(P2) clinical psychology Flashcards

1
Q

assumptions of clinical psychology

A
  • mental disorders are a form of illness to be diagnosed and treated (the medical model)
  • types of mental disorder can be grouped and classified.
  • types of treatment can be grouped within a particular approach to psychology (e.g. biological or non-biological)
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2
Q

define mental illness

A

mental illness refers to significant changes in thinking, emotion and/or behaviour. it also has a variety of effects (e.g. distress and/or problems in social, work and family activities)

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3
Q

how can mental health be seen as a ‘social construct’?

A

mental health intepretations and understandings differ across culture and societies. for instance, one society may interpret behaviour as deviant whereas another society may consider it the norm.

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4
Q

define psychopathology

A

the study of mental illness and the behaviours and experiences that may indicate illness/distress/impairment.

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5
Q

what are the two main classification systems for mental illnesses?

A

DSM-V- the diagnostic statistical manual of mental disorders

ICD-10- the international statistical classification of diseases and related health problems

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6
Q

what is the medical model of mental ill health?

A

an approach that treats mental illness in the same way as physical illness, using lists of symptoms, features and classifications to diagnose or categorise patients with a particular disorder.

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7
Q

what are the four D’s of diagnosis?

A

the four D’s are used to define abnormality.

deviance refers to behaviour and emotions that go against the social and cultural norms of society. these must be seen as socially unacceptable. (e.g. dancing alone in public may be seen as socially acceptable in some societies/cultures but socially unacceptable in others, which points towards mental illness). an example of deviance is paedophilia.
- Davis (2009) says betweeen 3% and 9% of males report interest in underage children. the intensity and frequency of urges is reported by considerably fewer.

distress refers to when someone with a disorder experiences negative feelings. it is thought that abnormality in a mental health sense is accompanied by feelings of distress.
- hypochondriasis, those who are deeply affected by the fear of illness even if they have been reassured.

dysfunction refers to a person being unable to carry out ordinary, daily tasks that they used to be able to. (e.g. not being able to go to work anymore or out with friends).

danger refers to danger towards others or to the individual. violent behaviour directed towards others signals danger, while behaviour that is a danger to individuals themselves would include suicidal thoughts.
- nicotine dependance is a mental health disorder linking to danger. davis (2009) cites figures showing that 10% of all current and former smokers in the USA have a smoking-related chronic disease, which illustrates the ‘danger’ from smoking-related diseases.
- davis (2009) also cites that individuals suffering from mental illness have a 25% higher chance of dying from unnatural causes.

fifth D:

duration refers to how long the symptoms have been present for.
- schizophrenia illustrates duration because for a diagnosis, episodes must happen over time.

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8
Q

who came up with the four D’s?

A

davis

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9
Q

when are the four D’s used?

A

the four D’s are useful in summarising how mental health professionals might define abnormality.

davis (2009) suggests that using the four D’s can help practitioners to see when a condition might need a DSM diagnosis. the four D’s can assist enough to become a diagnosis.

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10
Q

(AO3) evaluate the four D’s of diagnosis

A

STRENGTHS
- (davis, 2009) has shown how the four D’s can be used with the DSM-IV-TR and adds a fifth - duration. the four D’s have practical application because they are useful for a professional when considering when a patient’s symptoms or issues become a clinical diagnosis.

WEAKNESSES
- there is the potential for issues of subjectivity and a lack of objectivity, which raises issues about their reliability. if the four D’s are used by two different professionals, they may not reach the same conclusions about mental disorder. this is because ‘deviance’ for instance, may be considered different in one society/culture vs. another.
- it may be claimed that (davis, 2009) having to add another, fifth D (duration) means that the four D’s are insufficient themselves as a tool.

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11
Q

issues when using the four D’s to diagnose

A

deviance can be difficult in diagnosis because different mental disorders show similar deviance. however, some diagnoses are clearly illustrated by deviance (e.g. paedophilia) where the symptoms in the DSM clearly indicate deviance.
- Davis (2009)

dysfunction can be difficult to diagnose because many life events and issues can be dysfunctional. may be subjective.

distress is quite hard to measure because a person may be unable to function and carry out everyday tasks but they do not experience feelings of distress.

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12
Q

define neuroses

A

mental health issues that fall just outside of normal functioning, but the individual is still in touch with reality and knows they are ill.

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13
Q

define psychoses

A

mental health issues where the individual has lost touch with reality and is not on a continuum with normal mental health.

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14
Q

define prevalence

A

the proportion of the population that has a disease at a point in time.

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15
Q

define incidence

A

the rate of occurrence of new disease during a period of time

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16
Q

differences in DSM-IV-TR (2000) versus. DSM-5 (2013)

A

DSM-IV-TR
multi-axial system that consists of 5 axes:

axis I: considers clinical, major mental, developmental and learning disorders.
axis II: looks at underlying personality conditions, including mental retardation.
axis III: general medical conditions such as diabetes.
axis IV: psychosocial and environmental factors that affect the disorder (e.g. poverty, dysfunctional families).
axis V: assessing someone’s overal functioning using a rating score.

DSM-5
one of the goals of the DSM-5 is to harmonise with the ICD system, which was not the case for previous DSMs.

section I: explains the DSM-5’s organisation and the changes from the DSM-IV-TR (away from the multi-axial system).
section II: gives diagnostic criteria and codes and covers all of the mental disorders listed in chapters. such as bipolar disorder, schizophrenia.
section III: covers emerging measures and models, looking to the future of diagnosis.

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17
Q

AO3 evaluating the DSM, including the DSM-5

A

STRENGTHS
- DSM-5 underwent field trials before publication, which included re-test reliability where different clinicians independantly evaluated the same patient.
- the DSM is ultimately the best attempt at diagnosis in existence, given the limited understanding of mental disorders. albeit its criticisms, it has stood the test of time.

WEAKNESSES
- the british psychological society (BPS) has expressed concern about the DSM-5 because the DSM-5 brought in social norms to be considered when making a diagnosis and this requires the clinicians to make judgements about such norms or to use their own social norms, which may differ to the patient’s. deviance and dysfunction relate to culture and social norms as they might be different in different cultures.
- there was a criticism that when reviewing the DSM-5, individuals had to sign an agreement that they would not discuss the process of reviewing this version of the DSM-5. this is a problem because it means there is no transparency, meaning that the DSM-5 potentially lacks credibility because the results of any testing could not be challenged, which almost opposes scientific credibility.

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18
Q

differences between ICD and DSM

A

(1) ICD is produed by a global health agency with a constitutional public health mission
- whereas DSM is produced by a single national professional association

(2) ICD’s development is global, multidisciplinary and multilingual
- whereas DSM’s primary constituency is US psychiatrists

(3) ICD is distributed as broadly as possible at very low cost, with substantial discounts to low-income countries and available for free on the internet.
- whereas DSM generates a substantial portion of the American Psychiatric Associations Revenue; therefore, it is expensive.

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19
Q

operationalisation
(in relation to validity of the DSM)

A

operationalising variables means making them fully measurable so that what is done in a study is precise, replicable and clear.

if the DSM is to define mental disorders then mental disorders need to be operationalised. lists of symptoms and behaviour are the result of making a mental disorder measurable.

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20
Q

cultural issues: validity, diagnosis and the DSM
culture does NOT affect diagnosis, mental disorders are ‘scientific’

A

the DSM was developed in the USA but is used in many other cultures. this is a valid use if mental disorders are clearly defined with specific features and symptoms. mental disorders are scientifically defined illnesses that are explained in a scientific way like any other illness.

LEE 2006
supports this because he found that the DSM-IV-TR had construct validity for diagnosing korean boys with ADHD. the diagnosis occured in a non-western culture, which supports the idea that the DSM does have cross-cultural validity.

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21
Q

cultural issues: validity, diagnosis and the DSM
culture DOES affect diagnosis - a spiritual model

A

some studies have shown that culture can affect diagnosis. for example, symptoms that are seen in Western countries as characterising schizophrenia (e.g. hearing voices) may be interpreted in other countries as showing possession by spirits, which renders someone special in a positive way rather than negative.

EVRARD 2014
writes about how hearing voices can be because of a mental disorder but also because of individual differnces and interpreted as an exceptional experience. depending on cultural interpretations of what is being measured, the DSM is not always valid.

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22
Q

cultural issues: validity, diagnosis and the DSM
culture DOES affect diagnosis - a spiritual model

A

some studies have shown that culture can affect diagnosis. for example, symptoms that are seen in Western countries as characterising schizophrenia (e.g. hearing voices) may be interpreted in other countries as showing possession by spirits, which renders someone special in a positive way rather than negative.

EVRARD 2014
writes about how hearing voices can be because of a mental disorder but also because of individual differnces and interpreted as an exceptional experience. depending on cy

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23
Q

cultural differences in schizophrenia
differences in how hallucinations are interpreted and understood

A

LUHRMANN ET AL. (2015)
found that in the USA, hearing voices was a negative experience whereas in India and Ghana it was considered a positive experience because it was seen as a spiritual revelation. this suggests that the experiences of a mental disorder may differ across cultures, which challenges the validity of diagnoses as clinicians may be from a different culture.

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24
Q

cultural differences in schizophrenia
differences in how treatment affects people

A

MYERS (2010)
found from a case study that by using the recovery model, efforts to help people become more empowered citizens tended to generate more stress for those diagnosed with schizophrenia is their lives were already stressful. this shows that cultural differences (around work patterns) can lead to different reactions to treatment. myers cautions against using the same model of treatment in all cultures and says that sociocultural conditions affect outcomes.

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25
Q

culture bound syndromes

A

culture bound syndromes are a set of mental health problems found and recognised as illness only in a particular culture.

for example, penis panic

in some cultures, males think that their penis will retract into their bodies and women believe the same about their breasts. this is known as genital retraction syndrome (GRS) and such panics have been found mainly in asia and africa. it is thought to be related to witchcraft.

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26
Q

AO3 evaluation of cultural issues, validity, diagnosis and the DSM

A

STRENGTHS
- the DSM-5 provides updated criteria on cross-cultural concepts of mental illness. this is a strength because accounting for culture-bound syndromes and accounting for culture improves the validity of diagnosis.

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27
Q

what makes a valid classification system?

A
  • In order to be valid a classification system must accurately diagnose a mental health disorder, and lead to the right treatment for the diagnosed mental health disorder.
  • If a classification system has concurrent validity then it should come up with the same diagnosis for the same symptoms at the same time as
    another classification system.
  • Predictive validity is when upon diagnosing a mental health disorder accurate predictions can be made about how the disorder will progress, and how it will respond to treatment.
  • To have a valid classification system then symptoms of a disorder have to be operationalised and measurable e.g. social withdrawal for
    schizophrenia.
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28
Q

(AO3) evaluating reliability of diagnoses using DSM

A

CREDIBILITY the reliability of diagnoses can be significantly improved when clinicians communicate with other clinicians when making diagnosis because this increases inter-rater reliability. (Spitzer & Fleiss)

OBJECTIONS (W) lack of objectivity in interpretation of the four D’s, which also raises issues about the reliability of using them. for example, if the four D’s are used by two different therapists, they may not reach the same diagnosis (e.g. dissociative identity disorder/multiple personality, is a recognised disorder in the USA but not in Britain).

RELIABILITY (S) Goldstein (1988) tested the reliability and validity of diagnosis between the DSM-II and DSM-III. She used the single blind technique, where clinicians carry out the rediagnosis separately, without knowing the previous diagnosis, so they were not affected by bias/expectations. She found that there was evidence of reliability within the DSM-III, i.e. separate clinicians agreed on diagnosis. (They were consistent).

VALIDITY (W) Rosenhan’s (1973) study found that clinicians using DSM were unable to distinguish well, ‘normal’ participants from those with real psychiatric symptoms. This challenged the validity of DSM as a diagnostic tool. This led to important revisions in DSM, leading to a number to updated editions in the light of new evidence.

APPLICATION (S) DSM-V reflects social changes in society (e.g. there is more awareness of cultural differences in mental health) the DSM-V replaces the ‘culture bound syndromes’ and replaces it with advice on ‘cultural concepts of distress’, which is more inclusive and representative within our multicultural society.

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29
Q

(AO3) evaluating the validity of diagnoses using DSM

A

STRENGTHS
- there is supportive evidence from lee (2006) who conducted a study to investigate whether the DSM-IV-TR diagnosis of ADHD was suitable for korean children. using a questionnaire method with 48 primary school children, he found that there was construct validity between the DSM-IV-TR and the questionnaire data. this is a strength because it shows that different research methods (e.g. questionnaires) yield the same diagnosis as the DSM, proving validity. it also shows that there is cross-cultural validity using the DSM as a diagnostic tool in a different (non-western) culture.
- it may be said that great efforts have been made to improve the validity of the DSM-IV-TR till the current version now DSM-5 where it accounts for culture-bound symptoms now.
- the claim that the DSM is valid is supported by the claim that it is reliable because the two go hand in hand. if the DSM is reliable, it must be valid. Goldstein (1988) tested the reliability and validity of diagnosis between the DSM-II and DSM-III. She used the single blind technique, where clinicians carry out the rediagnosis separately, without knowing the previous diagnosis, so they were not affected by bias/expectations. She found that there was evidence of reliability within the DSM-III, i.e. separate clinicians agreed on diagnosis. (They were consistent).

WEAKNESSES
- (COUNTER-ARGUMENT TO LEE 2006) it’s possible that questionnaires produce the findings that they are searching for. for instance, if ADHD is classified by children being ‘hyperactive and impulsive’, teachers know that the children have that label and they will then say that the children are impulsive and hyperactive. this is a problem because the diagnosis is self-fulfilling.
- it has been said that co-morbidity is hard to diagnose using the DSM- a system that relies in health professionals choosing the closest match from a list of symptoms and features.
(co-morbidity refers to the state of having more than one mental disorder, or more generally more than one illness or disease).
- it may be claimed that splitting a mental disorder into symptoms and features is reductionist and a holistic approach might be more valid. for example, in counselling they aim to treat the person by considering whole aspects rather than symptoms. the DSM lacks this because diagnosis appears to be more important than treatment.

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30
Q

define construct validity

A

construct validity refers to the degree to which a psychological test or assessment represent that mental disorder.

*(e.g. in the case of depression, the number of days the patient has lacked the motivation to go to work).

construct validity can be increased by operationalising the mental disorders by creating lists of symptoms and behaviour that are measurable.

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31
Q

define concurrent validity

A

concurrent validity shows you the extent of agreement between the different measures or assessments taken at the same time.

*(e.g. if a diagnosis using the DSM comes up with the same mental disorder that another diagnosis has given at the same time, then the new diagnosis is likely to have concurrent validity).

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32
Q

define predictive validity

A

predictive validity assesses how well a test predicts a criterion that will occur in the future. it measures the test’s ability to foresee the performance of an individual on a related critetion measured at a later point in time. it gauges the test’s effectiveness in predicting subsequent real-world outcomes or results.

  • to find predictive validity, a test would be carried out and results collected. then another/different measure would be done the same time later that would test that same feature. if the tests matched the earlier measure then this shows predictive validity.
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33
Q

define convergent validity

A

a subtype of construct validity. it assesses the degree to which two measures that theoretically should be related, are related.
- a correlation test would be carried out. if two scales measure the same construct, for example, then a person’s score on one should converge (correlate) with their score on the other.

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34
Q

type I error / false positive

A

diagnosing someone with a mental disorder when they are healthy

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35
Q

type II error / false negative

A

diagnosing someone as healthy when in reality they are ill

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36
Q

(AO3) evaluating reliability of diagnoses using DSM

A

CREDIBILITY the reliability of diagnoses can be significantly improved when clinicians communicate with other clinicians when making diagnosis because this increases inter-rater reliability. (Spitzer & Fleiss)

OBJECTIONS (W) lack of objectivity in interpretation of the four D’s, which also raises issues about the reliability of using them. for example, if the four D’s are used by two different therapists, they may not reach the same diagnosis (e.g. dissociative identity disorder/multiple personality, is a recognised disorder in the USA but not in Britain).

RELIABILITY (S) Goldstein (1988) tested the reliability and validity of diagnosis between the DSM-II and DSM-III. She used the single blind technique, where clinicians carry out the rediagnosis separately, without knowing the previous diagnosis, so they were not affected by bias/expectations. She found that there was evidence of reliability within the DSM-III, i.e. separate clinicians agreed on diagnosis. (They were consistent).

VALIDITY (W) Rosenhan’s (1973) study found that clinicians using DSM were unable to distinguish well, ‘normal’ participants from those with real psychiatric symptoms. This challenged the validity of DSM as a diagnostic tool. This led to important revisions in DSM, leading to a number to updated editions in the light of new evidence.

APPLICATION (S) DSM-V reflects social changes in society (e.g. there is more awareness of cultural differences in mental health) the DSM-V replaces the ‘culture bound syndromes’ and replaces it with advice on ‘cultural concepts of distress’, which is more inclusive and representative within our multicultural society.

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37
Q

ICD-10

A

the ICD includes a look at the general health of a population and is used to measure incidence (when health problems occur) and prevalence (proportion of population that have a health condition). it is the ICD that provides mortality (number of deaths) and morbidity (number of diseases) for the WHO, world health organisation.

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38
Q

categories of the ICD-10

A

ICD-10 starts with the following categories:

I- certain infectious and parasitic diseases
II- neoplasms
III- diseases of the blood and blood-forming organs and certain disorders involving the immune system
IV- endocrine, nutritional and metabolic diseases
V- mental and behavioural disorders
VI- diseases of the nervous system

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39
Q

CLASSIC STUDY: Rosenhan (1973) the pseudopatient study

A

AIM Rosenhan aimed to test the reliability of mental health diagnosis to see if medical professionals could tell the sane (pseudo patients) from the insane in a clinical setting. He also wanted to investigate the effect of labelling on medical diagnosis.

SAMPLE staff and patients in the psychiatric hospitals in the United States. The hospitals were in 5 different states.
*pseudopatients were observers NOT participants

PROCEDURE pseudopatients went to clinical interviews and reported their symptoms.
After admission, they started behaving normally and stopped reporting hearing voices. They took a notepad and pen along with them to record what they saw and heard (unstructured observation).
They tried to do this covertly, but if the staff detected them they carried on recording things overtly.
As soon as they were admitted, pseudopatients requested to be discharged and they secretly disposed of the medication (e.g. flushed pills down the toilet) but otherwise, acted polite and friendly and obeyed all the instructions asked of them.
structured observation Rosenhan conducted two structured observations during the study:
- in 3 hospitals, a record was kept of how many patients voiced suspicions about the pseudopatients and how much time the staff spent on the ward, interacting with the patients.
- in 4 hospitals, the pseudopatient approached staff with a scripted question: “Pardon me, Mr [or Dr or Mrs] X, could you tell me when I will be eligible for grounds privileges?” (or “ . . . when I will be presented at the staff meeting?” or “. . . when I am likely to be discharged?”). The member of staff’s answer and body language were recorded.
follow on study After the main study ended, Rosenhan contacted his own hospital and revealed the results. The hospital agreed to a second study, but this time they would be aware that new pseudopatients would be seeking admission over the next 3 months. Staff were issued with a questionnaire to rate each new patient on a 10-point scale: 9-10 meant high confidence that the patient was really ill but 1-2 meant a strong suspicion that this was a pseudopatient.

RESULTS All 12 hospitals diagnosed the pseudopatients as mentally ill. 11 hospitals diagnosed schizophrenia, 1 hospital (the private hospital) diagnosed manic-depression (bipolar disorder). The pseudopatients went to hospitals that had diagnosed them with schizophrenia.
None of the staff recognised that the pseudopatients were healthy. It took between 7 and 52 days for the pseudopatients to be discharged; the mean length of stay was 19 days.
The pseudopatients were discharged with a diagnoses of “schizophrenia - in remission” (meaning the person has schizophrenia but the symptoms appear to have stopped) in 7 cases; 1 pseudopatient was discharged with a diagnosis of “schizophrenia” on their medical record.
- although staff were not suspicious of the psedudopatients, other patients were. 35/118 patients accused the pseudopatients of not being genuinely ill.
The pseudopatients observed many disturbing things while in the hospitals.

Staff abusing patients: The pseudopatients were well-behaved and none of them were harmed in any way, but they observed other patients being verbally or physically abused by staff. Rosenhan reports that patients were awakened in the morning by an attendant shouting “Come on you m—- f—-s, out of bed!” and one patient was beaten for saying to an attendant “I like you”.
Patients refusing medication: The pseudopatients disposed of their pills but when they went to flush them down the toilet, they often observed that other patients had done the same thing
Depersonalisation & powerlessness: The patients weren’t treated as persons. There were no doors on toilet cubicles and staff would inspect their medical records and personal belongings without asking permission. Staff would not make eye contact with patients. Staff would discuss patients within earshot, as if the patients could not hear them. Attendants would abuse patients while other patients were watching, but not when doctors were present.

CONCLUSIONS
“it is clear that we cannot distinguish the sane from the insane in psychiatric hospitals” (Rosenhan)

Rosenhan draws attention to the private hospital that diagnosed a pseudopatient with manic-depression. This is a more treatable disorder than schizophrenia. Rosenhan notes that wealthier people are more likely to get diagnosed with milder problems that have better therapeutic outcomes, which shows that your class background affects the way you are diagnosed.
In particular, Rosenhan identifies a tendency toward false positives (Type I errors) in normal diagnoses, but Type II errors (false negatives) when “the stakes are high” (ie. when the hospital knows its diagnoses are being assessed).
Rosenhan is very concerned that the conditions in psychiatric hospitals do not help with therapy; in fact, they make patients worse. Rosenhan agrees with Goffman (1961) that conditions in psychiatric hospitals are psychologically mortifying - they make healthy behaviour and healthy thoughts more difficult.

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40
Q

(AO3) evaluating Rosenhan (1973)

A

GENERALISABILITY (S) Rosenhan made a point of using a range of psychiatric hospitals - private and state-run, old and new, well-funded and under-funded - from across the United States.
(W) Nevertheless, 12 is a small sample for a country as big as the USA and a few “bad apples” could have skewed the results of Rosenhan’s observations.
(W) There’s been a lot of progress in mental health care since the 1970s (indeed, Rosenhan’s study prompted many reforms), so perhaps the results are “time-locked” and cannot be generalised to psychiatric diagnosis and care today. For example, Rosenhan’s pseudopatients were diagnosed using DSM-II. Today’s DSM-5 requires the patient to show TWO symptoms (not just one) and have the symptoms for at least 6 months.

RELIABILITY (W) Rosenhan trained his pseudopatients beforehand, but they didn’t all follow the same standardised procedures.
Data from a 9th pseudopatient was not included in Rosenhan’s report because, among other things, he did not follow procedures.
The graduate student asked his wife to bring in his college homework to do, revealing he was a psychologist.
Another pseudopatient revealed that he was going to become a psychologist and one of his visitors was a college Psychology professor
One pseudopatient struck up a romantic relationship with a nurse.
Rosenhan explains this as the pseudopatients resisting the effects of depersonalisation and powerlessness. However, it also suggests they failed to follow instructions and act consistently.

APPLICATION (S) This study had a huge impact on mental health care, not just in America but worldwide. It caused psychiatric hospitals to review their admission procedures and how they trained their staff to interact with patients. It started the move away from dependency on the “chemical straitjacket” of drugs to treat mental health. Today, the study is a compulsory part of training in psychiatric medicine and nursing.
Along with Robert Spitzer’s criticisms, this study was a major influence on reforming the DSM. DSM-III (1980) defined mental illnesses much more carefully, with clear guidelines for including or excluding people from each classification. For example, in DSM-III, a hallucination needed to be repeated several times; in DSM-IV (1994) hearing voices needed to be experienced for over a month before a diagnosis of schizophrenia can be made and DSM-5 makes this 6 months.

VALIDITY (W) despite being a field-study, it lacked ecological validity. Seymour Ketty (1974) criticised Rosenhan, saying that, because the pseudopatients were faking an unreal mental condition, it doesn’t tell us anything about how people with genuine mental conditions are diagnosed. Psychiatrists don’t expect someone to carry out deception in order to be admitted to a psychiatric hospital; therefore, the study lacks EV.

ETHICS (W) The hospital staff were deceived about the pseudopatients’ symptoms being real. The doctors and nurses in the hospitals could not consent to take part or exercise their right to withdraw from the study. The other patients in the study had no possibility of consenting or withdrawing and didn’t enter psychiatric hospitals in order to be in psychology research
(S) Rosenhan did protect confidentiality - no staff or hospitals were named.
(W) Rosenhan may be criticised for failing in a duty of care towards his own researchers - the pseudopatients. He put them in a harmful environment where they experienced tension and stress. None of them were physically abused but they witnessed physical abuse going on. They were instructed in how to avoid taking medication, but if they had been forced to take medication, it could have produced side-effects on them.
- However, Rosenhan took a few precautions. In his own case, he notified the hospital manager and chief psychologist of what he was doing. For all the pseudopatients, he prepared lawyers who would intervene to get the pseudopatients out of hospitals if they requested it.
(W) A different ethical issue with Rosenhan’s study is that it contributed to a crisis of public confidence in the American mental health system - which may have prevented people who genuinely needed help from seeking it.

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41
Q

what is schizophrenia?

A

a psychotic mental disorder where patients may experience, perceive and interpret things differently from others and may lose the ability to distinguish between the real and unreal. this is characterised by symptoms like hallucinations, delusions, disorganised thinking etc.

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42
Q

what are symptoms of a mental disorder?

A

the behaviours, thoughts and feelings experienced by the patient/client associated with their diagnosis e.g. hallucinations. They may be observable, or may be reported to the clinician by the patient (privately experienced, self-report).

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43
Q

+ symptoms

A

Symptoms that are found in patients with schizophrenia that are not found in the normal population such as hearing voices (auditory hallucinations).

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44
Q
  • symptoms
A

the absence or lack of normal levels of functioning such as apathy or avolition, poor self care, lack of speech (also known as poverty of speech or alogia), and the absence or ‘flattening’ of normal emotional responses (also known as flattened affect).

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45
Q

cognitive symptoms of schizophrenia

A

poor working memory, poor executive functioning (understanding and decision-making), difficulty in concentrating, difficulty in memory

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46
Q

features of a mental illness

A

Features of a mental illness are facts about the illness, such as age of onset of symptoms; how commonly it occurs in a particular population (prevalence); whether there are gender or culture differences, or groups at higher risk of diagnosis; the course of the illness; subtypes of the illness (in DSM-IV)

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47
Q

DSM-V diagnostic criteria for schizophrenia

A

To receive a schizophrenia diagnosis using DSM-5, someone can have any of the symptoms and features, but he must have the following:
1) At least two symptoms from Criteria A:
Delusions, Hallucinations, Disorganised Speech, Disorganised Behaviour, Negative Symptoms
2) Level of functioning has declined. This means that the symptoms must impair one’s life and get in the way of her ability to work (or go to/participate in school), have positive relationships (or any relationships at all), and practice self-care.
3) These must have been present for at least one month.
4) Schizoaffective disorder, major depression, and bipolar disorder have been ruled out
5) Substance use/abuse has been ruled out as a cause

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48
Q

features of schizophrenia

A
  • Lifetime Prevalence - Schizophrenia is found in any nation at a rate of 1.4 - 4.6 per 1000 people (Jablensky, 2000)
  • age of onset is typically 18 to early 20’s in men
  • age of onset is typically late 20’s to early 30’s in women
  • schizophrenia is more common in lower socio-economic backgrounds
  • schizophrenia is more common in urban rather than rural areas
  • risk factors of schizophrenia include drugs like marijuana
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49
Q

what are delusions in schizophrenia?

A

false ideas you feel convinced are true. common delusions include:

(1) paranoia the belief that people are watching you or want to hurt you

(2) delusions of grandeur the belief you are important, heroic or super powers

(3) delusions of identity thinking you are someone else like Jesus for example

(4) thought insertion the belief that your thoughts are not your own and have been put in your mind by someone else

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50
Q

what are hallucinations in schizophrenia?

A

when you see or hear things that aren’t real.

seeing (visual hallucinations)

hearing (auditory hallucinations)

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51
Q

what are disorganised thoughts in schizophrenia?

A

a key aspect of schizophrenia where speech may become tangential (jumping from one topic to another) or speech may be highly circumstantial (speaking continuously and never getting to the point).

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52
Q

types of schizophrenia
paranoid schizophrenia

A

paranoid schizophrenia is characterised by someone being suspicious of others and having delusions of grandeur. there are often hallucinations as well.

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53
Q

types of schizophrenia
disorganised schizophrenia

A

disorganised schizophrenia is characterised by speech being disorganised and hard to follow, as well as the person having inappropriate moods for a given situation. there are no hallucinations.

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54
Q

types of schizophrenia
residual schizophrenia

A

residual schizophrenia is where there are low level positive symptoms but psychotic symptoms are present.

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55
Q

types of schizophrenia
catatonic schizophrenia

A

catatonic schizophrenia is when someone is very withdrawn and isolated and has very little movement.

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56
Q

types of schizophrenia
undifferentiated schizophrenia

A

when someone doesn’t fit any of the above types.

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57
Q

schizophrenia key terms
thought insertion

A

if someone thinks their thoughts are put there by someone else

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58
Q

schizophrenia key terms
catatonic supor

A

standing motionless like a statue in bizarre postures

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59
Q

schizophrenia key terms
flatness

A

no emotional response can be elicited from any stimulus, face is immobile, eyes are lifeless, speech is toneless, staring vacantly

60
Q

schizophrenia key terms
inappropriate affect

A

responding inappropriately in certain situations (e.g. laughing when hearing terrible news)

61
Q

schizophrenia key terms
apathy

A

loss of interest in normal goals

62
Q

(AO3) evaluating the validity of schizophrenia diagnoses using the DSM

A

(S) Lee (2006) conducted a study to determine if the DSM-IV-TR diagnosis of ADHD would be suitable for Korean children. Lee’s study used a questionnaire with 48 primary school teachers and ask them to rate the behaviour of the children they taught. They intended to compare the DSM-IV-TR diagnostic criteria with the questionnaire data. They found that the two agreed, which shows concurrent valdity.
- This strengthens the validity of diagnoses using DSM criteria.

(S) the claim that DSM is valid is supported bt the claim that it is reliable. (e.g. Goldstein’s study found high reliability; therefore, the DSM also has high validity).

(S) DSM revisions have made more of an attempt to include culture-bound syndromes. (e.g. Penis panics in Africa and Asia which is known as genital retraction syndrome. The origin of this idea may be related to Witchcraft and the DSM acknowledges this as a culture-bound syndrome).

(W) It has been said that co-morbidity (having one or more mental disorder) is difficult to diagnose using the DSM.

(W) It may be claimed that splitting a mental disorder into symptoms and features is reductionist and that a holistic approach may be more valid. (e.g. a counselling session focuses more on the individual as a whole and treatment rather than focusing on diagnosis).

63
Q

(AO3) reliability of schizophrenia diagnosis using ICD-10

A

(S) supporting evidence from studies shows that ICD-10 is a reliable measure of schizophrenia.
(Jakobsen et. Al 2005) used a random sample of Danish in-patients diagnosed with schizophrenia and a sample of out-patients diagnosed with a history of psychosis to compare the reliability of ICD-10 with regard to schizophrenia. They found 87% predictive value when it came to diagnosis of schizophrenia and showed good agreeability when using another measure. This shows reliability.

(S) Studies use inter-rater reliability, which means more than one person can use the classification system and reach the same diagnosis. There are careful controls to ensure raters work independently free from bias.

(W) Schizophrenia was diagnosed more frequently in the ICD-10 than the DSM-IV.
**(Cheniaux et. Al 2009) They looked at various diagnoses including schizophrenia, bipolar disorder etc, and compared the inter-rater reliability across ICD-10 and DSM-5. They found that schizophrenia was more frequently diagnosed in ICD-10 than DSM-IV (possibly because of the duration), which shows low reliability.

(W) low inter-rater reliability, (Cheniaux et. Al 2009) showed 0.50 agreement, which suggests it is unreliable.

64
Q

(AO3) evaluate the validity of schizophrenia diagnoses using ICD-10

A

(S) there is supportive evidence from Pihlajamaa et al. (2008) who aimed to look at the validity of diagnoses using the DSM-III-TR, the DSM-IV and the ICD-10 in people born in helsinki (877 patients) who had at least one schizophrenia diagnosis. They found that using the Register and ICD-10 diagnosis, they reached the same diagnosis 78% of the time. this shows inter-rater reliability and agreement between two measures, which supports the idea that the ICD is valid.

(W) Jansson et al. (2002) aimed to compare the ICD-10 criteria with other diagnostic systems. they looked at concurrent validity between ICD-9 and ICD-10 and they found that different classification systems focused on different features and symptoms in schizophrenia (ICD-9 and ICD-10) which threatens the validity of the two systems. there is a general suggestion that there is a different focus and so validity of diagnosis is less likely.

(W) studies of validity of diagnosis of schizophrenia are hard to carry out given the differences in disorders (e.g. schizoaffective disorder). the complexity of the disorders seem to affect the validity of diagnoses. ellason and ross (1995) suggest that people diagnosed with dissociative identity disorder have more features and (positive) symptoms of schizophrenia than those with schizophrenia.

65
Q

what is the biochemical explanation for schizophrenia?

A

the biological explanation for symptoms of schizophrenia is that they are caused by abnormalities in the brain’s biochemistry.

66
Q

what is the dopamine hypothesis?

A

the idea that schizophrenia is caused by excessive activity at synapses that use dopamine as their primary neurotransmitter. this causes abnormal functioning of DA-dependant brain systems, resulting in schizophrenic symptoms.

it is possible that an increase in dopamine in one site in the brain (the mesolimbic pathway) contributes to + symptoms of schizophrenia like hallucinations.

and in another site (the mesocortical pathway), contributes to - symptoms of schizophrenia like avolition (lack of motivation).

67
Q

(AO3) evaluation of the dopamine hypothesis

A

(S) supporting evidence Wise & Stein (1973) found that schizophrenia patients who died in accidents showed abnormally low levels of Dopamine Beta Hydroxylase (DBH) in the brain fluid. DBH is an enzyme whose function is to break down the neurotransmitter Dopamine after release.
- The dopamine hypothesis suggests that an imbalance in dopamine neurotransmission is associated with the development of schizophrenic symptoms. This evidence supports the dopamine hypothesis because it proves how the reduced activity of DBH might lead to lower levels of dopamine. This aligns with the belief that dysregulated dopamine transmission is implicated in schizophrenia.

(S) supporting evidence: Barlow & Durand (1995) report that chlorpromazine is effective in reducing schizophrenic symptoms in about 60% of cases. It appears to have the most impact on the positive symptoms hallucinations, delusions) and treated patients may still suffer from severe negative symptoms.
- Since the dopamine hypothesis attributes schizophrenic symptoms to excessive activity at the synapses, this study supports the credibility of the dopamine hypothesis. Since Chlorpromazine works by blocking the dopamine receptor sites, it means excessive activity is unable to occur at the synapses. As it is effective in alleviating positive symptoms, it aligns with the idea that dopamine dysregulation plays a role in the occurrence of these symptoms.

(S) supporting evidence from brain scanning Hietala et al. (1994) found an increase in DA in patients with schizophrenia (not in remission) compared to controls, using PET scanning.
- They found an increase in dopamine in the these patients compared to the control. This aligns with idea that dysregulation of dopamine neurotransmission is a factor in the symptoms of schizophrenia. The elevated levels of dopamine observed in their study, is consistent with the notion that excessive dopamine contributes to positive symptoms of schizophrenia.

(W) amphetamines produce only + symptoms. amphetamines only produce symptoms like the + symptoms in schizophrenia. this is a problem because it suggests that the dopamine hypothesis is an insufficient explanation.

(W) the dopamine hypothesis may be criticised for its insufficiency. the dopamine hypothesis fails to establish a cause-and-effect. this means that there is a potential for misrepresentations where they may be potential confounding factors that influence the observed variables in the above evidence. for instance, a patient may take medication which could skew the effects of the neurotransmitters.

(W) PET scans show that blocking dopamine receptors does not always remove symptoms
PET scans have suggested that drugs that block dopamine do not reduce the symptoms of schizophrenia in patients who have had schizophrenia for 10 years or more.

68
Q

what is the glutumate hypothesis?

A

when glutamate activity increases, dopamine activity decreases, so glutumate has an inhibitory effect on dopamine activity. in relation to schizophrenia, what was assumed to be the result of excessive dopamine might actually be the result of too little glutumate activity.

69
Q

what is dopamine?

A

dopamine is a type of monoamine neurotransmitter. it also acts as a hormone and plays an important role in:
movement, memory, pleasurable reward/motivation, behaviour and cognition, attention, sleep and arousal, mood, learning.

70
Q

what is glutamate?

A

glutamate is the most abudant excitatory neurotransmitter in the brain. it plays a major role in learning and memory. for your brain to function properly, glutamate must be present at the right concentration in the right brain areas at the right time.

71
Q

what is chlorpromazine?

A

an antipsychotic drug that blocks dopamine receptor sites without activating them.

72
Q

what are amphetamines?

A

a drug of abuse that increases levels of dopamine in the brain by interrupting dopamine reuptake. the drug causes euphoria and psychomotor agitation and prolonged exposure to high doses of amphetamines. this can lead to a paranoid, delusional psychotic state, which can be accompanied by hallucinations.

73
Q

what is PCP?

A

a drug of abuse, also known as Angel Dust, which can induce symptoms that are almost indistinguishable from those associated with schizophrenia. It is an NMDA glutamate receptor antagonist, meaning that it blocks glutamate receptors without activating them.

74
Q

antagonist

A

blocks the receptor at the site of the receptor and deactivates it

75
Q

agonist

A

activates the receptor at the site of the receptor so a message is passed on.

76
Q

(AO3) evaluation of the glutumate hypothesis

A

(S) the glutamate hypothesis works with the dopamine hypothesis and expands on it, rather than replacing it.
- This is a strength because it means evidence for the dopamine hypothesis can also be incorporated in the glutamate hypothesis.

(S) supportive evidence Malhotra et. Al (1997) found that if schizophrenia patients are given PCP or ketamine the result is a marked increase in their symptoms that lasts for some time.
- The fact that PCP and ketamine, which act on the glutamatergic system, can induce symptoms similar to schizophrenia supports the idea that abnormalities in glutamate neurotransmission may be implicated in the disorder. Therefore, this is strong supportive evidence for the glutamate hypothesis.

(W) A weakness may be that using PET scanning to obtain evidence about neurotransmitter functioning. Carlsson et. Al (1997) mentions how under pressure, under a scan, humans may react differently and unnaturally. This means that the findings, espcially those focused on brain activity linked to psychosis might not have validity.

77
Q

what is the structural biological explanation for schizophrenia?

A

another biological explanation for symptoms of schizophrenia is that symptoms are caused by structural abnormalities of the brain.

This brain disease model of schizophrenia suggests that there are differences between the brains of people with a diagnosis of schizophrenia and the brains of most people in the population.

The theory claims that the symptoms of schizophrenia such as disordered thinking, hallucinations and delusions, are caused by these abnormalities in the structure and function of the brain.

Abnormalities found in the brains of people with schizophrenia (in comparison to controls) include reduced brain weight and volume, enlarged ventricles (fluid-filled spaces in the brain); cellular disarray; and hypofrontality (reduced levels of activity in the frontal lobes of the brain

78
Q

cellular disarray

A

Brain tissue samples from the brains of patients with schizophrenia show neurons that appear to be disorganised in the way they are structured/arranged in comparison to normal controls.
- causes disorder among signalling brain calls and thus may be related to hallucinations, for example.

79
Q

ventricular enlargement and asymmetry

A

The fluid filled spaces in the brain called ‘ventricles’ are enlarged in patients with schizophrenia in comparison to normal controls, and may be more enlarged in one hemisphere than the other.
- leads to severe cognitive impairments

80
Q

hypofrontality

A

Reduced activity in the frontal lobes of the brain, which are involved in higher level cognitive functioning, planning, problem solving and integrating information. This is measured in fMRI scans
- hypofrontality said to cause cognitive deficits in schizophrenia. these have been observed with neuropsychological tests of executive function. these impairments affect planning abilities, as well as regulating goal-directed behaviour (contributing to apathy)

81
Q

reduced brain weight

A

at post-mortem, the brains of patients with schizophrenia weigh less, on average, than normal controls.

82
Q

reduced brain volume

A

MRI scans of discordant MZ (identical) twins show reduced brain volume and increased fluid filled spaces in affected twins (with schizophrenia) in comparison to their well twins.
- causes deterioration in symptom severity, level of function and cognition

83
Q

(AO3) evaluate the biological/structural explanation for schizophrenia

A

(S) supporting evidence Gaser et al. (2000) compared the MRI scans of the brains of MZ (identical) twins, and found that the affected twins, with schizophrenia, had enlarged ventricles and reduced brain volume in comparison to the brains of the controls - the unaffected twins.
- This is a strength because it is consistent with the belief that structural abnormalities like reduced brain volume/enlarged ventricles have an effect on the display of schizophrenic symptoms.

  • Van Erp et al. (2015) conducted a meta-analysis of research into sub-cortical brain abnormalities in patients with schizophrenia and reported that in comparison to controls individuals with schizophrenia have smaller volume in the hippocampus, amygdala, thalamus, nucleus accumbens and intracranial space than controls, and larger pallidum and ventricle volumes.

(W) nature vs. nurture debate: the biological explanation only accounts for the nature debate. this may be considered reductionist as it does not take into account other psychosocial factors.

84
Q

CONTEMPORARY STUDY Carlsson et. Al (1999/2000)

A

AIM a review of studies aimed to present the current view of the relationship between schizophrenia and dopaminergic dysfunction (problems with dopamine). Another aim was to explore a rival theory: glutamergic deficiency or hypoglutamergia (too little glutamate).
- this is a review- summing up the research so far, NOT an investigative study.

SAMPLE reviewed 32 studies (conducted by other researchers).

PROCEDURE Carlsson et al. aren’t carrying out empirical research so they don’t have a procedure. However, they refer to a number of studies that use positron emission tomography (PET).

PET is a brain imaging technique which injects the participant with a radioactive tracer that dissolves in the blood stream. The tracer is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. A PET scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red.
Some PET tracers are designed to bind to receptors on neurons in the brain. They won’t be able to do this if certain neurotransmitters are over-active in the brain. Therefore, on a PET scan, these areas will show up as lacking in radioactivity, coloured green or blue. On the other hand, if these neurotransmitters are under-active in the brain, the tracers will bind themselves to lots of receptors and show up on the PET scan as yellow and red areas.

RESULTS (1) the dopamine hypothesis revisited 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.
- 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)

(2) beyond dopamine Carlsson et al. focus on glutamate:
- Drugs like PCP (“angel dust”) and ketamine produce psychotic symptoms, but instead of activating dopamine they stimulate glutamate receptors called NMDA.

(3) Glutamatergic control of dopamine release Glutamate seems to regulate the behaviour of dopamine and sheds some light on the behaviour of dopamine in the brain. Carlsson describes how it acts as an “accelerator” (increasing dopamine activity) or a “brake” (decreasing it).

(4) Glutamate-dopamine interaction at the postsynaptic (striatal) level 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 (in the basal ganglia) and in the cerebral cortex (which includes the frontal lobe, where conscious behaviour happens).

(5) The thalamic filter Carlsson has his own theory about what’s going on. The thalamus is an important brain structure between the stratium and the cerebral cortex. Carlsson proposes that the thalamus “filters off” neurortransmitters coming out of the stratium to stop the cerebral cortex from overloading. There are two “pathways” through the thalamus:
Picture
In the indirect pathway, too much dopamine (hyperdopaminergia) or too little glutamate (hypoglutamatergia) reduces the “protective influence” of the thalamus - this links to positive symptoms
There’s also a direct pathway, which has the opposite effect; abnormal dopamine and glutamate activity here will “excite” the thalamus, starving the cerebral cortex of stimulation - this links to negative symptoms.

CONCLUSIONS 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. In other words, even though only normal levels of dopamine are being produced, the dopamine receptors have an extreme reaction.

Researchers should start looking into the role of other neurotransmitters, like gaba, acetylcholine and neuropeptides.

85
Q

(AO3) evaluate contemporary study: Carlsson et. Al (1999)

A

(S) reliability The studies Carlsson et al. cite are all lab experiments, many of them on animals, which use modern PET or SPECT brain imaging techniques. These techniques are standardised and replicable, making the research reliable.

(S) application value The main application of this study is in the development of new antipsychotic drugs - improved dopaminergic drugs that have fewer side-effects based on a better understanding of dopamine pathways and new atypical drugs that affect other neurotransmitters like serotonin and glutamate.

(W) validity Carlsson is questioning the validity of the Dopamine Hypothesis that he himself pioneered back in the 1960s. He lists some of the evidence that has called it into question, such as the new atypical antipsychotics like Clopazine which reduce psychotic symptoms without influencing dopamine. He considers an alternative, the Glutamate Hypothesis.

86
Q

what is the cognitive explanation for schizophrenia?

A

The Cognitive explanation for schizophrenia suggests that faulty cognition is the cause of positive and negative symptoms such as hallucinations and delusions, disorganised speech and cognitive deficits. Faulty cognitions include poor attention and memory, difficulties with language and disorganised thinking.

87
Q

source monitoring as part of the cognitive explanation of schizophrenia

A

the ability to distinguish between self-generated thoughts and externally presented stimuli.

88
Q

subvocalisation as part of the cognitive explanation of schizophrenia

A

tiny but detectable movements that adults make with their speech muscles when they are ‘talking to themselves’ - their thoughts or ‘inner voice’

89
Q

schemas as part of the cognitive explanation of schizophrenia

A

information from past experiences that are stored in our long term memories, which help us to make predictions about the future and make sense of our experiences.

90
Q

JTC bias as part of the cognitive explanation for schizophrenia

A

stands for the jump to conclusions bias. this is the much replicated finding that patients with schizophrenia reach decisions with less information than normal controls. (Garety et. Al 1991)

91
Q

evidence for faulty source monitoring

A
  • In adulthood, inner speech is accompanied by ‘subvocalisation’ – covert activations of the speech muscles that can by detected by electromyography. It has been known for many years that subvocalisation is evident when patients experience voices (e.g. Gould, 1948; McGuigan, 1966) which suggests that auditory-verbal hallucinations occur when inner speech is misattributed to an external source.
  • Bentall & Slade (1985) observed that people who hear voices, when asked to detect an externally presented voice against a background of white noise, have an abnormal response bias, leading them to say a voice is present on trials when it is not
  • Johns et al. (2001) found that hallucinating patients are especially likely to mistake their own voice, after it had been electronically distorted, for speech by someone else.

Evidence to support the idea that source monitoring errors reflect a failure to monitor one’s own intentions comes from Blakemore et al. (2000) who found that voice-hearing psychotic patients had a greater ability to tickle themselves than non-psychotic patients.

92
Q

evidence for delusions (cognitive explanation)

A

The psychological abnormality that has been most robustly linked to delusional thinking is a tendency to ‘jump to conclusions’ (sometimes described as the ‘JTC bias’) when reasoning about probabilities.
Garety et al., (1991) presented deluded patients and controls with two jars containing red and white beads. The jars were taken away, the participants were presented with a sequence of beads and were asked, once they had obtained sufficient information, to decide which jar the beads had come from. Deluded patients requested less information before reaching a decision.

93
Q

treatments for schizophrenia (1) antipsychotic drugs

A

antipsychotic drugs can help to alleviate symptoms of schizophrenia.

The first antipsychotic medication that was helpful in alleviating symptoms of schizophrenia was developed in 1951. It was called Chlorpromazine (one of a group of drugs called the Phenothiazines) and radically transformed the treatment of schizophrenia, leading to many more patients living in the community rather than in psychiatric hospitals, with a greatly improved quality of life.

Chlorpromazine is a ‘typical antipsychotic’ - the first generation of antipsychotic drugs to be developed. These first generation antipsychotics have some severe and unpleasant side-effects that make non-compliance with medication a problem, when patients are discharged from hospital.

In the 1970’s, new generation ‘atypical antipsychotics’ were developed including Clozapine, which blocked serotonin as well as dopamine, proving to be an effective alternative treatment for patients who experienced severe side-effects from the typical antipsychotics, or for whom they were not effective.

Clozapine, appeared in 1971. Risperidone followed in 1993 and olanzapine in the 2000s.

94
Q

typical antipsychotic drugs

A

established drugs that were introduced in the 1950s. these drugs alleviate symptoms of schizophrenia by blocking dopamine receptors.

95
Q

Phenothiazines (PTZs)

A

a family of typical anti-psychotic drugs including: chlorpromazine (CPZ)

96
Q

chlorpromazine (CPZ)

A

They can be taken as a pill or via injection and are effective at the synapse within 48 hours. The drugs may take weeks to be effective however they do reduce symptoms of schizophrenia in around 60% of patients. They are less effective at controlling negative symptoms than positive symptoms and have some unpleasant side effects, including dry mouth, constipation, drowsiness and sleep dysfunction, and extrapyramidal side- effects (EPSE) including tremors and rigidity.

97
Q

atypical antipsychotics (AAPs)

A

newer antipsychotic drugs that have fewer side-effects and are more effective in alleviating both positive and negative symptoms. Although AAPs have fewer side-effects than PTZs, they do have some serious side-effects for some patients, including blood disorders and diabetes. A treatment of last resort, they are useful for treatment resistant patients or patients for whom the side-effects are intolerable.

98
Q

what are side effects of antipsychotic drugs for schizophrenia?

A

sleepiness + tiredness
shaking + muscle spasms
low blood pressure
problems with sex drive
weight gain

99
Q

(AO3) evaluation of taking antipsychotic drugs as a treatment for schizophrenia

A

(S) time effective antipsychotic drugs take a few weeks to work. It are quick and easy to take medication (no social interaction), which some individuals may prefer.

(S) effectiveness davis et. al conducted a study into the effectiveness of taking antipsychotic mediciation to reduce schizophrenia symptoms. they found that there was a STM beneficial effect in 75% and a LTM beneficial effect in 55-60%. this suggests that there was a significant improvement in the patient’s dysfunction, meaning they are able to return to their occupational and home lives.

(W) acceptability taking medication raises a certain stigma across certain individuals and cultures. for instance, the south asian culture primarily utilises herbal and natural remedies to cure illnesses or diseases. as a result, it may be difficult to put a schizophrenic patient onto antipsychotics because they may not be accepting of it.

(W) side effects the biggest weakness of antipsychotic drug use as a treatment for schizophrenia, is the side effects. neuroleptics (e.g. chlorpromazine, bind to the DA receptors without activiating them. they often cause severe side effects like weight gain or fatigue. these may be uncomfortable for the patient and may disrupt their quality of life.
- (counter argument) this may be more severe in terms of typical antipsychotic drugs like chlorpromazine. Bilder et al., (2002) found that newer (atypical) drugs (e.g. clozapine) were as effective as typical drugs for positive symptoms; better for negative symptoms. this suggests that newer drugs may not induce as negative side effects; nonetheless, they are still present (e.g. lowered WBC count).

100
Q

what is cognitive-behavioural therapy for schizophrenia?

A

The main aim of Cognitive Behavioural Approaches to treatment for schizophrenia is modifying hallucinations and delusional beliefs (Roth & Fonagy, 2005). Other aims are to help improve cognitive function and developing coping strategies to manage symptoms that are not addressed by medication, as well as normalising symptoms to reduce stigma, fear and distress.

Stress Management (SM) helps patients to cope with their symptoms, using cognitive techniques such as distraction from intrusive thoughts and challenging their meanings; increasing or decreasing social activity to help with intrusive thoughts; and breathing and other relaxation techniques (Bennett, 2006).

Another main approach is belief modification
or reattribution therapy
, which is directly aimed at changing the patients thinking.

Cognitive remediation (CR) aims to improve cognitive function, including patients ability to concentrate, remember, plan and solve problems, typically through computer software or pencil and paper exercises (Saperstein and Kurtz, 2013).

101
Q

what is stress management in CBT for schizophrenia?

A

helps patients to cope with their symptoms, using cognitive techniques such as distraction from intrusive thoughts and challenging their meanings; increasing or decreasing social activity to help with intrusive thoughts; and breathing and other relaxation techniques (Bennett, 2006).

102
Q

what is belief modification in CBT for schizophrenia?

A

delusional thinking is challenged directly and there is testing against reality. Evidence for the delusional belief is challenged.

103
Q

what is cognitive remediation (CR) in CBT for schizophrenia?

A

aims to improve cognitive function, including patients ability to concentrate, remember, plan and solve problems, typically through computer software or pencil and paper exercises (Saperstein and Kurtz, 2013).

104
Q

techniques/interventions of CBT for schizophrenia

A

CBT is the first recommendation of the NICE guidelines for the prevention of psychosis. CBT focuses on the individual, with one-to-one weekly sessions, over a number of weeks or longer.
The therapeutic relationship is important and focuses on the therapist being supportive and non-threatening.

There is collaboration between the therapist and the client to identify specific symptoms, problems and experiences, triggers and consequences. Once the problems have been identified the therapist and client work together to develop coping strategies to help them to cope more effectively with them.

Belief Modification

Focusing and reattribution aims to reduce the frequency of auditory hallucinations and reduce the distress that they cause. The therapist focuses first on the physical attributes of the voices (number, loudness tone, gender etc), then looks at the content of the voices, and the patient keeps a record of what the voices say for homework). The underlying aim is to show that the voices are self-generated, and not to be feared, but accepted.

105
Q

(AO3) evaluate the use of CBT for schizophrenia

A

(S) effectiveness CBT is significantly effective at improving the positive symptoms of schizophrenia (like hallucinations). Bentall (1994) considered reattribution of auditory hallucinations as a strategy for helping patients with schizophrenia, finding that 3 out of 6 patients reattributed the voices to themselves. Another (different) three patients reported fewer hallucinations as well as a reduction in stress levels. (no control group or follow up)

(S) relapse CBT has a long-term benefit and helps reduce the likelihood of relapse. Through belief modification and the collaborative relationship achieved between the patient and the therapist, it becomes empowering and supportive. This is a strength because it equips patients with coping stategies and reduces their likelihood of relapse as they have safer ways of coping. Kingdon and Turkingdon (1991) found that 35 out of 65 patients with schizophrenia (54%) were free of symptoms at 5 year follow-up, after normalising and CBT techniques were used (no baseline measure or comparison/ control group). This evidence proves that CBT is effective in reducing the symptoms of schizophrenia over a long-term.

(W) time CBT is relatively time-consuming and expensive. It is typically conducted by weekly sessions over a number of weeks or months. Furthermore, the travel to and from therapy may be disrupting to the individual’s day. This might deter schizophrenic patients to seek CBT as a treatment option because of its cost-benefit analysis. It is fairly time-consuming and expensive in contrast to antipsychotic medication.

(W) acceptability going to therapy may not be widely accepted because it holds stigmas in certain cultures or individual’s feel uncomfortable sharing their thoughts. This means it is not entirely accessible and an interaction-free, discrete option like antipsychotic medication may be more preferrable.

(W) distressing CBT can be distressing for the invididual as they often have to focus on their distressing symptoms such as hallucinations and delusions. they must also question their own beliefs, which includes questioning their own sanity which may also be stressful. this may be a weakness from an ethical perspective.

106
Q

unipolar depression or major depressive disorder (MDD)

A

is a mood disorder characterised by low mood (sadness, feelings of worthlessness) and a lack of energy, interest in or enthusiasm for activities. there are a range of social, physical, cognitive and affective (emotional) symptoms that are associated with depression.

107
Q

features of unipolar depression

A
  • Nearly a fifth (19%) of British adults have reported an episode of depression
  • Depression is more prevalent among women (30%) than men (15%)
  • Depression is reported by 27% of divorced or separated people, compared to 20% of people who are single and 16% of people in stable relationships.
  • People in lower-income households are more likely to report depression compared to wealthier households.
  • Average age of onset is mid to late twenties.
  • The most at-risk age group is 50-54
108
Q

types of symptoms of unipolar depression

A

**Affective symptoms: ** depressed mood, feelings of worthlessness and guilt, pessimism about the future and a lack of interest in things that used to be enjoyable are all reported by people with depression. This is called negative affect.

Cognitive symptoms: other symptoms include fatigue, difficulty concentrating and indecisiveness (these are mental symptoms but they’re not to do with emotion).

Social symptoms: people with depression often abandon hobbies and pastimes, work and study; they withdraw from relationships with friends and family.

Physical symptoms: people with depression often experience loss of appetite (or sometimes increased appetite) along with unexplained aches and pains; they move and speak slowly and there are changes in their sleep patterns (some sleep all the time, some can’t sleep at all).

109
Q

list affective symptoms of depression

A

depressed mood, feelings of worthlessness and guilt, pessimism about the future and a lack of interest in things that used to be enjoyable are all reported by people with depression. This is called negative affect.

110
Q

list cognitive symptoms of depression

A

Cognitive symptoms: other symptoms include fatigue, difficulty concentrating and indecisiveness (these are mental symptoms but they’re not to do with emotion).

111
Q

list social symptoms of depression

A

people with depression often abandon hobbies and pastimes, work and study; they withdraw from relationships with friends and family.

112
Q

list physical symptoms of depression

A

people with depression often experience loss of appetite (or sometimes increased appetite) along with unexplained aches and pains; they move and speak slowly and there are changes in their sleep patterns (some sleep all the time, some can’t sleep at all).

113
Q

what is the diagnostic (DSM 5) criteria for unipolar depression?

A

Low mood and/or loss of interest or pleasure in life activities for at least 2 weeks.

AND at least 5 of the following symptoms are present, causing significant interference in ability to function in social, work or other important areas of life, almost every day:

(1) Depressed mood most of the day.

(2) Diminished interest or pleasure in all or most activities.

(3) Significant unintentional weight loss or gain.

(4) Insomnia or sleeping too much.

(5) Agitation or psychomotor retardation noticed by others.

(6) Fatigue or loss of energy.

(7) Feelings of worthlessness or excessive guilt.

(8) Diminished ability to think or concentrate, or indecisiveness.

(9) Recurrent thoughts of death.

114
Q

features: gender differences in depression

A

One feature of depression is that it is experienced differently by men and women. For women the primary emotion is usually sadness, whereas for men it is more typically anger or irritability, often coupled with recklessness. Hormones are a major candidate for explaining this male-female difference (Westly, 2012).

Another feature of depression is that it affects up to twice as many women as men (Freeman and Freeman, 2014). However, this may been disputed. The difference in prevalence may be due to men under-reporting health problems - relying on self-report of symptoms may lead to under-diagnosis in men. When this is allowed for, the difference in prevalence between men and women disappears (Martin et al., 2013).

115
Q

cultural differences in diagnosis of depression

A

Davison & Neale (1994) state that in Asian cultures, a person experiencing emotional disturbance is praised if they do not express their feelings.

However, in some Arabic cultures, the outpouring of emotions is encouraged.

116
Q

what is the biochemical explanation for depression?

A

The Monoamine Hypothesis (MAOH) is the longest-standing and most persistent biological theory of depression (Claridge and Davis, 2003). According to the MAOH, the symptoms of depression are caused by low levels of a group of neurotransmitters known as monoamines, which are important for emotions and cognition as well as sleep regulation. These include serotonin (5-HT), noradrenaline (also known as norepinephrine) and dopamine.

The main reason to accept this hypothesis is that drugs that increase levels of these neurotransmitters in the synaptic gap have an anti-depressant effect, alleviating the low mood and other symptoms of unipolar depression (MDD). Most research has focused on serotonin

117
Q

Monoamine oxidase (MAO) neurotransmitters

A

a group of neurotransmitters including Serotonin, noradrenaline and dopamine. All have been implicated in depression.

118
Q

SSRI- Specific Serotonin Reuptake inhibitor

A

This antidepressant drug acts only on serotonin reuptake, reducing the amount that is taken back up by the presynaptic neuron’s serotonin transporters (SERT) and thereby increasing the amount of serotonin in the synapse.

119
Q

Tricyclics

A

a type of antidepressant drug that prevents some of the reuptake of noradrenaline and serotonin, increasing the amount of these neurotransmitters in the synaptic gap.

120
Q

MAOIs - Monoamine oxidase inhibitors

A

a type of antidepressant that works by preventing the enzyme monoamine oxidase (MAO) from breaking down the neurotransmitters 5HT and noradrenaline, thereby increasing the levels of these neurotransmitters in the synaptic gap.

121
Q

what are the 3 monoamine neurotransmitters in the biochemical explanation for depression?

A

noradrenaline (NA)

serotonin (5-HT)

dopamine (DA)

122
Q

how does serotonin contribute/reduce the implications of depression?

A

Serotonin regulates NA activity, so too little allows abnormal fluctuations in NA (permissive amine hypothesis)

123
Q

how does noradrenaline contribute/reduce the implications of depression?

A

Too little leads to depression, too much to mania (catecholamine hypothesis)

124
Q

how does dopamine contribute/reduce the implications of depression?

A

Involved in reinforcement, so too little results in anhedonia (dopamine hypothesis)

125
Q

(AO3) evaluation of the biochemical (monamine hypothesis) explanation for depression

A

(S) supporting evidence anti-depressants are effective as they are supported by evidence. SSRI (Specific Serotonin Reuptake Inhibitors) work primarily on serotonin reuptake. They work to reduce the amont that is taken up by the pre-synaptic neuron’s serotonin transporters (SERT) and increase the amount of serotonin in the synapse. this alleviates symptoms of depression like low mood. This can be supported by Haase and Brown’s research review in 2015. They conducted a review and concluded that as SSRI’s do help to alleviate depression by preventing serotonin from being taken back up into the presynaptic neuron, it follows that low levels of serotonin cause depression.

(W) contradictory evidence Claridge and Davis (2003) report that experimental monoamine depletion studies - where participants are given drugs that reduce levels of 5-HT and noradrenaline - do not cause depression in healthy volunteers with no depressive illness.

Nor does it worsen symptoms in depressed patients not taking medication (Delgado, 2000).

(W) evidence is insufficient Haase and Brown only prove the efficiency of SSRI’s. there appears to be limited evidence on the other explanations in the monoamine hypothesis.

(W) hormones it is possible that a different biological explanation accounts for depression better. it may be understood that the nervous system is related to stress and includes an increase in cortisol. this goes against the monoamine hypothesis.

126
Q

(AO3) evaluation of the biological treatments (anti-depressants) for depression

A

(S) time biological treatments like antidepressants do not take a long time to work. they take around a few weeks to work and treatment continues for a period of months or years, depending on the severity of the patient’s depression. this is a strength because it is time effective and easy to take; therefore, it may be preferrable.

(S) effectiveness anti-depressants are effective as they are supported by evidence. SSRI (Specific Serotonin Reuptake Inhibitors) work primarily on serotonin reuptake. They work to reduce the amont that is taken up by the pre-synaptic neuron’s serotonin transporters (SERT) and increase the amount of serotonin in the synapse. this alleviates symptoms of depression like low mood. This can be supported by Haase and Brown’s research review in 2015. They conducted a review and concluded that as SSRI’s do help to alleviate depression by preventing serotonin from being taken back up into the presynaptic neuron, it follows that low levels of serotonin cause depression.

**(W) a weakness may be that drug treatment has low acceptability. Caproino & Karver (2013) asked adolescent girls to rate treatments for depression on their acceptability. They found that teenage girls would prefer psychotherapy over drug treatment because it was deemed more acceptable than drug treatment on its own.

(W) side effects antidepressants have a variety of side effects. these range across each anti-depressant but side effects of typical antidepressants include: nausea, fatigue, weight gain, blurred vision, dry mouth. This is a disadvantage of using biological treatments because it is uncomfortable for the individual.

127
Q

what is the cognitive expanation for depression?

A

The Cognitive explanation of depression suggests that the negative, pessimistic thinking found in depressed individuals is the underlying cause of their symptoms and low mood, not just a symptom.

Aaron Beck (1967, 1976) suggested that depressed people have negative schemas; patterns or clusters of ‘Core beliefs’ about how the world works. This leads a Cognitive Triad of negative beliefs about the self, world and the future, which are maintained and fueled by cognitive biases and distortions that change their perceptions and interpretations of events.
This negative pattern of thinking results in a low mood and low self- esteem

the cognitive triad (a triangle)

1) negative views about the world
(e.g. everyone hates me because i’m worthless)

2) negative views about the future
(e.g. i’ll never be good at anything because everyone hates me)

3) negative views about oneself
(e.g. i am worthless)

128
Q

negative schema (cognitive explanation for depression)

A

these are clusters of pessimistic core beliefs - ideas about the world and how it works that develop during childhood as a result of early trauma and unhappy experiences, such as bullying or critical parents/teachers.
These core beliefs lead to rigid, perfectionist goals, rules and assumptions such as ‘I must be perfect in everything I do’; ‘If I make mistakes, then people will think I am worthless’.

129
Q

negative automatic thoughts (cognitive explanation for depression)

A

these self-critical thoughts are like an ‘internal dialogue’ of negative statements about the self, world and future come from the person’s core beliefs about themselves, the world, other people and relationships. Example might be ‘I’m unlovable’…’no-one could ever love me’, ‘I’m a bad person for feeling like this’.

130
Q

the cognitive triad (cognitive explanation for depression)

A

is what Beck called the pattern of negative thinking about the self, world and future, that triggers depression (see diagram, left).

131
Q

cognitive distortions (cognitive explanation for depression)

A

these are systematic errors in reasoning that lead to faulty assumptions and misconceptions - “logical errors” that distort objective reality. Events are interpreted with a negative bias that supports the underlying negative core beliefs. Examples of cognitive distortions are selective abstraction, magnification/minimisation, personalisation and overgeneralisation.

132
Q

(AO3) evaluating the cognitive approach to explaining unipolar depression

A

**(S) supporting evidence: D’Allessandro (2002) found that students’ negative views about their futures were strongly associated with an increase in depressed mood. Those with dysfunctional beliefs about themselves who did not get into their first choice of college then doubted their futures and developed symptoms of depression; this is consistent with the application of cognitive distortion linking to a negative belief about the future. This aligns with Beck’s cognitive triad that negative patterns of thinking triangulate an individual’s life and lead to automative negative thoughts, which are a cognitive symptom of depression.

(S) the cognitive model is not reductionist the cognitive model takes into account genes, family history and childhood and patterns of learning. This is important as it highlights the developmental issues that may contribute to negative thought processes. This can be supported by Noelen-Hoeskma et al (1992) found that children who had a habitual negative thinking style were more likely than a comparison group to develop depressive symptoms when affected by stressful
life events. Therefore, the cognitive approach is not reductionist and accounts for a variety of factors.

(W) there is a difficulty to distinguish between thinking which causes depression and thinking that is caused by depression. It is impossible to determine this; therefore, there is a sense of ambiguity within the cognitive approach as you cannot certainly pinpoint the cause of negative thoughts.

(W) contradictory evidence / inconsistency A longitudinal study by Lewinsohn et al (1981)
found no evidence that negative thinking or a
pessimistic bias preceded the onset of
depressed symptoms. this suggests that there is no relationship between negative thinking and the onset of depressed symptoms, which devalues Beck’s cognitive triad.

133
Q

how does cognitive therapy/CBT aim to treat depression?

A

Cognitive approaches to psychotherapy attempt to change the faulty, negative thinking that causes the low mood and self-esteem and lack of motivation found in people with depression. The aim is to challenge and replace irrational thinking and replace it with rational thinking, which leads to a healthier more positive response to experiences, leading to an improvement in mood and motivation.

134
Q

summarise the procedure of a CBT programme for treating depression

A

Typically a programme of CBT lasts for 6-8 sessions of 50 minutes. The first begins with contracting (agreeing to participate in the programme of 6 sessions) and setting boundaries (e.g. privacy and confidentiality). At first the client will talk about themselves so that the therapist can understand their frame of reference. A range of techniques may be used, including the downward arrow technique, which involves ‘drilling down’ from the automatic thoughts of a patient, to find their underlying core beliefs. These can then be disputed and homework tasks may involve identifying faulty thinking and finding evidence to challenge negative core beliefs.

135
Q

what are core beliefs in the cognitive approach towards treatment for depression?

A

deeply held beliefs that form schemas about the self, world and others. These develop in response to childhood experiences. E.g. ‘I am unlovable’.

136
Q

what are negative automatic thoughts in the cognitive approach towards treatment for depression?

A

sometimes called ‘hot thoughts’ these are the immediate, emotionally laden thoughts that the client has when in triggering situations, such as something going wrong, a failure or perceived rejection, a difficult social situation. They are usually accompanied by physical sensations and accompanying behaviours, such as feeling sick and an urge to get up and leave.

137
Q

what is frame of reference in the cognitive approach towards treatment for depression?

A

This is the way a particular client sees things, what their words mean to them.

138
Q

what is the downward arrow technique in the cognitive approach towards treatment for depression?

A

A method of asking the client questions to find their underlying core beliefs. If the client is upset about something that has happened that week and says they messed up and it was a disaster! The therapist would ask “If that were true, why would it be a problem? What would it mean about you?”. Drilling down, is continuing to use this technique until underlying core beliefs are revealed .

139
Q

(AO3) evaluation of cognitive treatments/CBT for depression

A

(S) supportive evidence on its effectiveness Kuyken et al. (2008), compared the effectiveness of anti-depressants and a Mindfulness-based CBT (MCBT) They found that MCBT was at least as effective in treating depression as medication such as Prozac, even in the long term. MCBT was found to be better at preventing relapse, in comparison to antidepressants alone, and offered a more effective change in quality of life and was more cost-effective.

(S) accessible and relatively cheap CBT is backed by government funding in the UK, because it is fairly quick to show results and relatively cheap to provide.

(W) many of the data about the effectiveness of CBT comes from self-report data. This is a problem because it may lack validity. The client may want to please the therapist and display demand characteristics or unreliable data to show that the therapy is working in order to appease them.

(W) contradictory evidence CBT is not effective enough as a stand alone treatment. It should be combined with drug treatment therapy to obtain the best results for the patient. Chan et al. (2006) found that drug therapy could be useful as an addition to CBT and a combination was more effective than just using CBT.

140
Q

what are the HCPC guidelines for clinical psychologists?

A

‘Practitioners’ are psychologists who work directly with clients, assessing and changing their behaviour. Areas of professional practice in psychology are: clinical, forensic, health, educational, sports and occupational psychology.

In order to work under one of these titles, a psychologist must be suitably qualified and registered with the Health and Care Professions Council. Anyone who called themselves e.g. a clinical psychologist, counselling psychologist but who is not licenced by the HCPC is committing a criminal offence. Registered practitioners must renew their registration regularly, and keep to a strict code of conduct. If they act unprofessionally, they may be disciplined by the HCPC. If found guilty, they could be required to retrain, or be suspended or barred from practice.

141
Q

in relation to the HCPC guidelines, what is practice referring to?

A

the use of specialised knowledge in the workplace. In psychology, it generally means using psychology to assess or deliberately change people’s behaviour, as opposed to doing research studies or developing theory (although practitioners may also be doing these things).

142
Q

in relation to the HCPC guidelines, what is fitness to practise referring to?

A

having the appropriate skills, knowledge, character, and health to be able to fulfil the professional role. A profession who never updated their training would not be maintaining their fitness to practise.

143
Q

in relation to the HCPC guidelines, what is professional boundaries referring to?

A

the lines between what is and is not permissible when working in a professional role with clients. This covers both legal boundaries (i.e. a professional is not supposed to break the law) but also the lines between e.g. work and friendship. For example, a clinical psychologist who started a romantic relationship with a client would be breaking professional boundaries.

144
Q

what are the HCPC code of practice (guidelines) for psychologists?

A

1) be able to practise safely and effectively within their scope of practice.

2) be able to practise within the legal and ethical boundaries of their profession.

3) be able to maintain fitness to practise.

4) be able to practise as an autonomous
professional, exercising their own professional judgement

5) be aware of the impact of culture, equality and diversity on practice

6) be able to practise in a non-discriminatory manner

7) understand the importance of and be able to maintain confidentiality

8) be able to communicate effectively

9) be able to work appropriately with others

10) be able to maintain records appropriately

11) be able to reflect on and review practice

12) be able to assure the quality of their practice

13) understand the key concepts of the knowledge base relevant to their profession

14) be able to draw on appropriate knowledge and skills to inform practice

15) understand the need to establish and maintain a safe practice environment

145
Q
A
146
Q
A
147
Q
A