Clinical psychology

The 4d of diagnosis: deviance

Deviance from social norms:

• Based around the idea of social norms (agreed ways of acting/normal behaviours within a society).

• Those who break them are abnormal (abnormal in society), e.g., hearing voices

• Affected by:

  • Culture (different cultures have different social norms)

  • Context (e.g., the clothes you wear in certain situations)

  • Age (certain behaviours expected by different age groups)

  • Gender (certain behaviours expected in males vs females)

  • Historical context (e.g., behaviours that used to be considered abnormal, such as homosexuality, are not abnormal now).

Statistical deviations:

• Those in society who have a characteristic which is infrequent are ‘abnormal’ e.g.,

• If you’re more than 2Sd away from the mean then you might be abnormal

• Illnesses examples - schizophrenia, OCD

The 4d of diagnosis: dysfunction

• If behaviours interfere with a person’s everyday life, it can be used as a way to diagnose mental disorders.

• Dysfunction can affect their working life, for example, not being able to go to work everyday, or complete work that is required if you are there.

• Inability to function normally, live life effectively etc is abnormal. For example, not going out with friends, not going food shopping etc.

• Illnesses examples: schizophrenia, OCD

The 4d of diagnosis: distress

• An abnormal behaviour is abnormal because it causes upset to the individual. E.g., they are unhappy with the symptoms they experience e.g., the symptoms that relate to OCD, Phobias, Depression, Schizophrenia

• Can be thought of on a continuum. Everyone can feel distress at times but persistent and serious distress is a concern and should be considered abnormal.

• Deals with subjective experience – each individual feels their distress uniquely.

• Illnesses examples - schizophrenia, depression, OCD

The 4d of diagnosis - danger

• This relates to people who are a danger to themselves or others (usually because of faulty thinking/behaviour).

• Examples include self-harm, suicide and violence towards themselves, or towards other individuals.

• Can be thought of on a continuum (varying degrees of danger to themselves or others).

• Illnesses examples - schizophrenia, depression

Strengths of deviance

• Deviance takes into account so many factors which make something a social norm e.g. gender, age, historical context etc → it makes this a little more holistic as a definition as it doesn't just say there is only one social norm. One clear example is the inclusion of 'context' as a factor which takes into account the fact that different behaviours may be allowable in different situations.

• Deviance (statistical) makes it more objective as there is a statistical cut off

Weaknesses of deviance

• Some behaviours may be considered deviant by some doctors but not by others, e.g., talking to yourself → using deviance may be subjective because it depends on the psychiatrist's perception of why the person is taking part in something that is deviating from social norms.

• Thomas Szasz suggests that Deviance has an issue with Social Control. In his work 'the myth of mental illness' we take behaviours we view as negative and use our power to diagnose them as a mental health issue.

• It is a reductionist way to decide on abnormality because it does not consider anything about the patient other than whether they fit within norms → means it fails to take into account other factors (like the other Ds) which might be important to make that decision.

• Deviance doesn't take into account the patient's wellbeing like D's such as Distress do. It only considers whether they fit into a social norm or not rather than how their behaviour impacts on them → making it a less complete/useful definition

• One issue is that this can be impacted by cultural factors because hearing voices is seen as normal in some cultures → this makes it a less valid/credible definition of abnormality because it isn't objective if it can change between cultures.

• Some behaviours may be considered deviant but not a symptom of a mental disorder → this makes the definition less valid/credible because if a behaviour breaks a social norm but isn't linked to a mental disorder then we can question how good a definition it is.

Strengths of dysfunction, distress and danger

• This definition is better than deviance as it considers the life quality of the patient as a factor because it talks about dysfunction/ life quality/ distress in their lives (which will damage life quality) → This means it takes into account factors about the wellbeing of the patient themselves rather than just social norms.

• We try to create objective measures of this D which doctors can use to test various illnesses, for example the 5th axis of DSM IV measured 'global functioning' which measures this.

Weaknesses of dysfunction, distress and danger

• Some behaviours may be considered dysfunctional by some doctors but not by others, such as gambling/drinking → using dysfunction may be subjective because it depends on the psychiatrist's perception of why the person is taking part in something that is 'dysfunctional'.

• This definition runs into problems because many behaviours are dysfunctional/ cause distress/ may be dangerous without being classed as an abnormality/ mental health problem e.g., repeated drunkenness → therefore questioning the validity of this definition.

DSM - diagnostic statistical manual

• Created in USA by APA in the 1950s to diagnose mental health conditions to improve the reliability of diagnosis (standardised criteria)

• Illnesses are grouped by family e.g., psychotic illness, affective disorders

• Patient will go to a doctor and explain their symptoms and the doctor will make notes - try to compare that against the symptoms listed for each illness

• Contains diagnostic criteria for all the different mental health illnesses e.g., Depression must show 5 of 9 items from the list of symptoms for a two week period

• Each diagnosis also lists things like: comorbid illness, differential diagnosis, prevalence, progression, cultural and sex differences

• Updates now on DSM V

The diagnostic interview process

• Clinician interviews the patient finding out about their symptoms and what is going on, eg hearing voices or unable to sleep

• Note key words describing symptoms

• Matches symptoms to ICD symptoms

DSM-V

• Diagnostic criteria - groups illnesses into categories and criteria

• Emerging models/ cultural formations

• Each diagnosis might contain: diagnostic criteria, diagnostic features, associated features, development and course, risk factors, culture and gender related issues, differential diagnosis, comorbidity

• Changes included removing the 5 types of Schizophrenia

• Removing the axis system

• Removing the clause for bereavement in Depression

• Combining Aspergers with Autism to become ASD

• Culturally bound syndromes included

ICD

• Published by the World Health Organisation (WHO)

• Creates a universal language for healthcare professionals worldwide

• Example: Depression diagnosed in Japan = Depression diagnosed in UK = Depression diagnosed in Brazil

• Translated into 43 different languages--Not just translation- it uses cultural adaptation (Different cultures express mental health differently for example some asian cultures describe anxiety as "heart discomfort" rather than "worry" and other cultures emphasise physical symptoms (tiredness, aches) over emotional ones (sadness)

• Has physical and mental illnesses in it

• Mental disorders are in section F with each illness being given a specific code, eg schizophrenia is 20 - subtypes of the illness are listed under it in other codes

• Patient will go to a doctor and explain their symptoms and the doctor will make notes - try to compare that against the symptoms listed for each illness

• Schizophrenia you need to have two symptoms including a main one such as hallucinations/ delusions

• Each diagnosis also lists things like: comorbid illness, differential diagnosis, prevalence, progression, cultural and sex differences

• Updated ‘regularly’ - change symptoms etc

ICD dimensional approach

• Old way (Categorical): You either have depression or you don’t

• New way (Dimensional): Mental health exists on a spectrum

• Tracks severity: Mild → Moderate → Severe

• Monitors changes over time e.g.

  • Month 1: Severe symptoms - can't get out of bed

  • Month 2: Moderate symptoms - functioning but struggling with low mood

  • Month 3: Mild symptoms - occasional low days but mostly managing

ICD changes

• ICD-11 removed Asperger's as a possible diagnosis and again incorporated it within the 'Autism Spectrum disorder'

• ICD 11 includes training material to help clinicians use it as well as a table to compare it with ICD 10 to help clinicians use it to diagnose patients with mental disorders.

Strengths of diagnostic manuals

• Using a diagnostic manual means doctors have standardised symptoms to diagnose people by → This improves the reliability of diagnosis as having the same symptoms should mean that doctors should be diagnosing the same way

• Allows for diagnosis which means it is useful as it means people can be given a medical label and can access help and support

• The manuals are ‘regularly’ updated to reflect new understanding of the illnesses and to iron out issues in the criteria → This improves the validity of the diagnosis as it will now better reflect what we know about the illness rather than being outdated.

Weaknesses of diagnostic manuals

• One issue is that the DSM and ICD differ from each other in some of the symptoms/criteria used to identify some disorders. E.g., duration needed for diagnosis. This means that there is a question about the validity of those durations and there could be issues of reliability when using the two manuals.

• Updates may hinder the reliability of the diagnosis because the criteria change. Now when people are re diagnosed later on their diagnostic label may change meaning their diagnosis was not a reliable one.

Aim of Rosenhan study 1

To investigate if sane people who present themselves to a psychiatric hospital would be diagnosed as being insane.

Sample of rosenhan study 1

• 12 different hospitals from across 5 states and included a range of different psychiatric institutions (modern and old, well-staffed and poorly staffed, one was private).

• The pseudopatients in the experiment included 5 men and 3 women.

Procedure of rosenhan study 1

• Pseudo-patients call psychiatric hospitals claiming to be hearing a muffled voice, but they could make out the words 'thud' 'hollow' and 'empty'.

• Once admitted, all participants gave honest life stories.

• As soon as they had been admitted, they claimed the 'voice' had stopped.

• The pseudopatients were observed in a natural, participant, 'covert' observation.

Results of rosenhan study 1

• 100% of pseudo-patients were admitted for treatment for diagnosed mental illnesses - 11/12 hospitals admitted them with Schizophrenia, 1 diagnosed with manic depression

• They remained in hospital for between 7-52 days, with a mean stay of 19 days.

• They were then released with a diagnosis of Schizophrenia "IN REMISSION".

• When in hospital, normal behaviours were viewed as symptoms of the illness by medical staff, e.g., waiting outside the cafe for lunch = ORAL ACQUISITIVE SYNDROME & writing in diaries = PATIENT ENGAGES IN PATHOLOGICAL WRITING BEHAVIOUR.

• A total of 2100 pills were handed to the pseudo-patients (only 2 were actually swallowed).

• Each 'real patient' spent less than 7 minutes per day with psychiatric staff.

• 35 out of 118 patients voiced their suspicions about the pseudopatient not being a 'real' patient.

• Treated inhumanely - ignored

Aim of rosenhan study 2

To see if the tendency toward diagnosing the sane as insane could be reversed

Procedure of rosenhan study 2

A teaching & research hospital was told of the first study and warned that over the next three months one or more pseudo-patients will attempt to be admitted. In reality, no pseudopatients were admitted into any hospital. Staff members rated 'new patients' on scale 1 - 10 as 'how likely to be a fraud'. 193 patients were 'assessed'.

Results of rosenhan study 2

• 41 rated as a pseudo-patient (by staff)

• 23 rated as pseudo-patient (by psychiatrist)

• 19 rated as pseudo-patient (by both)

Conclusion of rosenhan study 1 and 2

We are unable to detect sanity vs insanity

Strengths of rosenhan

• Various style of hospitals over 5 states (and a large number of their staff) which makes the results more generalisable → This means the results about diagnosis could be applied to a wider population of medical staff.

• Standardised procedure e.g., the words (thud, hollow, empty) used when going for diagnosis → This makes the study more replicable as you could repeat it with the same words like thud to see if you get a reliable result about diagnosis.

• The study is high in ecological validity because it was carried out in the staff’s natural environment of hospitals → This means the results about diagnosis could be applied to a wider population of medical staff.

• The study is low in demand characteristics because doctors and nurses didn’t know they were being observed or that the patients being admitted was actually a pseudopatient → This means they wouldn’t have changed their behaviour relating to how they treated the pseudopatients making the results more internally valid.

• The fact that the pseudopatients began acting totally normally when they were admitted means that their misdiagnosis and treatment is a valid representation of real diagnosis and treatment (rather than being influenced by their acting up) → This makes the results about diagnosis and treatment more valid.

• Quantitative and qualitative data were gathered by the pseudopatients → This means the quantitative data about diagnosis can be compared effectively whilst the qualitative data e.g., how they were treated by staff, give more depth and detail so a better understanding of mental health facilities and diagnosis.

• All of the pseudo patients were trained by Rosenhan in their observations meaning there is a high possibility of interrater reliability.

Weaknesses of rosenhan

• Validity issues- As the pseudo patients were admitted, the staff had no reason to think they were faking it, as healthy people do not say they hear voices that are not there. They lied, can’t blame the doctors for getting it wrong (essentially they showed demand characteristics).

• USA hospitas only so the results about validity of diagnosis are ethnocentric and not generalisable → The results about validity of diagnosis might not apply in other cultures like the UK or collectivist cultures.

• Only 12 hospitals were used in this sample so it is small and not generalisable → This means the results about diagnosis might not be representative of diagnosis and treatment in the whole population

• The situations which the pseudopatients found themselves in each hospital couldn’t be standardised and so it might be difficult to replicate → This means the results about diagnosis from the study might not be reliable.

• Since this is a naturalistic observation there will be extraneous variables which impact on the behaviour/treatment of the staff/pseudopatients in each hospital → This might make the results about diagnosis and treatment less valid as the EVs could have an impact.

• There could be bias in the reporting of the pseudo-patients (as this is essentially a participant observation) because they were being held there for so long when not ill → They might have some interpretation in their analysis of the results which makes their reports of treatment etc less valid.

• No inter rater reliability as there was only one pseudopatient per hospital

• Cahalan - suggests rosenhan removed data from a pseudopatient who gave positive feedback about hospitals

Validity in diagnosis

Have we given the correct diagnosis/has the correct illness been diagnosed, and lead to the right treatment for the diagnosed mental health disorder

Predictive validity

• We can suggest how your illness will progress (and we’re right) and/or I can give you medication for your illness and your symptoms should go away

• Eg if I say in 6 months you’ll be having hallucinations, do you?

Aetiological validity

• People suffering from the same disorder should have the same causes for that illnesses

• Eg if depression is genetic then everyone with depression should be carrying that gene

Concurrent validity

• Two separate test/measures give the same diagnosis

• Eg you are diagnosed by both the ICD and DSM and you get the same illness

Construct validity

• Are we measuring the thing we say we are

• Eg are the symptoms for schizophrenia in the DSM the symptoms people get with schizophrenia

Retest (intra-rater) reliability

You get the same diagnosis again when rediagnosed

Inter-rater reliability

Two different doctors give the same diagnosis

Things which affect the validity and reliability of diagnosis

• Standardised symptoms in diagnostic manuals e.g. in depression, should improve validity and reliability

• Updates will increase construct validity - up to date with knowledge and understanding

• DSM 5 includes section 3 which advises cultural issues should be taken into account so these should have less of an effect on the reliability of diagnosis.

• If a classification system is not reliable then it cannot be a valid measurement of mental disorders.

• DSM and ICD differences in criteria might lead to different diagnoses, reducing the validity and reliability of diagnosis

• Co-morbidity – some illnesses overlap and could be diagnosed as one by one doctor and a different, overlapping illness by another doctor.

• Updates can reduce the reliability as the changes in criteria changes the diagnosis

• Patients may lie/omit information due to embarrassment, or not realising something is a symptom.

• Bias e.g. gender or racial bias – misdiagnosing based on race or gender

• Culturally bound syndromes – mental illnesses specific to one culture that may not be diagnosed if the patient is in a different culture when seeing a doctor.

Evidence that DSM is valid

• Kim-Cohen - children diagnosed with conduct disorder were more likely to describe themselves are having antisocial behaviours than comparison children. Also, during observational assessments these children were more likely to behave disruptively → This demonstrates construct & concurrent validity in diagnosis

• Lee found that the diagnosis of adhd had concurrent validity when using DSM and other measures such as questionnaire data, so diagnosis may be valid → suggests diagnostic manuals are a valid method of diagnosing mental illness

Evidence that DSM isn’t valid

• Rosenhan showed that patients can lie and get diagnosed as mentally ill → this shows that diagnosis isn’t valid even if we have the DSM criteria

• Ford and Widiger found that men and women with the sane symptoms could be diagnosed with different illnesses - doctor bias still possible

Evidence that ICD is valid

• Jakobsen found there was good agreement in the diagnosis of schizophrenia between ICD 10 and other classification systems → suggests its a valid method of diagnosis mental illnesses

• Andrews found that DSM IV and ICD had agreement rates for disorders such as depression → can be said that both systems have concurrent validity

• Powers found that women who had suffered complex past traumatic disorder also had higher levels of alcohol and substance misuse as predicted by ICD 11 → shows that ICD 11 does have good predictive validity

Evidence that ICD isn’t valid

Cheniaux looked at schizophrenia, bipolar and unipolar depression. Two trained psychiatrists used interviews to assess 100 patients. They found that schizophrenia was more common when using ICD 10 rather than DSM IV → doesnt have concurrent validity

Evidence that DSM is reliable

• Rosenhan found that 11 out of the 12 hospitals admitted the pseudopatients with a diagnosis of schizophrenia → this shows diagnosis using the criteria can be reliable

• Morey found that DSM 5 was more reliable than DSM 4 in diagnosing borderline personality disorder so diagnosis of mental health disorders should be reliable if DSM 5 was used

Evidence that ICD is reliable

Reed found that the vast majority of clinicians answered ‘extremely’ or ‘quite’ for how easy the ICD 11 was to use

Evidence that ICD isn’t reliable

Jansson compared ICD 9 to ICD 10 with 155 patients. They gathered data by interviews, diagnostic criteria, and family history. ICD 10 and DSM 4 give the best diagnostic agreement. There were some differences between ICD 9 and ICD 10.

Influence of culture in diagnosis - social norms

• Culture could impact what is seen as normal and abnormal and therefore who/what behaviours get diagnosed

• Eg hearing voices seen as normal in some cultures and abnormal in others

Influence of culture in diagnosis - ethnocentrism

• Only researching or finding out about one culture but then applying them to other cultures where they might not apply

• May also undervalue or downplay differences between culture

• How people describe their illness will affect their diagnosis

• Over diagnosis of black people in uk relative to population in society

Influence of culture in diagnosis - DSM vs ICD

• May have different criteria for the illness so depending where you are in the world you might be diagnosed differently

• Less of an issue with DSM 5 now because it is now acknowledging the differences

Influence of culture in diagnosis - culture bound syndrome

• Illnesses only found in one culture or at least an illness which is interpreted totally differently in a different culture

• Hikkikomori - japan severe social withdrawal

• Koro - ‘penis panic’ - east Asia delusional beliefs about retracting genitals

• Dhat - ‘depression’ - caused by bodily fluid loss

• Possibilities which could explain these culturally bound symptoms

  • Something about that culture causing the illness

  • It’s the same illness/ same symptoms but diagnosis is different

Evidence culture impacts diagnosis

• Chandresa shows that there are more rates of catatonia (21%) in Sri Lanka than in British white people (5%). However, this is thought to be mostly due to treatment options. In Britain there are more treatment options available to stop the illness progressing to catatonic stage, compared to in Sri Lanka.

• Burham - Mexican born Americans have more auditory hallucinations than American with Mexican origins

• Kastrup argues that as not all cultures see the separation of mind and body prevalent in Western society. If the patient and clinician do not share an understanding of how problems are described faulty diagnoses are likely to occur

• Escobar & Vega - The current version of DSM is still unsatisfactory in terms of cross cultural applicability because of its strong western bias

• Banyard only 5% of the British population is black but 25% of psychiatric patients are black suggesting lack of understanding within our own culture. This data indicates we are overdiagnosing black people within our own culture.

• Malgady demonstrated there is a difference in the interpretation of hearing voices between Costa Rican culture where it is interpreted as spirits talking to an individual and the USA where the same phenomenon is interpreted as a symptom of schizophrenia, suggesting cultural differences would impact the validity of diagnosis.

• Davidson - We need to be aware of cultural diversity. Asian-American women are more subservient/withdrawn. There is a similar cultural differences occur in UK e.g. Afro carribean population. So some cultural characteristcs could be mis-identified as mental illness without the cultural understanding.

• Sato - Clinicians may be unwilling to give culturally sensitive diagnoses e.g. schizophrenia in Japan.

• Lopez claimed that trying to redress cultural bias in the DSM, by taking cultural beliefs into account, can lead to missing some diagnoses as symptoms are dismissed as cultural norms. This makes it very difficult to judge whether DSM can be used as a valid tool outside the USA.

Evidence culture doesn’t impact diagnosis

• Lee researched the diagnosis of ADHD in Korea and found concurrent validity → This suggests cultural differences do not impact diagnosis.

• Lin - Schizophrenia around the world shares more symptoms than it differs in. The availability of treatment being the major factor in many ‘differences’.

Schizophrenia

Psychotic disorder characterised by a profound disruption of cognition and emotion, which affects language, thought, perception and a sense of self

Features of schizophrenia

• No disparity in the occurrence and onset of schizophrenia between men and women, though it is more closely associated with younger men. This may be due to the fact that women are more likely to experience the onset of Schizophrenia later than men.

• Affects men at a younger age (late teens) than women (in late twenties to mid 30s)

• <1% chance of getting it (0.3-0.7%)

• Episodes of psychosis tend to appear between the ages of late adolescence and the mid-thirties, with males having it at a slightly earlier age than females.

• People who have psychosis before late adolescence often have a worse prognosis that those who develop it later on, with it being more severe and lasting longer.

• About 50% of people with schizophrenia have times where they have the symptoms and times where they do not have the symptoms.

Symptoms of schizophrenia

• In order for a diagnosis to be made, two or more of the symptoms must be present for more than one month along with reduced social functioning

• Hallucinations - Auditory (hear things) and visual (see things) hallucinations.

• Delusions e.g., paranoid (someone is after them, is tracking their movements etc, grandiose (the belief they are all powerful, have magical powers, are important (e.g., royalty etc).

• Disorganised behaviour, including catatonia, little to no emotion (flat affect), inappropriate emotional responses e.g., laughing at something sad.

• Disorganised thoughts e.g., thought insertion (someone is putting thoughts in my head), thought withdrawal (e.g., someone is taking my thoughts).

• Negative symptoms - Alogia (poverty of speech), loss of avolition (severe lack of motivation), flattened affect (little to no emotion)

Neurotransmitter explanation of schizophrenia

• A group of drugs were developed called phenothiazines

• They block a particulate dopamine receptor in your brain effectively blocking the transmission of nerve impulses through these receptors. They worked by basically blocking/ reducing dopamine transmission in the brain. This seemed to reduce schizophrenia symptoms

Hypodopimanergia

Decreased dopamine in mesocortical system causes negative symptoms

Hyperdopimanergia

Increased dopamine in mesolimbic system causes positive symptoms

The original dopamine hypothesis

• Excess levels of dopamine are linked with schizophrenia

• Or receptors are too sensitive to dopamine

• Or there are too many receptors (the D2 receptor in particular)

The role of glutamate and serotonin - neurotransmitter explanation of schizophrenia

• Glutamate is thought to control the amount of dopamine released by the brain, and normally seems to lower levels of dopamine.

• If glutamate production is blocked, then this can also cause schizophrenia as it then leads to an increase in the amount of dopamine in the brain

• An increase in serotonin activity can also lead to the positive and negative symptoms of schizophrenia

Strengths of neurotransmitter explanation of schizophrenia

• Anti-psychotic drugs work by blocking dopamine receptors and are effective in reducing the symptoms of schizophrenia → This suggests that excess dopamine does explain the development of schizophrenia as the medication which treats it does so by lowering the levels

• Davis injected schizophrenics with methylphenidate (a dopamine agonist) and found a marked increase in symptoms → This suggests that Dopamine levels might be a credible explanation of the cause of Schizophrenia

• Randrup and Munkvad raised Dopamine levels in the brains of rats by injecting them with amphetamines. The rats’ behaviour changed, becoming more stereotyped, aggressive and isolated, showing that changing the DA levels resulted in psychotic-type behaviours consistent with Schizophrenia.

• L-Dopa treats Parkinsons Disease by raising DA, side-effects are hallucinations → This suggests that Dopamine levels might be a credible explanation of the cause of Schizophrenia

• Scientific and objective because it is empirically measuring neurotransmitters → This means we can directly measure the levels of Dopamine, Glutamate etc so it is a credible explanation.

Weaknesses of neurotransmitter explanation of schizophrenia

• Kwon et al found a 25% reduction of grey matter in the frontal & temporal lobes so there may be other brain differences → the neurotransmitter explanation is not a full explanation.

• Researchers at Liverpool University in 2012 found that childhood trauma makes you three times more likely to develop schizophrenia → there is a strong relationship between the environment and the development of schizophrenia and it is not just due to genetics.

• Depatie & Lal found that giving people drugs that increase their production of dopamine does not create the symptoms of schizophrenia as would be expected if excess dopamine caused it → This means that Dopamine might not be a sufficient explanation of what causes Schizophrenia

• Cause and effect issues as most of the research is correlational → This means it might not be a good explanation as high levels of Dopamine could cause SZ or SZ causes high levels of Dopamine

• It is difficult to test the chemicals in the brain/synapses directly so often we use urine or blood tests which lowers the validity because it is not totally clear if the chemicals are in the brain or elsewhere

Aim of Bradshaw

To see if CBT was effective treatment for Schizophrenia in an Atypical case of a woman with schizophrenia

Sample of Bradshaw

• One adult female, carol, aged 26 at the start of the case study. Carol suffered from schizophrenia.

• Atypical for SZ first in family and young for a woman…delusions, hallucinations 30/100 on global functioning

Procedure of Bradshaw

• Studied for three years whilst undergoing CBT

• First stage she was building a rapport with the therapist

• Second stage she was understanding how CBT would work for her and her SZ (ABC model)

• Third (longest stage) was her undergoing CBT. Managing stress, challenging her thoughts, increasing activities…practicing this in the real world and the final 3 months her going without therapy sessions

• Various measurements of her (at beginning, end, 6m later, 1 year later) e.g. global functioning, how well she met her targets e.g. finding a job, symptom severity and number of hospitalisations

Results of Bradshaw

• At the conclusion of the study there were few symptoms and Carol reported little distress. After 1 year, RFS was stable at 27 (she had scored 6 at the start).

• At the end of the study, Carol's GPI score of 1 indicated there were few symptoms present and she reported little distress.

• GAS increased from 19.85 to 80.15, which shows that treatment goals had been attained. Goals included starting a college course, taking on a volunteer job and going out once a week with friends.

• Days in hospital (in the previous 3 months) dropped from 60 to 0 and maintained that throughout the follow up period

Conclusion of Bradshaw

Carol experienced improvement in functioning in all four measures after a 3 year course of CBT. Bradshaw concludes that CBT can be successful in treating schizophrenia.

Strengths of Bradshaw

• One strength is the study is longitudinal as it studied Carol over 3 years so gathers lots of depth and detail → The study is able to show development and change about her functioning with Schizophrenia following CBT (so gains depth and understanding)

• Lots of data gathered as it was an indepth qualitative study (and quantitative) about her progress with CBT → This means we get lots of understanding about her experiences with schizophrenia and CBT

• Quantitative data also gained from the scales and numbers of hospitalisations which can be analysed more easily/objectively and can be statistically analysed → This lets us see how effective CBT is/was for treating schizophrenia in Carol

• Triangulation of data (various methods being used like the goal attainment scale and number of hospitalisations → This allows the results from the different measures of her wellbeing during the CBT to be used to check each other and gain concurrent validity.

• Useful because it showed that the CBT was an effective one for Schizophrenia and Carol saw the benefits

Weaknesses of Bradshaw

• Difficult to repeat as they take a long time to conduct (this one took 3 years) → This means we can’t effectively test to see if the results about CBT and schizophrenia are reliable

• Since Carol was an Atypical case of schizophrenia it means it is a small sample so it isn’t generalisable → The results about Carol’s Schizophrenia and CBT treatment might not be representative to others.

• Case studies are typically naturally occurring circumstances where it can be affected by many extraneous variables that may affect validity e.g. events and situations going on in Carol’s life which could’ve impacted on the effectiveness of the CBT

• Ethically this is a naturally occurring case of a woman with CBT undergoing treatment which means no harm was actively done to her (in fact the study helped her recovery)

• Withdrawal and consent can always be an issue since it is longitudinal and people change their mind.

Schizophrenia biological treatment - drugs

• Anti-psychotics are drugs which lower dopamine levels (usually at D2 receptors) to reduce the symptoms of schizophrenia

• Prescribed by doctor - takes a few weeks - monitor and change as needed, such as dosage or type

• Typical are the older type which block D2 receptors which reduces the activity there, which reduces schizophrenia symptoms, eg haloperidol→ mainly for positive symptoms

• Atypical are newer and they block dopamine and serotonin, eg clozapine → both positive and negative symptoms

• Orally - tablet or liquid or slow release injection

Strengths of schizophrenia biological treatment

• Emsley found 84% of patients on anti-psychotic medications had at least a 50% reduction in symptoms if they were given early enough → This shows that the medication is an effective method to treat Schiozphrenia and reduce the symptoms

• Kane found that antipsychotic drugs help approximately 80-85% of patients → This shows that the medication is an effective method to treat Schiozphrenia and reduce the symptoms.

• Hogarty et al found relapse rates of 48% vs 80% without these types of medication → This shows that the medication is an effective method to treat Schiozphrenia and reduce the symptoms.

• Meltzer - Haloperidol gave significant improvements in all aspects compared to placebo (as did 2 of the other drugs) → This shows that the medication is an effective method to treat Schiozphrenia and reduce the symptoms

• Kane et al found that out of 200 patients who showed no improvement with the commonly used Haloperidol, 30% responded to Clozapine with an improvement in both positive and negative symptoms → This shows that medication is an effective method to treat Schizophrenia and reduce the symptoms, as long as the right medication is given to the patient.

• Drugs act relatively quickly allowing stabilisation of the patient’s condition during the acute phase of illness, improving the patients quality of life.

• Drug treatment allows the patient to return to and function effectively in the community. This makes drugs an effective treatment with major benefits and help patients avoid/reduce hospitalisation.

Weaknesses of schizophrenia biological treatment

• Leiberman - Many patients stop taking their medication because of the severe side effects, this affects the effectiveness of this treatment.

• Rosa found only 50% of patients complied with taking their anti-psychotics → This means the treatment is not an effective one because if half of patients stop taking them they’re not beneficial for most patients.

• Fenton et al - Rates of medication non-adherence among schizophrenic patients are approximately 50% within the first year, and up to 74% within the first two years after the onset of disorder. It is estimated that non-adherent schizophrenic patients have a risk of relapse 3.7 times greater than that of adherent patients, suggesting it is not a good treatment.

• Leucht et al found that drugs are good for treating ‘positive’ symptoms, however comparative affects on ‘negative’ schizophrenia are marginal → This means that the drugs might not be an effective treatment for all aspects of Schizophrenia.

• Can leave as many as 60% of patients with symptoms that do not respond to treatment → This suggests it is not an effective treatment as a large percentage of patients are not helped.

• Drugs cannot cure the disorder, at best they help the individual manage the disorder. They are not a long lasting cure and when you come off the medication the symptoms might reappear → This suggests that drugs might not be the most effective treatment.

• Anti-psychotics have serious side effects such as a decrease in motivation and Tardive Dyskinesia (involuntary movement of face and jaw), so schizophrenics may prefer not to take them → This means the treatment is not an effective one because people’s Schizophrenia will not be treated if they decide not to take them.

Cognitive explanation of schizophrenia (non biological)

• Schizophrenia is characterised by disturbance in language, attention, thought and perception. This has led to cognitive psychologists to explain the disorder as a result of faulty information processing.

• The positive symptoms of Schizophrenia have been consistently and effectively explained by biological factors such as increased dopamine levels.

• Other symptoms have been seen to be seen by them trying to make sense of their own experience. This is where the cognitive explanation comes in mainly.

Cognitive explanation of schizophrenia: Frith - attention deficit theory

• Schizophrenia is caused by a faulty attention system (sensory overload)

• Schizophrenia results from patient’s increased ‘self-awareness’ whereby they have an inability to filter out unnecessary cognitive ‘noise’. We can ignore all of the unconscious processes like thought, perception and decision making. Schizophrenics can’t tune this out - this causes hallucinations.

Cognitive explanation of schizophrenia: Frith - meta representation

• Meta representation is the ability to reflect and monitor your own thoughts and intentions

• Frith suggested that schizophrenics fail to monitor their own thoughts correctly, misattributing them to the outside world

• When a person hears voices, it is actually their own inner speech being misinterpreted however they may believe that someone or something in the external world is communicating with them

• Most of the symptoms can be explained in terms of deficits in three cognitive processes:

  • Inability to monitor willed action

  • Inability to monitor the beliefs and intentions of others

  • Delusions may be caused by an inability to process social situations appropriately, so leading to feelings of persecution

Cognitive explanation of schizophrenia: Helmsley

• A poor link between memory and perception can lead to disorganised thinking as people will not know what to expect from a situation

• People with schizophrenia have a disconnect between their memory and perception and what they actually hear and see. When they encounter new situations, their schemas are not activated.

• This causes sensory overload. It also means they struggle to predict what will happen next. This leads to disorganised thinking and behaviour.

• Some of the negative symptoms of schizophrenia may be the result of cognitive strategies used by the individual to keep mental stimulation to a manageable level, ie social withdrawal

Strengths of cognitive explanation of schizophrenia

• McGuigan Identified that immediately before episodes of auditory hallucination were reported, some schizophrenic patients showed activation of the vocal centres, which may suggest that they misinterpret their own inner voice as belonging to someone else → This suggests the cognitive theory is correct that some symptoms of Schizophrenia do come from maladaptive/faulty thought process/faulty attribution of thoughts so cognitive explanations are credible

• McGuire found during hallucinations the part of the brain in the temporal lobe responsible for identifying and monitoring ‘inner speech’ recorded reduced activity, showing that the individuals might have been experiencing an internal conversation, but were more likely to perceive the voice as belonging to another → This suggests the cognitive theory is correct that some symptoms of Schizophrenia do come from maladaptive/faulty thought process/faulty attribution of thoughts so cognitive explanations are credible

• Frith and Done found that schizophrenics were unable to decide/ figure out if they were in control of actions on a computer game less than others without schizophrenia → This suggests the cognitive theory is correct that some those with schizophrenia have issues with meta representation which means that it might be a credible explanation of schizophrenia

• The cognitive explanation is useful as it can lead to therapies like CBT which focuses on changing the misattributed thoughts → Since CBT works it would suggest that the cognitive explanation of Schizophrenia might be a credible explanation.

• Accounts for nature (talks about neurotransmitters) and nurture → this is more holistic so is a better explanation

Weaknesses of cognitive explanation of schizophrenia

• Carlsson found that glutamate activity causes schizophrenia → cognitive fails to account for this influencing schizophrenia as it only looks at faulty information processing → makes it an incomplete explanation of schizophrenia

• Sitskoom - cognitive deficits found in patients with schizophrenia were also found in relatives of the patients who did not have the disorder → Therefore there is a genetic component and it is reductionsit to just look at the cognitive issues without looking at the biology underlying it.

• Butler found using PET scans that there is less activity in the frontal lobes of those with schizophrenia, showing they are less likely to monitor information from the senses → this conflicts as cognitive doesn’t focus on biological aspects like brain activity

• Ignores other factors/explanations such as genetics/ neurotransmitters → reductionist explanation

• Difficult to test as you cannot empirically measure the cognition behind Schizophrenia → This means we don’t know if cognitive processes can explain schizophrenia effectively as it cannot be tested.

• The research into schizophrenia and fully processing is correlational so you don’t get cause and effect → we don’t know if the cognitive processes causes schizophrenia or if schizophrenia causes the cognitive processes so this isn’t a credible explanation

Schizophrenia non biological treatment - CBT

• Cognitive behavioural therapy sees the patient with schizophrenia once a week with 1:1 sessions in a supportive non-threatening environment where they can work together

• CBT aims to control their own behaviour rather than getting rid of symptoms

CBT - identify, challenge, change

• Work to identify their irrational thoughts, eg delusions, they might record this as part of ‘homework’

• They challenge, look for evidence for/ against their delusions and beliefs to see that they don’t match reality - which helps changing them and reduces their stress

• Change of behaviour: the therapist encourages the patient to come up with their own coping strategies for when they experience (or stress about them)

• Clients may also be asked to change their behaviour and record their experiences, such as going out with friends if social withdrawal is a symptom

CBT for schizophrenia - examples of ‘challenge’

• Belief modification: challenging those ideas around their delusions and how they come from irrational thinking and there is no evidence for them (or are alternative explanations) - also means that they don’t need to act upon them

• Focusing and reattribution: working with them to realise their auditory hallucinations are internal voices, eg focus on physical attributes of the voice such as the tone of the voice

• Normalising: therapists will discuss events that happened before the schizophrenia and cognitive distortions from illness in order to make the schizophrenia seem normal

CBT - ABC model

• Looking at activating events, beliefs about those events and the consequences of those beliefs

• The therapist will help the client work through some more adaptive thoughts for given situations

Strengths of CBT for schizophrenia

• Hoffman looked at 106 meta-analysis where CBT was shown to be very effective → this provides evidence that CBT does work for schizophrenia because across hundreds of studies in the meta analysis the techniques to reduce delusions were shown to be effective

  • OTOH it mainly looked at anxiety, anger control and stress, rather than Schizophrenia, so may not be generalisable.

• Chadwick and Lowe found that 10/12 patients showed a decrease in their conviction/belief in their delusions and 5/12 managed to reject their delusions at the end of their therapy as measured via self-report → This supports the idea that you can challenge and change peoples delusions to help them which suggests CBT is an effective treatment for schizophrenia

• Bradshaw assessed CBT in a case study with a female schizophrenic patient called carol and found considerable improvement in functioning and symptoms over a 3 year treatment period and 1 year follow up → this supports the process of CBT as it can reduce the severity of symptoms across the treatment period, eg challenging her delusions and so it is an effective therapy

• There is a collaborative relationship so the patient is not powerless in this therapy → This is good because it is less socially controlling than medication and can make the patient feel more positive about their treatment and progression.

• CBT is tailored to the individual needs of the patient, for example, the specific maladaptive thoughts and symptoms of Schizophrenia they have → This makes it a more effective therapy as it is directly tailored to that person and so will be able to help them specifically.

• No side-effects in comparison to drug therapies since it is not directly altering biology → This is beneficial for the treatment as it makes it more likely that people will stick with the therapy rather than non-compliance and relapse

• Cognitive behavioural therapy aims to give the client the tools they need to reduce the impact of their Schizophrenia so the client can use these tools in the future if further life events may lead to depression → This makes the therapy more long lasting in its ability to help Schizophrenics and therefore more effective.

Weaknesses of CBT for schizophrenia

• Sensky had some patients undergoing CBT (some from Newcastle, County Durham and London) and a control group doing ‘unspecific befriending’. Both interventions resulted in significant reductions in positive and negative symptoms of schizophrenia → this conflicts with the effectiveness of CBT as the control group who were not taught CBT techniques like belief modification saw a similar reduction so perhaps its not CBT techniques causing improvements in patients

  • OTOH at the nine-month follow-up evaluation,

• CBT can be distressing as it focuses on distressing symptoms, like hallucinations and delusions. Also, patients have to question themselves, which can be upsetting and difficult → This might make it less effective as a therapy because if it is difficult and uncomfortable it will have a higher attrition rate.

• Difficulties in measuring cognition/thought processes and attributions mean that it is not empirical → This can make if difficult to measure it’s effectiveness as we must rely on self- reports so cannot objectively measure the impact.

• If the causes of schizophrenia are due to neurotransmitters, then cognitive behavioural therapy will not treat the schizophrenia, and anti-psychotic medication would be more effective.

• CBT requires the patient to be able to express themselves and examine their thoughts, which patients with schizophrenia may not be able to do effectively (especially if they have any language related issues such as disorganised speech) → This makes the therapy less effective for the patients and means it might not be truly able to treat Schizophrenia.

Genetic explanation of schizophrenia

• The chance of anyone getting schizophrenia is less than 1%

• The chance increases when you’re related to someone with Schizophrenia, which means that genetics play a role in developing Schizophrenia.

• Risk rises with degree of genetic relatedness:

  • Spouse – 1% (same as the general population)

  • Child – 13%

  • DZ twin – 17%

  • MZ twin – 48%

• These genetic differences have been suggested to cause:

  • Critical neural pathways in the brain to be disrupted or damaged. This means behaviour controlled by these pathways will not be carried out/develop properly

  • Evolutionary link: these genes may be adaptive providing creative ways of thinking so the mutations are selected for…or some other adaptive process

  • The brain to alter how it works e.g., sensitivity to certain chemicals

• Polygenic - there isn’t one gene, there are multiple genes need/ can cause it

• C4-A - control neuron pruning - excess pruning → higher risk of developing schizophrenia

• COMT gene - controls enzymes that break down dopamine

Strengths of genetic explanation for schizophrenia

• Kety found that the biological relatives of Schizophrenia patients had a higher rate of Schizophrenia (8.9%) than the biological relatives of a control group (1.9%) → This shows that genetics could be a credible explanation of the causes of Schizophrenia

• Gottesman and shields found that 42% of the MZ twins both had a diagnosis of schizophrenia compared to 9% of the DZ twins → this supports that genes do play a role in the development of schizophrenia as those with more shared DNA had a higher/ greater concordance

• Sherrington - a gene located on chromosome 5 has been linked to schizophrenia

Weaknesses of genetic explanation of schizophrenia

• The concordance for MZ twins is not 100% which we would expect if it was purely genetic, therefore showing that the environment plays a role too. Saying it is solely due to genetics would be a reductionist explanation.

• Diathesis stress model says you need both genes and environmental stress

• Researchers at Liverpool University in 2012 found that childhood trauma makes you three times more likely to develop schizophrenia → suggesting that there is a strong relationship between the environment and the development of schizophrenia and it is not just due to genetics.

• Tienari compared high and low risk children who lived in various levels of ‘disturbed families’ and found that high risk children in healthy environments didn’t develop schizophrenia → this shows that its not just genetics and that environment also influences the chances of developing schizophrenia

• Tamminga and Schulz argue that research has failed to isolate a single recessive or dominant gene which causes the illness → This means the theory can be called into question as to how effective it is as an explanation of Schizophrenia

• Doesn’t include neurotransmitters/ cognitive differences → reductionist

Aim of Carlsson

To review studies that looked at the relationship between neurotransmitters and schizophrenia, especially dopamine and glutamate

Procedure of Carlsson

• Looked at 32 studies

• 8 animal studies - including rodents and primates, 5 drug studies, 12 brain scan studies, and 7 ‘other’ - including a cadaver study and a spinal fluid study

• Parkinson’s patients, acute schizophrenia and schizophrenia in remission, people on recreational drugs - cocaine and PCP, and people on schizophrenia medication

Results of Carlsson

• ‘Glutamate failure in the cerebral cortex may lead to negative symptoms, whereas failure in the basal ganglia (cognition, co-ordination and movement) could be responsible for positive symptoms

• Dopamine is high but there is unusual activity in other neurotransmitters too, eg serotonin, GABA, glutamate

• Low levels of glutamate has been shown to be linked to the development of psychotic symptoms

• Glutamate moderates dopamine - it controls the levels of dopamine

• NMDA antagonists seem to stimulate the turnover of serotonin more ‘consistently’ and so serotonin may also be implicated in schizophrenia too

• PCP causes lower glutamate, causing psychosis

Conclusion of Carlsson

Glutamate might be linked to schizophrenia, not just dopamine

Strengths of Carlsson

• 32 studies involving secondary data - large sample → results Carlsson found about neurotransmitters are more representative of a wider population than someone would be likely to get using a single study

• The fact that this study uses secondary data in a review study about neurotransmitters means it can be replicated → could use the same methods to gather studies about the same topic to see if the results about neurotransmitters Carlsson got would be reliable

• Brain scans were used in some of Carlsson’s research which are empirical → direct measurement of neurotransmitter in schizophrenic patients so is more valid.

Weaknesses of Carlsson

• A lot of the studies in the review are based on animal research, such as animals being given NMDA antagonists → the results may not be generalisable to humans as our brain structures and neurotransmitters are not identical.

• The secondary data collected may include studies which are old and lack temporal validity e.g., that have used an old classification system such as DSM-III to diagnose the patients or outdated information → the results may not be true of updated classification systems and so may not be valid for mental health disorders/treatments using neurotransmitters at the present time

• Publication bias

• Secondary data - dont know how it is operationalised → lowers validity on neurotransmitter because we don’t know the details in the studies

Unipolar depression

‘Normal depression’ - major depressive disorder

Symptoms of depression

• Specific symptoms, at least 5 of these 9, present nearly every day (for two weeks). One of which must be depressed mood or loss of interest/ pleasure.

  1. Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective report (eg feels sad or empty) or observation madd by others (eg appears tearful)

  2. Decreased interest or pleasure in most activities most of each day

  3. Significant weight change (5%) or change in appetite

  4. Change in sleep: insomnia or hypersomnia

  5. Change in activity: psychomotor agitation or retardation

  6. Fatigue or loss of energy

  7. Guilt/ worthlessness: feelings of worthlessness or excessive or inappropriate guilt

  8. Concentration: diminished ability to think or concentrate, or more indecisiveness

  9. Suicidality: thoughts of death or suicide, has suicide plan

Features of depression

• It’s the most common mental illness affecting almost 1/6 people

• Often comorbid with anxiety

• Moussavi et al said 15% of industrialised nations

• Women twice as likely to be diagnosed with depression

• Most common in young adulthoood (20-mid 20s)

Aim of Brown

To see if life events and self esteem are vulnerability factors for depression

Sample of Brown

• 395 working class women with at least one child at home were recruited by postal questionnaire (husbands in manual jobs or single mothers)

• All women were aged between 18 and 50, had a partner in manual labour and all lived in Islington (prospective study)

Procedure of brown

• Women were assessed twice, approximately a year apart using a variety of measures

• Prospective study

• Initially interviewed about self-esteem and social support they had in their lives

• Assessments were done by interview (some recorded and checked for inter-rater reliability) and included measurements of psychiatric stress

• At the second interview (303) participants were questioned about stressful life events in the intervening period and looked to see who had been diagnosed as depressed

Results of brown

• Of the women who had developed depression in those twelve months, 29 of the 32 had experienced some major life event (involving a loss, failure or disappointment) 91% Vs 23% of the women without depression

• 33% of those who developed depression had negative evaluation of the self and 13% did not.

• The majority of women with core crisis support (85 of 92) saw it as helpful, and there was no difference in their perception of support being helpful whether they had developed depression or not

Conclusions of brown

• Stressful life events is a risk factor for depression

• Low self esteem when coupled with stressful life events is a risk factor for depression

• Social support is protective

Strengths of brown

• A large sample of 395 women therefore generalisable → The results we get about the factors that impact and protect people from depression would make the results more representative to a wider population

• 21 interviews were checked by multiple researchers → inter rater reliability as other researchers checked to see patterns in depression

• Standardised questions in semi-structured interview about depression means it can be repeated → This means we can test the results about protective and risk factors for depression more reliable

• The semi-structured interviews on the women with depression means we can ask follow up questions to gain more detail and depth about depression risk factors → This means we get a better understanding of the protective and risk factors which impact on depression

• They eliminated women in the second stage who turned out to have depression in the first stage (and EV/bias) → This improves the internal-validity as it makes sure their depression in stage 1 doesn’t influence the measures taken during that stage.

• Very similar group minimises individual differences (but not fully), this removes extraneous variables which could impact the depression → The results about protective and risk factors in depression would therefore be more valid without individual differences impacting on them

• This is a prospective study means that there is no retrospective bias in the gathering of the data about the women’s depression → This makes it more valid because their current mental state doesn’t impact the data which has already been gathered about them before depression (retrospective data looking back would be)

Weaknesses of brown

• Sample only includes 395 women and therefore gynocentric and not generalisable → The results we get about risk factors for depression might not be equally representative in men

• Sample only includes people from the same doctors surgery (and had similar characteristics like husbands in manual jobs) who have similar backgrounds which makes the results only applicable in that group → The results we get about risk factors for depression might not be equally representative in people from other surgery’s

• Ethnocentric - all from Islington → results we get about risk factors for depression might not be representative in other continents

• Social desirability/demand characteristics could be a problem due to the self-report nature of the measures about depression → If the women lied about how they were feeling or how the risk and protective factors effected them then it would make the results less valid.

• Semi-structured interviews means some questions were only asked to some of the women with depression → This means there may be problems with reliability as the interviews are not fully replicable so we don’t know if the results about depression factors would be reliable

Biological explanation of depression

• Depression is caused by an imbalance of neurotransmitters in the brain which affects the signals (particularly in the dopamine/serotonin pathway)

• The monoamine hypothesis claims that low level of monoamines (noradrenaline, dopamine and serotonin) cause depression.

• Low levels of serotonin (or low receptors/sensitivity) have been linked to symptoms of depression like low mood/high anxiety (since serotonin is a calming hormone) and erratic brain functioning.

• Serotonin also regulates other monoamines like Dopamine (reward) and Noradrenaline (alertness/energy/concentration). Evidence indicates that low serotonin levels tend to cause low levels of the other monoamines.

• Low Dopamine would result in symptoms like no longer getting enjoyment (anhedonia) and lack of concentration.

• Low Noradrenaline would result in lack of energy/changes in sleep.

• High levels of the enzyme monoamine oxidase is also linked to low levels of monoamines. The monamine oxidase enzyme breaks down monoamines meaning you have less of them.

• Could be a faulty 5HTT gene causing less serotonin when under pressure/stress.

Strengths of biological explanations of depression

• Drevets found a reduced potential in serotonin to bind to receptors in unmedicated depressed patients → This shows that reduced monoamines/reduced binding of monoamines to receptors are a possible cause of depression.

• Versiani found that patients who had noradrenaline reuptake inhibitors increased their mood, therefore, if changing the biology can reduce symptoms, there may be a biological cause.

• Bunney found that urinary levels of noradrenaline decreased during episodes of depression, suggesting reduced noradrenaline in depressed patients.

• This is an objective and empirical theory as you can directly measure the levels of Monoamines through methods such as blood samples and urine samples → This makes it a good explanation of depression as it can be directly tested to show a person is low in Monoamines.

• Useful for drug treatment which works by increasing monamines and is effective → since drugs work to treat depression by increasing monoamines it is credible that low monamines causes depression