Schizophrenia and Diagnosis of Mental Disorders

A TWIN STUDY: GOTTESMAN & SHIELDS (1966)

THE GENETIC CAUSE OF SCHIZOPHRENIA

Common triggers include:

• Drug abuse (such as new types of potent cannabis)

• Stress

• Family tensions

Aims:

1. To find out if there is a genetic basis for schizophrenia.

2. Also, to replicate previous twin studies into schizophrenia to test their reliability. In particular, the researcher looks for concordance rates in MZ twins where one suffered from schizophrenia and compared these to concordance rates in DZ twins to see if there was a significant difference which would be explained by genes.
   
   IV
   
   This is an independent groups design, since it looks at the difference between DZ twins and MZ twins. Because zygocity is a naturally-occurring variable, this is a natural experiment.
   
   DV
   
   The researcher's measured the concordance rate for pairs of twins in four different categories.
   
   Sample
   
   62 schizophrenic patients, half male, half female and all aged 19 to 64. All had been patients at a large London hospital between 1948 and 1964 and all had a twin. The researchers originally identified 68 but had to reduce this because some were now out of the country or else it was impossible to tell if they were MZ or DZ twins.
   
   Procedure
   
   The researchers had to assign each twin pair to either MZ or DZ conditions. Zygocity was determined by:

• fingerprint testing (different patterns suggest DZ)

• blood testing (different blood groups means DZ)

• physical resemblance (different hair/eye colour and sex means DZ)

24 MZ twin pairs and 33 DZ twin pairs were identified.

Mental health in the twin was measured by a range of tests:

• hospital notes

• questionnaires and semi-structured interviews with twins and parents

• 30 minute tape recording of speech, to identify language problems (a negative symptom)

• personality testing

• psychometric testing to measured disorganised thinking (a positive symptom)

Results:

• In every category, there was a significant difference between MZ and DZ twins, with MZ twins being more likely to share a similar diagnosis of mental illness. The concordance was stronger for female twins than male twins and also stronger with more severe schizophrenia.

• There seems to be a genetic component to schizophrenia because the closer the genetic link, the more likely both twins are to show schizophrenic symptoms. However, the MZ concordance rate was significantly lower than 100%. This means that, despite their shared genotype, MZ twins do not always share schizophrenic symptoms - 21% of MZ twins with a schizophrenic brother or (less commonly) sister were perfectly healthy. This suggests that genetics is not the only cause of schizophrenia.

• Gottesman & Shields conclude that genes may predispose a person towards schizophrenia, but there needs to be an environmental trigger. This is called the diathesis-stress model (Rosenthal, 1963) and it takes into account nature and nurture.

STRENGTHS OF TWIN STUDY: GOTTESMAN & SHIELDS (1966)

Generalisability:

• This study has a fairly large sample and covers a range of ages, from teenagers to men and women in their 60s. There's a 50/50 mix of men and women and even a high proportion of 'rare' MZ twins in the study.

Application:

• The people need to know they have a genetic predisposition to schizophrenia so that they can avoid triggers (like drug abuse or excessive alcohol, highly stressful professions, etc). Armed with this research, doctors can monitor "at-risk" patients for early symptoms that might go unnoticed. Like most mental illnesses, schizophrenia cannot be cured but its harmfulness can be reduced if it is recognised early.

Validity:

• Gottesman & Shields' findings tie in with earlier research and Rosenthal's theory of the diathesis-stress model of schizophrenia. This gives their research concurrent validity (they agree with the previous studies) and construct validity (they agree with the theory).

Ethics:

• The participants in this study were mostly adults who agreed to take part knowing what was being researched. The youngest participants were teenagers and may have needed parental consent, but parents were heavily involved in the research process so that was surely given.

WEAKNESSES OF TWIN STUDY: GOTTESMAN & SHIELDS (1966)

Generalisability:

• The sample may not be representative. Besides the problem of twins being unusual people, these particular twins were particularly unusual. Many of them were admitted to hospital in the '40s and '50s after their experiences in WWII. Some of them had been prisoners of war (POWs). These traumatic experiences might have led to all sorts of lifelong problems, not just "ordinary" schizophrenia.

Reliability:

• By modern standards, the procedures are not reliable. Without DNA testing, assigning zygocity by physical resemblance and fingerprints is not accurate. However, in the Brendgen et al. (2005) study, Brendgen assigned zygocity based on appearance then checked this with DNA testing and found it to be 94% accurate, which is quite high.

• If Gottesman & Shields were that accurate, then at most 2 or 3 twin pairs were mis-assigned, probably DZ twins being mis-assigned to MZ. In this case, the real difference between MZ and DZ twins might have been even greater than it appeared!

Validity:

• The twins' illnesses might be nothing to do with schizophrenia - for example, having to care for a mentally ill twin is stressful and depressing, but that doesn't necessarily make you schizophrenic too.

Ethics:

• There are some concerns about obtaining consent from mentally ill participants who may not be competent to understand and agree to the research. However, parents and carers may give presumptive consent instead.

• This sort of research has a strong social responsibility to shed light on the causes of schizophrenia and perhaps help reduce the suffering it causes.

Heston (1966) - ADOPTION STUDY

Adoption studies use a correlational technique to see if there is a relationship between the children and their parents.

Aim: To test whether schizophrenia and other mental disorders were a cause of nature or nurture by seeing how many adopted children of biological mothers with schizophrenia would go on to develop it themselves.

Conditions: The participants were all born between 1915 and 1945 to schizophrenic mothers in an American psychiatric hospital. Children were selected if their mother: ● Had put them up for adoption ● Was diagnosed with schizophrenia ● Had evidence of behaviour consistent with schizophrenia ● Had no diseases ● The mother and child were separated from birth

Sample: 74 children satisfied the conditions, but 16 participants were dropped for reasons including death, contact with their mother, disease, and no control participant, which left 58 total participants. These 58 were matched with like controls on sex, type of eventual placement, and length of time in child care. A control group was used to possibly eliminate the fact that adoption itself was the cause of schizophrenia. However, due to further deaths and loss of contact via follow-up, there were a final 47 experimental participants (30 male, 17 female), and 50 controls (33 male, 17 female).

Procedure:

• Conducted personal interviews with the participants in their homes

• Conducted MMPI (Minnesota Multiphasic Personality Inventory - a mental health personality test)

• Collected their IQ scores (either from school/other records or one was conducted)

• Looked at police/retail credit/school/psychiatric hospital records, criminal and civil court actions, and reviewed newspaper files.

• Contacted relatives, friends, and employers

• Noted the social class of the participant’s first home and their current social class

Results:

• No differences in the number of participants, age, gender, adoption rate, or IQ.

• No differences in children, divorces, marriage rates, school years, social groups, or years serving in the armed forces.

• Differences found in psycho-social disability, schizophrenia, time spent in penal or psychiatric institutions, IQ deficiency, as well as sociopathic and neurotic personality disorder, crimes, and the number discharged from the armed forces due to psychiatric or behavioural issues.

• The rate of schizophrenia to those with schizophrenic mothers was 10.6% compared to 0% in those not born to individuals with schizophrenia.

Conclusion:

• The findings support the influence of genes in schizophrenia and that inheritance also contributes to psycho-social disability.

• However, Heston also reports that ½ of the participants born to schizophrenic mothers were successful adults who possessed artistic talented and imaginative adaptations to life which was not found in the control group. Therefore, it can be concluded that there must be other possible factors influencing the development of schizophrenia.

Strengths of Heston (1966) - ADOPTION STUDY

Reliability:

Several aspects followed a standardised procedure which allows for replication, e.g.:

• Each participant’s dossier was evaluated using the same approach (i.e., blindly and individually, then a third time by Heston). This allows for high inter-rater reliability as a total of 3 researchers confirmed the evaluative assessment of the adoptees and whether they had schizophrenia, making the study objective and removing bias with high scientific credibility.

• The interviews were standardised with the same questions being asked to each participant, meaning the results will be easily comparable and the procedure itself can be replicated.

Application:

There is a clear genetic link for schizophrenia. This finding can be used to develop research in order to prevent schizophrenia being passed on.

Validity:

High ecological validity as the experiments were conducted in a natural environment (the participants’ home) so their behaviour will be quite natural.

Weaknesses of Heston (1966) - ADOPTION STUDY

Generalisability:

There was a small sample of 47 adopted participants from Oregon, meaning the findings/conclusions cannot be generalised to other cultures outside of the USA/Oregon, especially collectivist cultures.

Ethics:

Participants were contacted by letter asking if they'd like to take part, meaning informed consent was obtained. However, some questions could've caused stress as they were very personal.

Reliability of the DSM-3

Spitzer (2012) and his colleagues felt that 0.7 on Cohen’s kappa would indicate ‘good agreement’.

Johnstone and Miners (2014)

Suggests psychologists are turning to ‘formulation’ as an alternative to diagnosis. This involves building up a personal story that allows the clinician to understand how past traumatic experiences have caused current distress.

Regier and colleagues (2013)

3 disorders including PTSD had kappa values ranging from 0.60-0.79 (very good) while seven more diagnoses including schizophrenia had kappa values of 0.40-0.59 (good).

Major depressive disorder (MDD) had one of the least reliable diagnoses (0.28)

Cooper (2014)

DSM-5 task force classified kappa values 0.2-0.4 as ‘acceptable’, so the fall in standards suggests DSM is less reliable than previous versions because of the risk of error during diagnoses.

Poniozovsky et al. (2006)

Strengths - Reliability of ICD:

• Compared reliability of ICD-9 and ICD-10 using PPV (positive, predictive value) which is the proportion of people getting the same diagnosis when reassessed.

Galeazzi et al. (2004)

Strengths - Reliability of ICD:

• Compared reliability of ICD-9 and ICD-10 using PPV (positive, predictive value) which is the proportion of people getting the same diagnosis when reassessed.

Mason et al. (1997)

Strengths - Validity of ICD:

• Good predictive Validity for Schizophrenia

• ICD-9 & ICD-10 were reasonably good at predicting disability in 99 people with schizophrenia 13 years later.

Luhrmann et al. (2015)

Cultural Differences in Hearing Voices:

• Interviewed 60 American, Indian & Ghanaian people with schizophrenia

• 70% of Americans - harmful, destructive voices.

• 50% of Ghanaians - mainly positive voices.

• 20% of Ghanaians - voices told them to kill or fight.

• Indian people tended to hear family members compared to only 10% of Americans.

Strengths - DSM-5 and ICD-10 are reliable because of consistent schizophrenia diagnosis

• Regier et al. (2013) - Kappa value was 0.46 in field trials of DSM-5.

• Sartorius et al. (1995) - high kappa value of 0.86.

Davis et al. (1991)

Dopamine Deficiency - Hypodopaminergia

Suggests:

Excess Dopamine in the mesolimbic pathway - positive symptoms of schizophrenia

Limited Dopamine in the mesocortical pathway - negative symptoms of schizophrenia

Insel (2010)

• Suggests schizophrenia stems from abnormalities in early brain development, starting in the first few weeks of gestation.

• People who exhibit schizophrenic symptoms in their late teens & early 20s exhibit similar prodromal (pre-diagnostic symptoms).

Howes & Kapur (2009)

Dopamine Dysregulation & schizophrenic symptoms:

• Describes dopamine dysregulation in the striatum as a common pathway to psychosis.

Tenn et al. (2003)

Strengths of Neurotransmitters (biological explanation of schizophrenia):

• Research Support - Found rats given 9 amphetamine injections over 3 weeks showed various schizophrenic symptoms, which can be seen as social withdrawal.

Snyder (1985)

Strengths of Neurotransmitters (biological explanation of schizophrenia):

• Support for D2 receptors - Chlorpromazine acts as an antagonist at many D1 & D2 dopamine receptors, has an antipsychotic effect.

Dépatie & Lal (2001)

Weaknesses of Neurotransmitters (biological explanation of schizophrenia):

• Showed that apomorphine, a dopamine agonist that stimulates D2 receptors, does not include psychotic symptoms.

• This challenges how hypodominergia is responsible for positive symptoms of schizophrenia.

Veling et al. (2008)

Weaknesses of Neurotransmitters (biological explanation of schizophrenia):

Second Generation Immigrants:

• Showed Moroccan immigrants in the Netherlands were more likely to be diagnosed than Turkish Immigrants & correlated with the amount of actual & perceived discrimination faced by each group.

Hilker et al. (2018)

Schizophrenia: Genetic Influence (One other biological explanation)

• A recent estimate for the heritability of schizophrenia is 79%.

Wright (2014)

Schizophrenia: Genetic Influence (One other biological explanation)

• As many as 700 genes have been linked to schizophrenia.

Houston et al. (2008)

Schizophrenia: Genetic Influence (One other biological explanation)

Diathesis-Stress Model: Schizophrenia genes are only triggered by biological and environmental factors.

• ‘Stress’ was often seen as psychological, created by harsh parenting.

• Stress is now seen as anything that risks triggering schizophrenia.

Susser & Lin (1992)

Schizophrenia: Genetic Influence (One other biological explanation)

Epigenetics: How genes are turned on and off by environmental stressors.

• Reported that women who became pregnant during the famine had low birth weight babies who were twice as likely to develop schizophrenia.

Mil et al. (2006)

Schizophrenia: Genetic Influence (One other biological explanation)

Epigenetics:

• Found MZ twins had up to 20% greater ‘methylation’ of two genes linked with schizophrenia.

Gottesman (1991)

Strengths for Schizophrenia: Genetic Influence (One other biological explanation)

Research Support:

• Found a clear relationship between genetic similarity and an increase in two related individuals having schizophrenia.

Gottesman & Shields (1966)

Strengths for Schizophrenia: Genetic Influence (One other biological explanation)

Research Support:

• Found a concordance rate of 42% for MZ twins and 9% for DZ twins.

Dahown et al. (2017)

Strengths for Schizophrenia: Genetic Influence (One other biological explanation)

Research Evidence on DISC1 and COMT genes:

• Reviewed 14 studies and concluded that DISC1 is associated with presynaptic dopamine dysregulation, a key factor in schizophrenia.

Egan et al. (2001)

Strengths for Schizophrenia: Genetic Influence (One other biological explanation)

Research Evidence on DISC1 and COMT genes:

• Proposed a link between decreased dopamine activity in the PFC and 1 form of the COMT gene.

Tienari et al. (1994)

Issues & Debates:

Strengths for Schizophrenia: Genetic Influence (One other biological explanation)

• A 21-year longitudinal study supports the diathesis-stress model.

• Adopted children whose biological mothers were diagnosed with schizophrenia were more sensitive to family dysfunction in adoptive homes than those from low-risk backgrounds.

Pederson & Mortensen (2006)

Weaknesses for Schizophrenia: Genetic Influence (One other biological explanation)

• Research demonstrates the longer a person is exposed to urban life (dense population), the greater the risk of developing schizophrenia.

What are the 4D’s?

DEVIANCE: These are behaviours and emotions that are viewed as unacceptable. Extremely abnormal behaviour conflicts with social norms; people feel anxious or threatened by the person who is deviant.

DYSFUNCTION: This is when the abnormal behaviour is significantly interfering with everyday tasks and living your life.

DANGER: They are a threat to society

DISTRESS: This is the simple view that abnormality involves being unhappy: experiencing negative feelings like anxiety, isolation, confusion and fear. Abnormality is when these negative feelings occur inappropriately or persist longer than they should.

APPLYING DIAGNOSES TO REAL LIFE (A02)

A serious problem with the application of diagnosis is false diagnosis. These false into two types:

• Type I Error or False Positive: diagnosing someone with a mental disorder when they are healthy

• Type II Error or False Negative: diagnosing someone as healthy when in reality they are ill

False Positives come from "reading too much" into the client's behaviour. It can also come from the fear of the consequences of a False Negative (if a mentally ill person is told they are normal then goes and hurts or kills themselves). False Negatives can come from the suspicion that the client is faking their illness or the belief that their deviant behaviour is deliberate wickedness.

Cultural Problems:

• People from other cultures presenting their symptoms to a Western doctor may express themselves in unfamiliar ways. For example, among African-Caribbeans it is not abnormal to talk to dead relatives while grieving. This can lead to them being diagnosed with a much more severe disorder than they really have (such as schizophrenia rather than mild depression) - a false positive diagnosis.

EVALUATING DIAGNOSES (A03)

Supporting Research:

• The use of diagnostic systems means more communication between clinicians, which increases inter-rater reliability (Spitzer & Fleiss, 1974).

• Factitious disorders (like Munchausen Syndrome) exist where people fake illness or psychological disorder to get medical attention. This indicates deviance from the norm, as well as distress felt by the individual through faking illness; there may be danger, as they may harm themselves to back up their claims; dysfunction may incur as faking the illness involves losing jobs, withdrawing from social life, etc.

Opposing Research:

• There has been found to be only a 68% agreement (Andrews et al, 1999) between the ICD and DSM.

• Rosenhan (1973) provides evidence that diagnoses are flawed, as staff were unable to tell mentally disordered patients apart from those who were healthy.

• The lack of objectivity of the four Ds raise issues about reliability of diagnosis. If the four Ds are used by two different therapists, they may not reach the same diagnoses. For example, Dissociative Identity Disorder (multiple personality) is a recognised disorder in the USA but not in Britain.

• Spitzer & Fleiss (1974) carried out a meta-analysis of 6 studies and found some similarities in how disorders were diagnosed by psychiatrists but many differences. They claim that reliability is not high for the diagnosis of any mental disorder and that reliability for schizophrenia is just 'fair' rather than 'good'.

Different Theories:

• Davies proposes that a 5th D - Duration - needs to be included. Grief is a good example, because a period of grief is normal after the death of a loved one (in fact, not grieving would be abnormal) but if the grief goes on too long (like Queen Victoria) then that becomes abnormal instead.

• Recovery Model - It grew out of a movement in the 1980s and '90s that rejected institutionalization and drug therapy and focused on the testimonies of people who "beat their illness" by changing their lives.

• Arenella (2015) argues that the recovery model is gaining ground over the medical model because drugs and psychiatrists are expensive but social workers are much cheaper.

Application:

• African-Caribbean people in the UK are 3-5 times more likely to be diagnosed with schizophrenia and hospitalised than other groups. You are also more likely to be diagnosed with serious mental disorders if you are poor. Women are more likely to be diagnosed than men.

Diagnosis

The process of matching a person’s behaviours, cognitions, feelings and desires to the signs and symptoms of a recognised mental disorder to provide information and prognosis.

The 4D’s of Diagnosis

Deviance:

• Unusual, bizarre behaviours.

• Statistical and social norms are necessary to determine how undesirable behaviour is.

• Failure to conform to social norms may lead to negative attention and social exclusion.

Dysfunction:

• Symptoms interfering with the ability to carry out daily responsibilities.

• Objective measures are used by psychologists to assess everyday functioning and the abilities to follow routines.

Distress:

• Symptoms causing emotional pain or anxiety.

• Quantitative data is collected using Kessler Psychological Distress Scale

Danger:

• Careless, hostile behaviour jeopardising safety

• Predicting violent behaviours are hard, but a record makes another incident more likely

• UK’s ‘Mental Health Act’ only needs 3 professionals to agree that an individual is a danger to themselves and others.

STRENGTHS OF Diagnoses using 4D’s

• All 4 features help avoid erroneous diagnoses.

• Avoids eccentric, harmless people being seen as abnormal, but common, debilitating symptoms of depression are missed.

WEAKNESSES OF Diagnoses using 4D’s

Lack of Objectivity:

• Feelings are subjective when rated

• Clinician requires information about the person and their community to apply the 4Ds properly.

Fazel et al. (2009)

• 4D’s create labels - media distortion can cause schizophrenic people to seem more dangerous than normal people.

Classification Systems: DSM-5

Features:

• Focuses more on mental and emotions

• Important introductory step for appropriate support and treatment

• Describes and classifies symptoms, features and associated risk factors of over 300 mental and behavioural disorders

Structure:

Consists of 3 sections:

• 1 - Guidance about using the new system

• 2 - Details of disorders, categorised according to current understanding of underlying causes and similarities

• 3 - Includes information about the impact of culture on the presentation of symptoms and how they are communicated.

Diagnosis using DSM:

• Unstructured and structured clinical interviews based on symptoms

• General practitioners can diagnose uncomplicated symptoms whilst difficult cases can take weeks or months.

Types of Validity for DSM-5

1. Descriptive Validity - 2 people with the same diagnosis exhibit similar symptoms

2. Aetiological Validity - 2 people with the same diagnosis have similar causal factors

3. Concurrent Validity - Clinician uses more than 1 method to reach the same diagnosis'

4. Predictive Validity - Accurately predicting outcomes

STRENGTHS OF DSM-5

• Good level of agreement for some disorders. Development of new criteria for PTSD.

• Kim-Cohen et al. (2005) found that DSM has predictive validity for conduct disorders in children.

WEAKNESSES OF DSM-5

• Issue of failing standards

• Acceptable level of agreement has fallen, reducing reliability and validity.

• Prone to cultural barriers, language barriers and miscommunication

• Patients can choose to lie or withhold information from the clinician

Classification Systems: The ICD-10

Features:

• It includes all diseases and disorders (physical and psychological), not just mental disorders. ICD-10 includes 10 groups of mental disorders, such as delusional disorders, mood disorders, clinical/personality disorders etc. It is bases its diagnoses around symptoms.

• Each disorder has a code starting with ‘F’, listed consecutively and there are 11 sections.

• Each section contains ‘leftover codes’ so new disorders can be added

Process:

• Select key words from client interview relating to symptoms

• Use alphabetical index

• Locate sub-category

Weaknesses of ICD-10

• Presentation, communication and interpretation of symptoms are shaped by language and culture.

• Culture bias can lead to different diagnoses from physicians of different cultures.

• Diagnostic practices and standards may differ internationally.

Strengths of ICD-10

• PPV scores for schizophrenia increased from 68% in 1989 to 94.2% in 2003, showing high reliability of ICD.

• Good predictive validity for schizophrenia.

APPLYING DIAGNOSTIC MANUALS (A02)

• It's normal and healthy to grieve when a loved one dies. DSM-IV contains a "bereavement exclusion criterion" for Major Depressive Disorder. This meant that you couldn't be diagnosed as depressed if you had been bereaved (lost a loved one) up to 2 months ago. DSM-5 removes this exclusion, allowing for a grieving person to be diagnosed with a mental disorder.

EVALUATING DIAGNOSTIC MANUALS (A03)

Supporting Research:

• Research by Rosenhan (1973) and Spitzer & Fleiss (1974) showed how important it was to make diagnosis more valid and reliable. Wilson (1993) suggests that DSM-III was developed precisely to tackle the unreliability of the previous systems.

• There is evidence that the DSM is improving. Brown et al. (2001) tested the reliability of the DSM-IV. They studied anxiety and mood disorders in 326 out-patients in Boston, USA. The patients underwent two independent clinical interviews and there was high level agreement for most of the DSM-IV categories.

Opposing Research:

• Normal grief being diagnosed as Major Depressive Disorder (MDD) because the bereavement exclusion criterion has been removed.

• Forgetfulness in old age might be diagnosed as Mild Neurocognitive Disorder, leading to the "worried well" being diagnosed with dementia

• Binge Eating Disorder will lead to a mental disorder being diagnosed for people who are just greedy. Behavioural Addiction is a diagnosis that be applied to anything we like doing a lot (like Pokemon Go).

• This can create a lot of Type 1 errors, leading to unnecessary prescribing of medical drugs which is expensive and harmful.

Different Theory:

• There has been found to be only a 68% agreement (Andrews et al, 1999) between the ICD-10 and DSM-IV on an assessment of 1500 patients. However, Andrews found agreement on diagnosis for depression, substance dependence and generalised anxiety.

• Hoffman et al. (2015) compared DSM-5 and ICD-10 in a study of alcoholism among over 7000 prisoners. The two systems agreed in diagnosing healthy individuals and those with severe alcoholism. However, the diagnoses differed when it came to mild-to-moderate alcohol disorders. About a third of those with mild alcohol disorder according to DSM-5 received no diagnosis from ICD-10.

Application:

• Patients increasingly self-diagnose using medical websites which are based on DSM-5

Diagnosis of Schizophrenia

1. DSM-5: The person must have at least 1 month of active symptoms and 6 months of disturbance to everyday functioning. Requires at least 2 of the 5 key symptoms.

2. ICD-10: Less focus on dysfunction and 6 months of disturbance is not necessary.

Positive Symptoms of Schizophrenia

Additions to normal behaviour:

• Delusions: Harmful fixed beliefs resistant to change

• Hallucinations: Unrealistic perceptual experiences (sensory)

• Thought Insertions: Believing thoughts are implanted by an external source

Negative Symptoms of Schizophrenia

Absence of certain behaviours:

• Disorganised thinking: Jumbled and unrelated thoughts leading to incoherent speech.

• Flat Affect (Lack of emotion)

• Mutism

• Avolition (lack of goal-directed behaviour)

Nurture - Cultural Differences in Schizophrenia

Luhrmann et al. (2015) interviewed 60 American, Indian & Ghanaian people with schizophrenia

1. 70% Americans heard destructive and harmful voices

2. 50% Ghanaians heard mainly positive voices

3. 20% of Ghanaians heard voices telling them to kill or fight

4. Indians tended to hear family members

Features of Schizophrenia

1. Onset slightly earlier in males than females

2. Prognosis is variable and hard to predict while only a minority recover

3. 0.3-0.7% lifetime prevalence (uncommon)

4. Males have poorer prognosis than females

Evaluation of Features & Symptoms of Schizophrenia

STRENGTHS:

• Reliability - Schizophrenia diagnosis is highly consistent using DSM-5 & ICD-10. Sartorius et al. (1995) - Kappa value of 0.86

• Detailed descriptors for reliable diagnosis

WEAKNESSES:

• Hard to distinguish with other mental disorders

• Accurate diagnosis requires awareness & sensitivity to cultural & linguistic differences

Biological Explanation of Schizophrenia

Desbonnet (2016) - ORIGINAL DOPAMINE HYPOTHESIS - HYPERDOPAMINERGIA

• Found overactive dopamine D2 receptors in areas like the limbic system linked to positive symptoms of schizophrenia.

• Negative & Cognitive schizophrenia symptoms can link to low functioning of dopamine D1 receptors in the PFC.

Causes of hyperdopaminergia:

1. Low levels of beta hydroxylase may build up excess dopamine in the synapse

2. Proliferation of D2 dopamine receptors in postsynaptic cells

Davis et al. (1991) - HYPODOPAMINERGIA

• Positive symptoms - excess dopaminergic activity in the mesolimbic pathway

• Negative Symptoms - lack of dopaminergic activity in the mesocortical pathway

Developmental Psychology:

Insel (2010) - schizophrenia stems from early abnormalities in brain development. Genetics overlap with other disorders.

Effect of Serotonin on Schizophrenia - CLOZAPINE

• Clozapine binds to D1 & D4 receptors but weakly to D2.

• Binds to serotonin receptors, greatly reducing positive & negative symptoms

• Negative symptoms may be caused by irregular serotonin activity

Dopamine Dysregulation

Howes & Kapur (2009):

• High presynaptic levels of dopamine can cause ‘psychosis proneness’ and not just schizophrenia

• Dopamine dysregulation explains referential delusions and aberrant salience (can lead to hallucinations and delusions)

Evaluation Of Biological Explanation of Schizophrenia

STRENGTHS

1. Tenn et al. (2003): supported by research on rats treated with amphetamines

• Rats given 9 amphetamine injections over 3 weeks showed various schizophrenic symptoms like social withdrawal.

2. Snyder (1985): Support for D2 receptors

• Chlorpromazine acts as an antagonist at many dopamine receptors and has an antipsychotic effect.

• Haloperidol is a dopamine antagonist with a narrower range of biochemical effects.

• Excess activity on D1 and D2 dopamine receptors can lead to development of schizophrenia

3. Application:

• Atypical drugs and dopamine antagonists allow schizophrenic individuals to live in residential care.

WEAKNESSES:

1. Dépatie & Lal (2001): apomorphine, a dopamine agonist that stimulates D2 receptors does not induce psychotic symptoms, showing how excess dopaminergic activity does not cause positive schizophrenia

2. Veling et al. (2008): Social stress can cause 2nd generation immigrants to be more prone to psychosis

3. Reductionist - only focuses on biological view

One Other Biological Explanation of Schizophrenia - GENES

Hilker et al. (2018) - 79% heritability of schizophrenia

DiGeorge Syndrome - deletion of 30-40 neighbouring genes located on chromosome 22 has a 25% chance of developing schizophrenia

COMT Gene: COMT is an enzyme that breaks down dopamine in the PFC, so the deletion of the COMT gene can cause negative symptoms of schizophrenia.

DISC1 Gene: Abnormality causes issues in the creation of GABA and people are 1.4 times more likely to develop schizophrenia (Kim et al. 2012).

Original Diathesis Stress Model: Genes are triggered by environmental factors. Stress was seen as a trigger for schizophrenia. Mil et al. (2006) found MZ twins had up to 20% greater ‘methylation’ of 2 genes linked to schizophrenia.

Evaluation Of One Other Biological Explanation of Schizophrenia - GENES

STRENGTHS:

1. Empirical Support - Gottesman (1991) found a clear relationship between genetic similarity and an increase in 2 related individuals having schizophrenia.

2. Gottesman & Shields (1966) found a concordance rate of 42% for MZ twins and 9% for DZ twins.

3. Egan et al. (2001) proposed a link between hypodopaminergic activity in the PFC and 1 form of the COMT gene, which causes negative symptoms of schizophrenia.

4. Dahoun et al. (2017) reviewed 14 studies and found DISC1 gene was associated with presynaptic dopamine dysregulation.

5. Support for the original diathesis model: Tienari et al. (1994) found adopted children from schizophrenic biological mothers were more sensitive to family dysfunction compared to those from low-risked backgrounds, showing how social and environmental stressors can trigger genes for schizophrenia.

WEAKNESSES:

1. Other factors also increase risk of schizophrenia - Pederson & Mortensen (2006) demonstrated that the longer a person is exposed to urban life, the higher the risk of developing schizophrenia.

2. Reductionist theory

One Non-Biological Explanation of Schizophrenia - SOCIAL FACTORS

1. Social Adversity - Basic human needs are not met by an individual. Eaton (1974) - city life is more stressful

2. Urbanity - Increased competition & population density elicits schizophrenic symptoms. Lederbogen et al. (2011) found urban participants had greater activity in the amygdala and ACC compared to rural areas using fMRI scans, showing stress and emotional regulation is higher in urban participants.

3. Faris (1934) - Schizophrenia can cause social isolation.

4. Social Defeat Hypothesis - when a person or animal is exposed to hostile confrontations, causing high stress.

Evaluation Of One Non-Biological Explanation of Schizophrenia - SOCIAL FACTORS

STRENGTHS:

1. Support for social causation hypothesis: Vassos et al. (2012) performed a meta-analysis of data from 4 studies and found risk of schizophrenia was 2.37 times higher urban than rural settings.

2. Veling et al. (2010) - Weak ethnic identity increases risk of developing schizophrenia.

3. Application - Importance of housing projects that encourage neighbourhood cohesion & cultural diversity.

WEAKNESSES:

1. DIATHESIS STRESS MODEL: Environmental factors only trigger the onset of schizophrenia for people already genetically predisposed.

One Biological Treatment

1. Typical Antipsychotics (FGAs):

• Chlorpromazine is a dopamine antagonist that greatly reduces positive symptoms by blocking postsynaptic dopamine receptors.

• Barlow & Durand (1995) - 40% of schizophrenic patients do not gain relief and still experience negative symptoms. Side effects like tardive dyskinesia can cause relapse.

2. Atypical Antipsychotics (SGAs):

• Clozapine blocks dopamine, serotonin and glutamate receptors (antagonistic effect), reducing both positive and negative symptoms.

• Lally & MacCabe (2015) - Provides relief for 60% but has fatal side effect of agranulocytosis.

• Risperidone - more recent SGA that binds stronger to dopamine receptors with less side effects.

2. TGAs:

• Glutamate agonists

Trials: 118 schizophrenic people, 4 week double-blind trial. Random allocation to 3 conditions:

1. 40 mg twice daily of new TGA

2. 15mg of a SGA

3. Placebo

Both new TGA and SGA showed superior response rates compared to placebo.

Individual Differences: Texas Medication Algorithm Project (TMAP)

STAGES

1. Risperidone

2. Different SGA/FGA

3. Clozapine

4. Different combinations of FGAs and SGAs along with mood-stabilising drugs.

5. ECT shocks to non-dominant hemisphere of the brain

Patel et al. (2014) - Medication use should be early for higher effectiveness. Maintenance dosage should be maintained for 12 months after remission to prevent relapse (only 18-32% schizophrenic patients relapsed after taking maintenance dosage).

Evaluation Of One Biological Treatment

STRENGTHS:

• Zhao used a large meta-analysis and found 17 antipsychotics tested had significantly lower relapse rates than the placebo. This shows drug treatments are cheap and effective if medicine fails.

• Application: Antipsychotics allow schizophrenic people to remain in the community and live normal lives.

WEAKNESSES:

• Patel found only 20% of schizophrenic patients showed consistent improvement after multiple FGA trials whilst 45% experienced partial improvement with severe side effects.

One Non-Biological Treatment

Cognitive-Behavioural Treatment: 5-20 sessions in groups or individually

Aim: Helping clients identify irrational thoughts & delusions and change them.

Process: Therapist encourages self-awareness in clients so that they can recognise specific situations to precede decompensation (decline of normal functioning to psychosis). Stress management and coping strategies are used.

• Verbally challenging the clients’ perceived reality through a recording.

• Evidence is then discussed so their delusions can be debunked.

EXAMPLE - Combs et al. (2007): LN

• LN was hospitalised for aggressive behaviour out of the delusion that social services were stealing from her. This was based on getting several phone calls where the caller immediately hung up and seeing people in the shared carpark. This was debunked when a family member helped find 3 missing items.

Evaluation Of One Non-Biological Treatment

STRENGTHS:

1. NICE (2014) - A meta-analysis of CBT studies found that CBT was effective in reducing re-hospitalisation for up to 18 months and time spent in hospitals. CBT also reduced symptom severity and improved psychosocial functioning 12 months after treatment.

2. Kuipers et al. (1997) - conducted a randomised control trial on CBT & found drug-resistant clients improved when given CBT which targeted delusions and hallucinations.

WEAKNESSES:

1. CBT overlooks individual differences - Bradshaw (1998) found that relationship between client and therapist was also important for the journey to self-recovery.

2. McKenna & Kingdon (2014) - CBT was only superior to routine treatment in 2/9 trials.

3. Challenging client’s delusions can be distressing.

Classic Study: Rosenhan (1973)

Aim: To reveal deep flaws in process of psychiatric diagnosis by providing evidence to support the idea that mental disorders are subjectively determined by the person making the diagnosis.

Procedure:

• 3 males and 5 females as pseudopatients who complained of the same symptom at a psychiatric hospital

• They claimed to hear same-sex, unfamiliar voice that said ‘empty’ and ‘hollow’ terms

• 12 hospitals in 5 states in the East and West coast

• Pseudopatients proved they were sane by cooperating with staff and socialising with other patients

• Pseudopatients then asked the staff about their release

Findings:

Initial study:

• 7 diagnosed with schizophrenia and 1 with bipolar disorder

• 19 day average hospitalisation

• 30% of patients voiced suspicion on pseudopatients

Follow-Up Study:

• At least 1 member of staff wrongly reported 41/193 were fake.

• Slater (2005) replica in 9 psychiatric wards was diagnosed with psychotic depression, which was later disagreed upon by many psychiatrists, showing how Rosenhan’s claims were not era-bound.

Conclusion:

1. Hospital environment created a set of situational factors that led to depersonalisation & segregation

2. Self-fulfilling prophecies

Evaluation Of Classic Study: Rosenhan (1973)

STRENGTHS:

• Covert Observation allowed for quantitative and qualitative data to be collected

• High ecological validity

WEAKNESSES:

• Only 1 pseudopatient per hospital and pseudopatients only recorded negative interactions.

• Clinicians were made to feel incompetent and real patients were discriminated against

Contemporary Study: Carlsson et al. (2000)

Aims: Biological Explanation of Schizophrenia

• To provide an up-to-date review of current status of dopamine hypothesis

• Glutamate, serotonin & GABA for new antipsychotics

Procedure & Findings:

Carlsson explains evidence from PET/SPECT that supports the Dopamine Hypothesis (dopaminergic dysfunction):

• Schizophrenic participants show more dopamine activity than a healthy control group, especially in a part of the brain called the basal ganglia

• However, Laruelle et al. (1999) found that schizophrenia patients in remission (not showing symptoms) only had normal dopamine activity

• Carlsson et al. point out the patients taking antipsychotics complain most about the side-effects while their symptoms are in remission - not surprising if their dopamine activity becomes normal during this time and the drugs are causing hypodopaminergia (too little dopamine)

Carlsson et al. focus on glutamate for two reasons:

• Drugs like PCP ("angel dust") and ketamine produce psychotic symptoms, but instead of activating dopamine they stimulate glutamate receptors called NMDA

• Lodge et al. (1989) claim glutamate activity at NMDA receptors produces psychotic reactions (it is "psychotogenic") in rats and humans

Low levels of glutamate (hypoglutamatergia) seems to link with both positive and negative schizophrenic symptoms. Carlsson locates this activity in an area of the brain called the striatum (reward centre) and in the cerebral cortex (which includes the frontal lobe, where conscious behaviour happens).

• The "treatment resistant" patients who don't respond to typical antipsychotics (that reduce dopamine) might have a more glutamatergic condition instead

• Clozapine is an atypical antipsychotic that has better results with "treatment resistant" patients and this might be because it doesn't target dopamine (it targets serotonin instead)

Conclusion: Carlsson suspects there are probably different groups of schizophrenia patients ("subpopulations") whose symptoms have different biological explanations - not always the Dopamine Hypothesis. There may be a subpopulation suffering from glutamatergic deficiency and these deserve "special attention". Lack of glutamate might cause patients to have an exaggerated response to dopamine at the post-synapse.

Evaluation Of Contemporary Study: Carlsson et al. (2000)

STRENGTHS:

1. PET scans makes research reliable and replicable

2. Development of new antipsychotic drugs that focus on serotonin and glutamate

WEAKNESSES:

1. His review of studies is not generalisable to modern society and research.

2. Evidence for dopamine hypothesis was based on acute schizophrenia but people with chronic schizophrenia may respond differently to drugs.