperdopaminergia
An excess of the excitatory neurotransmitter dopamine, caused when vesicles release dopamine too easy and often.
Amphetamines are agonists (increase the action of) dopamine, if normal people take them then they suffer similar symptoms to schizophrenics including hallucinations. This shows that schizophrenia may be the result of excess dopamine.
Antipsychotics reduce the mode of action of dopamine (binding to their receptor sites on the post-synaptic neurone) and have been found to reduce schizophrenic symptoms
Schizophrenia - neurotransmitters explanation - dopamine hypothesis - causes
Hyperdopaminergia - reduced beta hydroxylase (enzyme that breaks down dopamine in the synapse) leads to an increased likelihood of binding to the proliferation of D2 receptors on the post-synaptic neurone
Davis et al (1991)
Hyperdopaminergia explains positive symptoms of schizophrenia (hallucinations, distorted thinking, delusions and thought insertion), finding that schizophrenics with positive symptoms have increased dopamine in the meso-limbic pathway.
Hypodopaminergia explains the negative symptoms (flat affect, alagia)
Schizophrenia - neurotransmitters explanation - serotonin
Carlsson et al (2000) reviewed the findings of other studies finding that clozapine (antipsychotic) binds to D1 and D4 receptors but weakly to D2 receptors to reduce positive symptoms, however from existing knowledge we know that schizophrenics have high levels of D2 receptors suggesting that dopamine as a cause is reductionist. It also binds to serotonin receptors reducing both positive and negative symptoms as serotonin regulates dopamine in the meso-limbic pathway
Schizophrenia - neurotransmitters explanation - strengths
Tenn et al (2003)
Zhao et al (2016)
Schizophrenia - neurotransmitters explanation - weaknesses
Veling et al (2008)
Insel (2010)
Tenn et al (2003)
Rats given nine amphetamine injections over three weeks showed schizophrenic symptoms, which can manifest itself as social withdrawal or stereotypical movements.
Dopamine antagonists were successful in reversing these effects
Zhao et al (2016)
Conducted a meta-analysis comparing 18 antipsychotics from 56 randomised control trials with over 10,000 participants. They found that the antipsychotics tested had significantly lower relapse rates than placebos
Veling et al (2008)
Showed that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants in the Netherlands, this correlates with the amount of actual and perceived discrimination received by each group. The neurotransmitter explanation could not explain this.
Insel (2010)
Individuals with early onset schizophrenia often exhibit similar pre-diagnosis symptoms, specifically not hitting cognitive milestones. There is also a genetic overlap between individuals developing autistic symptoms from age three and schizophrenic ones from age 18, supporting an epigenetic role
Carlsson et al (2000) - aims
To look at the relationship between schizophrenia and dopamine
To look at glutamatergic deficiency
Carlsson et al (2000) - procedure
Using secondary data (meta-review)
A number of studies used PET scans
Overactivity of a neurotransmitter, would lack radioactivity, underactivity would appear yellow and red
Carlsson et al (2000) - results
Neurotransmitters interact and affect each other (looked at glutamate and serotonin as well as dopamine)
Focused on glutamate because drugs like PCP and ketamine produce psychotic symptoms but affect glutamate receptors (NMDA) instead of dopamine ones.
Lodge et al (1989)
Glutamate seems to regulate the behaviour of dopamine in the brain, when glutamate is high dopamine is low. Miller and Abercrombie (1996) showed that the release of dopamine is increased if glutamate activity is reduced
Low levels of glutamate seem to relate with both positive (low levels in the striatum) and negative symptoms (low levels in the cerebral cortex)
Lodge et al (1989)
Found that glutamate activity at the NMDA receptors produces psychotic responses in rats and humans
Carlsson et al (2000) - conclusion
Suspect that there are different sub populations of schizophrenia patients whose symptoms have different biological explanations, including a particular attention to those with glutamatergic deficiency
Carlsson et al (2000) - strengths
Application to the development of new drug treatments - glutamate agonists used to reduce both positive and negative symptoms of schizophrenia. By tackling neurotransmitters more directly side effects are also reduced, reducing dropouts from treatment
High reliability - Svensson and Carlsson (1990)
Svensson and Carlsson (1990)
Gave mice a drug to reduce motor activity and then one to reduce glutamate and increase serotonin and dopamine levels. This resulted in highly abnormal psychotic like behaviour
Carlsson et al (2000) - weaknesses
Gogos et al (2015)
Low generalisability - a person in remission is more likely to complain about side effects than during acute episodes, research needs to consider a wider range of phases
Luhrmann (2018)
Gogos et al (2015)
The experience of woman may be different due to the neuroprotective role of oestrogen which appears to regulate glutamate, serotonin and dopamine. Woman also have a later average onset and better prognosis
Luhrmann (2018)
70% of American people said their voices told them to hurt people, whereas 50% of Ghanaians said that their voices were mainly positive and only 20% said they told them to kill or fight. This shows that the symptoms present differently dependent on culture
Schizophrenia - genetic explanation
Hilker et al (2018)
Wright (2014)
COMT gene
DISC1 gene
Diathesis stress model
Epigenetics
Hilker et al (2018)
Heritability of schizophrenia is 79%, there is a high genetic influence
Wright (2014)
As many as 700 genes are linked to the development of schizophrenia
Schizophrenia - genetic explanation - COMT
The COMT gene codes for the enzyme catechol-O-methyltransferase, which breaks down neurotransmitters, including dopamine in the pre-frontal cortex. The deletion of this gene would result in the production of the enzyme stopping, leading to less dopamine regulation and hyperdopaminergia (linked with positive schizophrenic symptoms)
Schizophrenia - genetic explanation - COMT - strengths
Egan et al (2001)
Egan et al (2001)
Found a link between decreased dopamine in the pre-frontal cortex and the ‘val’ allele of the COMT gene. Concluded that having two copies of the allele increased the risk of schizophrenia by 50%
Schizophrenia - genetic explanation - DISC1
Codes for the creation of GABA, a neurotransmitter that regulates dopamine and glutamate. Dysfunction of the gene can lead to hyperdopaminergia, which has been linked to positive schizophrenic symptoms
Schizophrenia - genetic explanation - DISC1 - strengths
Kim et al (2012)
Dahoun et al (2017)
Kim et al (2012)
People with an abnormality in the DISC1 gene are 1.4 times more likely to develop schizophrenia
Dahoun et al (2017)
Conducted a review of 14 studies concluding that DISC1 was associated with pre-synaptic dopamine regulation.
Schizophrenia - genetic explanation - diathesis stress model
Schizophrenic correlated genes may be present but the development of the disorder only occurs due to the presence of other biological or environmental factors. These include cannabis, seven times more likely to develop schizophrenia due to interference with the dopamine system.
Schizophrenia - genetic explanation - diathesis stress model - strengths
Tienari et al (1994)
Tienari et al (1994)
Conducted a 21 year longitudinal adoption study, supporting the diathesis stress model. Adopted children whose biological mother had schizophrenia were more sensitive to family dysfunction in the adoptive home than those from low risk matched backgrounds
Schizophrenia - genetic explanation - epigenetics
Suggests that genes can be turned on or off due to environmental stressors, changing the way that the genetic code is expressed.
Schizophrenia - genetic explanation - epigenetics - strength
Sussar and Shang Lin (1992)
Pederson and Mortenson (2006)
Sussar and Shang Ling (1992)
Found that pregnant women during the Dutch famine of 1944 went on to have low birth weight babies, which were more than twice as likely to develop schizophrenia than normal.
Pederson and Mortenson (2006)
Stated that the longer a person is exposed to city life and a higher population density, the more likely they were to develop schizophrenia
Schizophrenia - genetic explanation - strengths
Gottesman and Shields (1966)
Application to genetic counselling - recurrence risk can be calculated to determine the risk of the heritability of the disease, affecting family planning
Gottesman and Shields (1966)
Identified a concordance rate of 42% for Mz twins compared to 9% for Dz twins, showing the genetic role in the development of schizophrenia.
Schizophrenia - genetic explanation - weaknesses
Gottesman and Shields (1966) - equal environment assumption, correlational study (not causal, diathesis stress model shows that other factors may account for this difference)
Schizophrenia - non-biological explanation
Social adversity
Urbanicity
Social isolation
Immigration and minority status
Schizophrenia - non-biological explanation - social adversity
Some children grow up in environments that are less favourable than others, making them more vulnerable to mental health disorders. For example, families exposed to unemployment and poverty may be exposed to more stress. People from lower socioeconomic groups may also not have access to treatment for schizophrenia.
Schizophrenia - non-biological explanation - urbanicity
Eaton (1974)
Increased population density makes life more competitive, increasing the stressor of chronic social defeat, a stressor which may elicit schizophrenic symptoms.
Eaton (1974)
City life is more stressful than rural life and long term exposure to such stress may trigger an episode of schizophrenia. These stressors include, noise, pollution, criminality and greater anonymity
Schizophrenia - non-biological explanation - social isolation
Faris (1934)
Faris (1934)
Suggested that people with schizophrenia withdraw because they feel that contact with others is stressful. This self-imposed isolation cuts the individual off from feedback about what behaviours or thoughts are inappropriate and in the absence of corrective feedback they begin to behave weirdly.
Schizophrenia - non-biological explanation - immigration and minority status
Boydell et al (2001)
Veling (2008)
Boydell et al (2001)
Research in many countries has shown that first and second generation immigrants are at greater risk of schizophrenia than the general population. However, this risk decreases as the number of people from that same ethnic background increases.
Veling (2008)
Schizophrenia may be a reaction towards the chronic experience of prejudice and discrimination. Second generation immigrants have a greater risk because they have a weaker cultural identity.
Schizophrenia - non-biological explanation - strengths
Vassos et al (2012)
Veling et al (2010)
Application to treating schizophrenia - can help deal with schizophrenia by drawing attention to factors affecting mental health at the community level. Housing projects reduce overcrowding and encourage neighbourhood cohesion.
Schizophrenia - non-biological explanation - weaknesses
Not a complete explanation - Gottesman and Shields show a genetic contribution to the development of schizophrenia, suggesting that environmental factors may only trigger the onset of the disorder in those that are genetically predisposed
Data is correlational - no causation between urbanicity and adversity and the development of schizophrenia. Social drift hypothesis suggests the opposite, people with schizophrenia find it hard to hold down a job, leading them to drift into lower social classes.
Vassos et al (2012)
Performed a meta-analysis of data from four studies conducted in Sweden, Denmark and the Netherlands, including nearly 24,000 cases of schizophrenia. They found the risk was 2.37 times higher for people living in the most urban areas compared to those in the most rural.
Veling et al (2010)
Found that people classified as marginalised (weak national and ethnic identity) and assimilated (strong national but weak ethnic identity) were at greater risk of schizophrenia than those that were classed as integrated (strong national and ethnic identity) or separated (weak national but strong ethnic identity). Suggests that a strong ethnic identity may be a protective factor against schizophrenia.
Schizophrenia - biological treatment
Drugs - antipsychotics
Schizophrenia - biological treatment - first generation antipsychotics (FGAs)
Dopamine agonists which greatly reduce positive symptoms by blocking post-synaptic dopamine receptors.
FGAs also have some unpleasant side effects such as tardive dyskinesia, potentially leading to poor compliance and subsequent relapse
Barlow and Durand (1995)
E.g. chlorpromazine
Barlow and Durand (1995)
Although FGAs are effective in reducing positive symptoms, as many as 40% see no effect at all. Many others also experience negative symptoms
Schizophrenia - biological treatment - second generation antipsychotics (SGAs)
Block dopamine receptors but also act upon serotonin and glutamate receptors. This reduces both positive and negative symptoms.
E.g. clozapine
Lally and MacCabe (2015)
Lally and MacCabe (2015)
One side effect is the blood condition agranulocytosis, however the drug is still useful with treatment resistant clients. It provides up to 60% relief for such people
Schizophrenia - biological treatment - protocol
Patel et al (2014)
Patel et al (2014)
Review on the efficacy of medication for schizophrenia, explaining that it is important to start medication use quickly to be effective. In the first seven days after a psychotic episode the objective is to decrease hostility and return the client to normal functioning. The individual is carefully monitored for side effects and changes in symptoms. Once the symptoms have begun to subside a maintenance dose is prescribed to combat relapse (18-32% in those that do and 60-80% in those that don’t).
Schizophrenia - biological treatment - additional considerations
Amphetamines, alcohol, caffeine and nicotine can all disrupt the effectiveness of anti-psychotic medications, therefore support for substance use may also be considered through treatment.
Schizophrenia - biological treatment - strengths
Zhao et al (2016)
Application to deinstitutionalisation - drugs have meant that people with schizophrenia have been able to live in society instead of living in institutional care
Zhao et al (2016)
A meta-analysis comparing 18 anti-psychotics utilising data from 56 randomised control trials with over 10,000 people. They found that 17 of the anti-psychotics tested had significantly lower relapse rates than placebos.
Schizophrenia - biological treatment - weaknesses
Kapur et al (2000)
Turner et al (2012)
Drugs treat symptoms and not causes, the effects will be reversed once the client has stopped taking them
Kapur et al (2000)
Cautions against overgeneralising from animal studies. High doses of medication can be given to animals so that D2 receptors can be effectively blocked out, but this would lead to severe side effects in humans. Such research may show how symptoms are reduced but not how side effects would interfere with everyday life.
Turner et al (2012)
There is publication bias towards studies that show a positive outcome for anti-psychotic drugs, therefore the effectiveness is exaggerated. Drug companies have a strong interest in the continuing success of antipsychotics and fund much of the research
Schizophrenia - non-biological treatment
CBTp
Schizophrenia - non-biological treatment - irrational thoughts
Thoughts identified as irrational
The therapist teaches the patient coping skills to cope with their symptoms
Decompensation - preventing schizophrenics from retreating into their delusions
Schizophrenia - non-biological treatment - ABC model
A - activating event (first experience)
B - leads to either rational or irrational beliefs
C - leads to consequences
The ABC model traces the origin of the patients symptoms helping them to understand them
Schizophrenia - non-biological treatment - behavioural experiments
Evaluating and disrupting the content of irrational thoughts - done by assuming the thought is true and breaking down the rational
Schizophrenia - non-biological treatment - behavioural activation
The therapist sets tasks for the patient to do and feedback on
Schizophrenia - non-biological treatment - strengths
Directive - the patient decides whether to complete the homework or not
Effectiveness - NICE (2014)
Side effects - Kuipers et al (1997)
Expense - more cost effective than other talking therapies due to limited umber of sessions (16), solves problems payment for drugs is constant
Reasons - looks at underlying reasons for the disorder
Types of people - Addington and Addington (2005)
NICE (2014)
Meta analysis showed that CBT reduced rehospitalisation rates for 18 months and reduced the amount of time in hospital. Symptom severity and psychological functioning also improved
Kuipers et al (1997)
Randomised control of CBT, finding that drug resistant clients improved when given CBT.
Addington and Addington (2005)
In the acute phase (sever symptoms) self reflection is not appropriate, however once stabilised CBTp is an effective treatment
Schizophrenia - non-biological treatment - weaknesses
Directive - therapist is in control of the tasks set and determine which beliefs are irrational
Effectiveness - Jauhor et al (2014)
Side effects - behavioural experiments may cause high levels of stress and anxiety.
Expense - more expensive than drug therapies due to high levels of training
Reasons - reductionist - focuses on thought processes controlling the behaviour (not all of which are conscious)
Types of people - Kingdon aand Kirschen (2006)
Jauhor et al (2014)
Large scale meta-analysis found a small therapeutic effect on key symptoms, however these disappeared when the study was blind (researchers did not know who was getting CBTp)
Kingdon and Kirschen (2006)
Investigated 142 schizophrenic patients within a psychiatry hospital, finding that many were not suitable for CBTp because they have to want to change
Clinical case study
Lavarenne et al (2013)
Lavarenne et al (2013) - aims
Used an outpatient therapy group to describe how a group can provide a firm boundary within which individuals can explore their own fragile ego boundaries
Lavarenne et al (2013) - procedure
The therapy group met consistently and usually consisted of ten members that had a vulnerability to psychosis. Four members were not present at the session used as the casestudy. All members were receiving drug treatments, and the sessions were not taped or recorded but the emotions expressed and verbal content was coded
Lavarenne et al (2013) - findings
Earl - rejected gifts from Brett, potentially representing his fear of being annihilated. He responded by discussing a multi-national oil project that was interpreted as an attempt to hold the pieces of his self together, identifying a boundary between himself and the others
Dan - had been silent for the first six months attending the group, but did not stop talking. Told the group that he had an out of body experience
Lavarenne et al (2013) - conclusion
The notes from sessions show that all patients were working hard to hold themselves together. Interactions with other people threaten their fragile boundaries, so they cut themselves off from human relations
Lavarenne et al (2013) - related AO1
In depth look at one group (outpatient therapy group)
Looked at unusual behaviours (all had vulnerability to psychosis)
Emotions expressed and verbal content were coded (qualitative data collected and turned into quantitative data)
Focused on one individual session
Lavarenne et al (2013) - related AO3
Confidentiality may be impaired (named Brett, Earl and Dan in findings)
No before and after comparison (lack of generalisability)
Therapists conducted the group (may lock objectivity)
Clinical interview
Vallentine et al (2010)
Vallentine et al (2010) - aims
Investigated the usefulness of psycho-educational material provided via group work for offender patients in a high security psychiatric hospital
Vallentine et al (2010) - procedure
42 male patients detained under the mental health act, referred to understanding mental illness psycho-educational group as they were judged to be able to gain from further information. Using ICD-10 80% diagnosed with schizophrenia, they took part in four 20 session groups over three years.
Two outcome measures given to pre and post group:
Self concept questionnaire - 30 item questionnaire measuring self esteem
Semi-structured interview - to evaluate patients experience of the group
Vallentine et al (2010) - related AO3
Used content analysis, subjective identification of themes
Recorded data - reanalysed by a second researcher, 60% level of agreement
Semi-structured interview - different experience for each participant
