3/1/2012

A2 EDEXCEL PSYCHOLOGY

UNIT 3: CLINICAL PSYCHOLOGY

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3.1

Clinical psychology
An introduction to clinical psychology

What is clinical psychology?

Clinical psychology is about the study of mental health and mental disorders. This application of psychology focuses on diagnosing, explaining and treating mental illness. As part of this course, areas of clinical psychology which you will cover include methods of mental disorder diagnosis (and the reliability and validity of such diagnosis tools) and definitions of what it means to be abnormal. For this module, you are also required to study two mental disorders. One of these disorders must be schizophrenia, and you are presented with a list of options for the second choice. For both of your disorders, you must learn the key features and symptoms of the disorder, how it is diagnoses, two explanations from different AS approaches and two treatments.

Course outline: clinical psychology

This unit is separated out into the following sections. Tick the boxes as you go through them Methodology Primary data and secondary data: methods used to collect primary and secondary data, and strengths and weaknesses of each type of data Features of reliability and validity Research methods into studying schizophrenia (your course specifies interviewing and twin studies) Content What is clinical psychology? Describe and evaluate two definitions of abnormality: the statistical and social norms definitions Use at least one other definition of abnormality, in brief, to evaluate the other two definitions Describe the DSM as a mental diagnosis tool, and with the use of studies for support and evaluation identify issues of reliability, issues of validity and issues of culture with regards to diagnoses with the DSM Discuss two mental disorders, including schizophrenia and one other disorder from: unipolar depression, bipolar depression, phobia, obsessive-compulsive disorders, anorexia nervosa and bulimia nervosa For schizophrenia, you must be able to: Describe key features and symptoms of schizophrenia Explain and evaluate two explanations for schizophrenia, including a biological explanation and one other explanation from a different AS approach Describe and evaluate two treatments for schizophrenia from two different AS approaches For your other chosen disorder from the above list, you must be able to: Describe key features and symptoms of your chosen disorder Explain and evaluate two explanations from any two AS approaches for your chosen disorder Describe and evaluate two treatments from any two AS approaches for your chosen disorder Describe and evaluate five other treatments for mental illness (one from each of the five AS approaches) Studies in detail You must be able to describe and evaluate three studies: Rosenhan (1973), a study on being sane in insane places any one study into schizophrenia, from Gottesman and Shields (1966) and Goldstein (1988) any one study of your choice into your other chosen mental disorder Key Issue Describe one key issue from the following and conduct a practical which covers the key issue: the issue of understanding mental disorder (focusing on one of your chosen disorders) the issue of caring for someone at home who suffers from a mental disorder the issue of the portrayal of mental illness in the media

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3.2

Definitions of abnormality
The statistical and social norms definitions of abnormality

Normality and abnormality

It has been hard to describe exactly what is meant by abnormal for a number of reasons. First of all, there is no clear definition of what is normal making it difficult to identify what is not normal. Also, there is no one shared characteristic between everything that is described as abnormal, making it difficult to operationalise. Different cultures also interpret behaviours differently, so whereas Westernised countries may see something as abnormal, others may see this as perfectly normal, but you will come across cultural issues later on. Therefore, there are a range of definitions of abnormality used by different psychologists. There are two discussed in detail as part of this application, and two others (abnormality as dysfunction and distress and deviation from ideal mental health) may also be looked at for evaluative purposes.

Deviation from statistical norms

Under this definition of abnormality, a persons trait, thinking or behaviour is classified as abnormal if it is rare or statistically infrequent. What is regarded as statistically unusual all depends on normal distribution. A distribution curve can be drawn to show what proportions of people share the traits, characteristics or behaviours in question. The graph shows the distribution of IQ scores. 34.1% of people either side of the mean score (100 in this case) lie within 1 standard deviation of that mean, either higher or lower, and 13.6% of the population either side of that sit within 2 standard deviations. Anything further than two standard deviations is said to be statistically infrequent.

frequency

34.1% 0.1% -3SD 2.1% 13.6% -2SD -1SD

34.1% 2.1% 13.6% 0.1%

mean

+1SD

+2SD

+3SD

Therefore, a very small subset of the population (2.2% in total) have an IQ which is more than two standard deviations from the statistical norm, and are said to have an abnormally low IQ (this means less than 70). Similarly, anyone with an IQ above 130 is said to have an abnormal IQ score, and these people site within the 2.2% above 2 standard deviations from the mean. Normal distributions are calculated by mathematicians based on formulae which are designed to give standard distributions. A normal distribution curve has 95.4% of scores either side of the mean which are within two standard deviations, and since this is a high percentage, it is considered statistically frequent. The more a person deviates from that mean, the more they are considered to be abnormal, although anyone within that centre 95.4% is considered t be normal. Anyone outside that percentage group is considered to be abnormal, approximately 2.2% at either end. The statistical definition gives a quantitative measure which is objective, and is more likely to be reliable because the scores come from tests or studies which can be repeated Some measures of abnormality under this definition highlight a lack of normal functioning and therefore this is a scientific measure of whether or not someone is entitled to assistance, support and funding What is considered abnormal from a statistical sense may actually not be undesirable, for example people within the top 2.2% of the population with high IQs (above 130) are considered abnormal, but this is actually seen as a good trait and they are not treated as though they have mental health disorders Single cut-off points present difficulties, for example, saying that anyone with an IQ below 70 is abnormal makes it difficult to justify someone having an IQ of 69 being abnormal and then someone else of 70 being normal Abnormal behaviour itself is not actually rare, most people are likely to show atypical behaviour at some point in their lives, and mental disorders such as depression are actually very statistically common, so may not be as valid

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Deviation from social norms

The deviation from social norms definition of abnormality suggests that all behaviour which is socially unusual is abnormal. Behaviour should conform to social norms in order to be considered normal. These norms are social rules that people abide by, and are more often than not specific to one culture. There are a number of influences on social norms that need to be taken into account when considering the social norms definition: different cultures and subcultures are going to have different social norms culture for example, hearing voices in one culture may be seen as abnormal behaviour and signs of mental illness, whereas in other cultures it may be a sign of being connected with spirits at any one time, a type of behaviour might be considered normal whereas another time the same behaviour could be abnormal, depending on both context and situation context and situation for example, wearing a chicken suit in the street for a charity event would seem normal, but wearing a chicken suit for everyday activities such as shopping or going to church, it would be socially abnormal time must also be taken into account, as what is considered abnormal at one time in one culture may be normal another time, even in the same culture for example, one hundred years ago, pregnancy outside of marriage was considered a sign of mental illness and some women were institutionalised, whereas now this is not the case different people can behave in the same way and for some will be normal and others abnormal, depending on age and gender (and sometimes other factors) for example, a man wearing a dress and high heels may be considered socially abnormal as society would not expect it, whereas this is expected of women

historical context

age and gender

Behaviour which goes against social norms may be incomprehensible to others, and it can make others feel threatened and uncomfortable, or at the least surprised and confused. What this definition states is abnormal matches with what society normally means when it uses the term abnormal as we normally mean odd behaviour, so traits such as having high IQs are not considered abnormal by this definition This definition helps to explain why different cultures have different ideas about what is normal, and the definition itself takes into account that there is no universal rule about what abnormality is When culture, context, situation, historical context, age and gender have to be taken into account for a proper understanding of abnormality, it makes it difficult to have a reliable idea of what is abnormal, so diagnosis using this definition is difficult Some people might be mentally ill, perhaps suffering from extreme anxiety disorders, but not breaking any social norms and therefore would not be considered abnormal and ill by this definition Criminals, for example, break social norms, and are seldom considered mentally ill

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3.3

DSM
The Diagnostic and Statistical Manual [of Mental Disorder] and an evaluation of the DSM

Diagnostic classification systems

There is no one manual for diagnosing mental illness. There are two classification systems which are most widely-used in western cultures: the APAs (American Psychiatric Association) Diagnostic and Statistical Manual of Mental Disorder (known as the DSM) which is the most commonly-used manual, and is now in its fourth edition, the latest being the text-revised version, called DSM IV-TR the WHOs (World Health Organisation) International Statistical Classification of Diseases and Related Health Problems (known as the ICD), which is similar to the DSM although not quite as widely-used, but it shares the same sort of strengths and weakness the ICD is now in its tenth edition, ICD-10 The DSM provides criteria from which mental health disorders can be diagnosed. The content of the DSM has changed significantly since the publication of DSM-I in 1952, and there are to be many more updates and amendments in the upcoming fifth version, DSM-5 (previously DSM-V) which is due to be published May 2013. With each new version of the DSM, definitions have become more precise (for example, by including the duration of symptoms needed for a diagnosis), and also changed have been made in line with changing social norms (for example, homosexuality in DSM-I and DSM-II was considered a mental illness). New disorders are also outlined in each edition.

The multi-axial system

The DSM is used as a diagnostic manual, and the DSMs system of diagnosis uses a five-axes model. Each axis measures a different aspect in relation to the disorder. Axes 1-3 are compulsory, whereas axes 4 and 5 are optional, although are usually included as well for a more reliable diagnosis. Having multiple axes allows a patient to be assessed by more than one criterion, so a patient is put into a category on each axis using their symptoms and a diagnosis can be made from this. Axis I measures the clinical disorder, this gives the major diagnostic category arrived at by the diagnostician, so disorders such as schizophrenia, depression, bulimia , sleep disorders, etc would be described under this axis (axis I will also include anything which requires immediate intervention, such as history of sexual abuse or stress-related physical symptoms which need quick attention) Axis II measures personality disorders and mental retardation (based on a ratings scale), and these chronic conditions often go alongside the axis I disorders, and help understand these disorders these are clinical syndromes that are a permanent part of the patient and may affect treatment, such as OCR or paranoid personality disorder Axis III assesses general medical conditions, these are physical problems that are of relevance to the condition or treatment for example, if the patient has diabetes, this could contraindicate the use of certain drugs and these conditions may contribute to the patients ability to cope and their self-image Axis IV measures psychosocial and environmental problems (life problems that influence the psychological wellbeing of the patient) examples include homelessness, family issues and unemployment Axis V gives a score for the global assessment of functioning, whereby a score from 1 to 100 is used to classify the patient based on an evaluation of how well the individual functions socially, occupationally and psychologically where a score of 1 means severe danger of harm to self or others and 100 shows the individual has superior functioning in a wide range of activities (generally, a score of 50 or below indicates severe symptoms)

Strengths and weaknesses of the DSM

The main strength of the DSM is that it is in such wide use and is commonly agreed upon. This allows for a common and universal diagnosis. Through its many revisions, the DSM has stood the test of time. Having a diagnostic companion such as the DSM or ICD allows, theoretically, for two doctors to make the same diagnosis on the same patient if the symptoms are the same, a more agreeable diagnosis is likely using the DSM. However, some criticise the DSM because it serves as confirmation that sufferers of these conditions are sufferers who need treatment, although some suggest mental illness is often just another way of living, whos to say theyre actually suffering a mental disorder? Laing (1960) suggested that schizophrenia is just another way of living and not a condition.

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3.4

Issues of reliability, validity and culture with diagnosis

Evaluating the DSM with regards to reliability and validity, and culture affecting diagnosis

Reliability and validity in clinical psychology

To be reliable as a diagnostic classification system, there would have to be consistency with the DSM. This means that the DSM is reliable if the clinicians using it consistently arrive at the same diagnoses as each other. The term inter-rater reliability is used to describe the extent to which different clinicians agree on the same diagnosis for the same patient. Traditionally, reliability is calculated mathematically, often using a measure known as positive predictive value (PPV). The PPV of a disorder shows the reliability, taking the example of depression, of the DSM with that disorder; so if depression had a PPV value of 80, this means that 80% of diagnosed depression patients will have the same subsequent diagnosis when re-assessed. However, there may also be a cultural element to reliability, for example with Cooper et al. (1972) who showed the same patient interview tapes to various American and British psychiatrists, and American clinicians diagnosed schizophrenia twice as often as the British, and the British clinicians diagnosed depression twice as often as the American. Validity is the extent to which a measure of a psychological variable measures what it sets out to measure. Essentially this means the correct variable (in clinical psychology, this variable will be a mental disorder) is measured, by arriving at the correct diagnosis. Needless to say, if the DSM were not reliable, it would not be valid either. This is because if it is unreliable it means inconsistent diagnoses are made, and so it must not be valid either as surely the correct diagnosis is being made. construct validity refers to whether or not a classified disorder is actually a good indicator of what youre really trying to measure, for example, in operationalising (see below) a disorder such as depression by drawing a list of symptoms and features, you begin to lose some understanding of the real nature of the disorder so the DSM becomes invalid concurrent validity is when the results of a study matches the result of another study done at the same time, so this would mean that if a diagnosis made using the DSM arrives at the same mental disorder that another diagnosis has, it is likely to have concurrent validity predictive validity, on the other hand, is when the results of a test or study match the result of another done at a different time, so instead of looking at two diagnoses to see if they back each other up, the comparison is made over two different time periods, for example the DSM could be used for a diagnosis, then some time later another measure (perhaps a doctors view or observations by mental health personnel) would agree with the diagnosis to be valid convergent validity is when a test result converges (gets close to) the result of another test measuring the same thing a correlational test would be carried out to see the convergence (the difference between convergent validity and concurrent/predictive is that convergent validity must be measuring the same thing, it can be different measures in concurrent and predictive validity)

Operationalising mental disorders

Mental health disorders need to be operationalised is they are to be definable within the DSM. This would mean arriving at lists of symptoms and behaviours to make the disorder measurable. It has been argued, however, that in operationalising a concept such as depression, something is lost from the understanding of the nature of the whole experience of depression, which means that the DSM is not a valid tool in that is lacks construct validity, in that the constructs which are drawn up may not actually be sufficient to represent the disorder. A further possible problem with validity and the DSM is that although taking into account axes IV and V in the later versions of the DSM (personal and social factors and how well the patient is functioning in society), taking such factors into account when diagnosing can actually lead to an invalid diagnosis. For example, someone diagnosed with depression may not be functioning well in society at all, but this might not be due to their diagnosed disorder but actually for another reason, possibly unemployment (for example), and so such a diagnosis would not be valid. It has also been argued that since there has been significant change in the content of the DSM with regards to categorising certain disorders that the manual is invalid. For example, homosexuality and epilepsy have both been considered mental disorders and been included in the DSM at one stage, but are no longer, which might suggest that the DSM has low validity.

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Studies evaluating the DSM in terms of reliability

The course requires that you know studies to evaluate the use of the DSM as a classification system in terms of reliability and validity. Outlined here are three studies supporting the DSM in terms of reliability, and one criticising the DSM.

Goldstein (1988)
[For the full study by Goldstein, see 3.9 Goldstein (1988) in this section] Goldstein tested the DSM for reliability using the at-the-time current version, DSM-III. One of the aims of her study was to test the DSM-III, comparing the results of the re-diagnoses of 199 patients who had been originally diagnosed with schizophrenia using DSM-II. Experts carried out a re-diagnosis of a random sample of eight patients using a single-blind technique (not allowing the experts to know the hypothesis, so their answers are not biased, whereas Goldstein herself was aware of the hypothesis). She found that 169 of the 199 patients diagnosed according to DSM-II as having some form of schizophrenia met the DSM-III criteria too, so reliability was seen as good with the DSM. Of the patients assessed by the clinical experts as well, she found high levels of inter-rater reliability.

Brown et al. (2001)

In 2001, Brown et al. studied anxiety and mood disorders in 362 outpatients in Boston, to test reliability of the DSM-IV and patients underwent two independent interviews using anxiety disorder interview schedules for DSM-IV, known as the life-time version. Brown found good-to-excellent reliability for most of the DSM-IV categories (most of the disagreements tended not be on what the symptoms were, but simply if there were enough of them). However, they found some boundary problems with certain disorders, which made it hard to diagnose patients with disorders if they were at boundary level. Overall, the study highlights some problems with the DSM but generally proves it to be a reliable tool.

Stinchfield (2003)
Stinchfield studied both reliability and validity by looking at the diagnosis of pathological (behaviour which is considered abnormal due to its extreme or excessive nature) gambling. 803 people were studied from the general population, and 259 people on a gambling treatment programme, all from Minnesota, and they were assessed using a questionnaire of 19 items used to measure the DSM-IV diagnostic criteria for pathological gambling. The DSM criteria were used to sort those linked to pathological gambling and those who were not. There were other validity measures as well. It was found that the DSM-IV criteria were both reliable and valid.

Kirk and Kutchins (1992)

In a review paper, Kirk and Kutchins argued that methodological problems with studies conducted to test the reliability of the DSM up until 1992 had limited the generalisability of their findings. For example, they argued that there had been insufficient training and supervision of interviewers, and studies tended to take place in specialised research settings, and so could lack validity as well as reliability. Assessment of Kirk and Kutchins points Due to the specialised settings the findings may not be valid as they may not relate to the conclusions of real clinicians Their review paper was published in 1992, before the studies of Brown and Stinchfield, who showed the DSM-III and DSM-IV to be reliable, so it is suggested that reliability of the DSM has improved since then The accuracy of their criticisms is debatable, as the above three studies all found the DSM to be a reliable tool Some of the points about interviewing such as that different interviewers may affect the situation and lead to different data might be important, when considering generalising findings from studies; Goldstein, however, did not use interviewing to test reliability, she used re-diagnosis using secondary data and still found reliability Another study you could use for evaluation is Nicholls et al. (2000), which showed that using the DSM-IV there was not good inter-rater reliability for the diagnosis of eating disorders in children.

Studies evaluating the DSM in terms of validity

The studies on the following page have evaluated the use of the DSM in terms of validity. It is recommended that you learn at least two studies from this selection.

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In order to be valid, the diagnoses must identify a distinct condition that has different symptoms from other conditions and that is likely to progress in a certain way and respond to one treatment over another. A valid diagnosis for a mental disorder is more difficult than for a physical disorder because of a lack of objective physical signs. To be valid, the DSM also has to be reliable.

Kim-Cohen et al. (2005)

In 2005, Kim-Cohen et al. undertook a longitudinal study of conduct disorder in five year olds, to test the concurrent, convergent and predictive validity of the DSM-IV. There were 2,232 children involved in another, existing, longitudinal study which was used as a focus. The childrens mothers were interviewed and teachers received postal questionnaires asking about conduct disorder symptoms over the previous six months. They found that 6% were diagnosed as having conduct disorder (displaying three or more symptoms), and 2% of the children with severe conduct disorder (five or more symptoms). Children diagnosed with conduct disorder were more likely to describe themselves are having antisocial behaviours than comparison children. Also, during observational assessments these children were more likely to behave disruptively. Different measures were said to show the diagnoses had validity, as different data sources were used to check validity.

Hoffmann (2002)
Hoffmann studied prison inmates to look at diagnoses of alcohol abuse, alcohol dependency and cocaine dependency, to see if differences would occur in a computer-prompted structured interview, compared to the DSM-IV-TR criteria. It was found that the DSM-IV-TR diagnosis was valid and that the interview data supported the idea that dependence was more a severe syndrome than abuse. The symptoms from the automated interview matched those of the DSM criteria.

Lee (2006)
Lee studied the DSM-IV-TR diagnosis of ADHD to see if it would be suitable for Korean children, and looked at gender differences in the features of ADHD in the DSM. The DSM lists eighteen criteria for ADHD linked to childrens behaviour. In total, 48 primary school teachers rated the behaviour of 1,663 children (904 of which were boys, the remaining girls) using a questionnaire. Lee looked for concurrent validity by comparing the DSM-IV-TR criteria with criteria arising from the questionnaire, and compared DSM behavioural and psychological characteristics with those found in an ADHD test. Previous studies had showed that ADHD children had oppositional deficit disorder, ODD, as well, having problems with peers and discipline. Lee decided that finding the same correlation would support the diagnosis and show the DSM to be a valid tool. The same relationship was observed, and so it was said that the DSM-IV-TR had concurrent validity. Also found it to be reliable, as the correlation could check for similar diagnoses. However, the study found that for girls, the DSM-IV-TR symptoms and diagnoses were less compatible than they were for boys, which was a weakness found with the DSM as a diagnostic tool.

Culture affecting diagnosis

Whilst all of these above studies show the DSM to be a reliable and valid tool, the area it receives most criticism is in its usefulness across different cultures. There are two schools of thought, outlined below: Culture doesnt affect diagnosis: mental disorders are scientific The DSM was developed in the USA and is used widely across many other cultures this is a valid use if mental disorders are clearly defined with specific features and symptoms In other words, this school of thought suggests mental disorders are scientifically defined illnesses that are explained in a scientific way and therefore culture does not affect diagnosis as it should be the same cross-culturally The study of Lee (2006) can be used to support this, as the DSM-IV-TR was used deliberately in a non-western culture to see if ADHD diagnoses were valid in Korea Culture does affect diagnosis: a spiritual model There have been studies which have shown that culture can affect diagnosis, for example, hearing voices in western cultures is normally an abnormal sign of, for example, schizophrenia, whereas in other countries this may be seen as a positive characteristic, such as a sign of being connected to spirits Depending on cultural interpretations of what is being measured, the DSM is not always shown to be valid

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Cultural differences in the symptoms of schizophrenia You are required to know how culture affects the symptoms of schizophrenia, the required mental disorder you should know about for your course. It has been reported that catatonic schizophrenia (see 3.5 Schizophrenia) is on the decline, and this could be because of health measures that prevent the development of this type of schizophrenia. Auditory hallucinations were reported to doctors by patients more in Mexican-born Americans than in non-Mexican-born Americans. Burnham et al. (1987) looked at this using self-reports and interviewing, and checked the evidence and found that there was a difference. No other explanation could be found except that culture had led to the difference. White Americans were reported, using patients records, as showing more grandiosity as a symptom compared with Americans of Mexican origin, again showing cultural differences. However, it should be noted that schizophrenia in all countries has more similarities than differences.

Culture-bound syndromes
A culture-bound syndrome (CBS) is a disorder which is isolated to one culture, usually only diagnoses exclusively in one region or country. Psychiatrists tend to reject culture-bound syndromes, although some are listed in the DSM-IV. Two examples of culture-bound syndrome are described below: one example is hikikomori (literally meaning to be pulled away and translated to English as complete social withdrawal), a condition which has attracted concern in Japan recently, affecting mainly male teens who are otherwise perfectly healthy. The condition makes them withdraw completely, locking themselves in their rooms sometimes for up to twenty years, in extreme cases leaving only occasionally to commit violent crimes, although must sufferers are not violent, just depressive. The Japanese government have described hikikomori as a social disorder rather than a mental disorder, and say it is representative of the economic downturn the country is going through a second syndrome is amok which comes from the Malay people, first described in the fifteenth century as an understandable reaction to frustration, but now recognised as a mental disorder requiring treatment. Although the disorder has been described elsewhere, it is most often found in Malay males, beginning with depressive brooding and often following violent outbursts using weapons, commonly homicidal. The turn of phrase running amok or running amuck came from this, describing the sensation of rage leading to a killing spree

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3.5

Schizophrenia
Schizophrenia as a mental disorder: symptoms, features, two explanations and two treatments

Your course requires that you study two mental disorders: one being schizophrenia, and the other your choice from a list provided by the board. The latter disorder is covered in the next section, and for this series of notes the chosen disorder is unipolar depression, although other choices are available. This document covers the compulsory disorder, schizophrenia and what you have to know: key features, key symptoms, two explanations and two treatments (both from different approaches to psychology).

Symptoms and features of schizophrenia

Schizophrenia is a chronic mental health condition that causes a range of different psychological symptoms. Common symptoms include: hallucinations hearing and seeing things that do not exist delusions believing things that are not true and so schizophrenia is therefore a psychosis, not a neurosis, as the patient does not realise they have a condition. The exact cause of schizophrenia is unknown as of yet, although there are a number of possible explanations. Two are covered in this unit. The NHS suggests that as many as 1 of every 100 people will suffer at least one episode of acute schizophrenia in their lifetime, although Jablensky (2000) suggested that the disorder is found in about 1.4 to 4.6 people in every one thousand for any nation, on average. Men and women appear equally affected by schizophrenia, although in men it is typically active between the ages of 15 and 30, whereas in women it usually becomes active between 20 and 30. It is commonly thought that schizophrenics have a split personality, acting perfectly normal one minute, and then irrationally the next. However, this is not the case, and though schizophrenia derives from Greek and German words meaning split mind, it is not a split personality disorder. Sufferers are said to suffer episodes of dysfunction, however. Most studies confirm that there is some link between schizophrenia and violence, although the media tends to exaggerate this. In reality, a sufferer is actually more likely to be the victim of violence than the initiator of a violent attack. Experts at the RCP estimate that less than 1% of UK violent crime is committed by schizophrenics. When discussing mental disorders, symptoms are what characterise the disorder, describing ways in which sufferers think, feel and behave. Symptoms of schizophrenia are broken down into positive symptoms and negative symptoms. Positive symptoms are additions or changes to the behaviour of a patient, whereas negative symptoms are removals from the character or personality of the patient: first-rank symptoms include hearing voices and believing that others are guiding you, for example these are positive symptoms such as hallucinations and delusions, they are added to the patients behaviour as they were not there before the disorder became active second-rank symptoms include flattened emotions and other negative symptoms, such as lack of energy, sex drive, etc (so these are all removals from the personality) these often start well before the positive symptoms and any diagnosis, in what is known as the prodromal period
POSITIVE SYMPTOMS delusions firmly held erroneous beliefs due to distortions or exaggerations of reasoning delusions of grandeur one specific type of delusion, where the patient believes they are more powerful than they are hallucinations auditory and visual distortions, the hearing voices can be critical, providing a commentary on what the person is doing, controlling or telling them what to do disorganised thinking/speech or thought disorder this is usually noticed through confusing speech and incoherency grossly disorganised behaviour may include unpredictable agitation, social disinhibition and other bizarre behaviour NEGATIVE SYMPTOMS affective flattening a reduction in range and intensity of emotional expression, including eye contact, voice tone, body language and facial expression alogia (lack of speech) lessening of speech fluency avolition (lack of energy) reduction or difficulty to undertake normal daily tasks (sometimes mistaken for lack of interest apathy) anhedonia (lack of pleasure) inability to experience pleasure from previously-enjoyable activities/experiences, including hobbies, social interaction, exercise and sex social withdrawal avoidance of interaction with others

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The features of a disorder are aspects about how a disorder develops and consider the disorder on a wider scale, often include facts and statistics. The key features of schizophrenia include: schizophrenia appears to be a universal disorder (the condition can affect anyone in any place, males and females) the profile of sufferers seems to be as follows: - of patients will have one episode of schizophrenia and then fully recover - of patients will suffer chronic schizophrenia, having continuous schizophrenic episodes - of patients will have occasional schizophrenic episodes but do not have a chronic disorder positive symptoms (those added to the sufferers being) can be overcome (e.g. hallucinations, delusions), whereas the negative symptoms (those lacking in sufferers) tend to remain male sufferers tend to experience a more severe course of the disorder than females (Goldstein, 1988) there are five categories which psychiatrists and diagnosticians use to describe different types of schizophrenia

Types of schizophrenia
One feature of the disorder is that there are different types. The five types are described below: paranoid schizophrenia is when the patient is suspicious of others (delusions of being watched or followed are common, and thinking that messages in TV and radio programmes or newspapers are aimed directly at them) and common symptoms are delusions of grandeur and hallucinations disorganised schizophrenia is when the patients speech is hard to follow and behaviour may be bizarre, acting with inappropriate moods for certain situations, although there are no delusions or hallucinations catatonic schizophrenia is when the patient becomes very withdrawn and isolated and has little physical movement, they appear to be in a trance-like state, with very little speech or activity residual schizophrenia is when there are low-level positive symptoms but there are psychotic symptoms present undifferentiated schizophrenia is when the patient does not fit any of the four above types

The dopamine hypothesis: a biological explanation

The dopamine hypothesis is a theory that argues a biological explanation of schizophrenia. It suggests that the unusual behaviour and experiences of schizophrenia can be explained by changes in dopamine function in the brain. Dopamine is one of many chemical neurotransmitters which send messages of neuronal synapses. The hypothesis suggests that there are an excess number of dopamine receptors at the post-synaptic membrane (receiving end of the dopamine) of neurones in schizophrenic patients. This is partly based on a number of studies that look at the effects of drugs on dopamine receptors and behaviour. It is also suggested that positive symptoms of schizophrenia might be due to an increase in dopamine in one part of the brain, and negative symptoms due to an increase in another part. Both PET scanning and animal studies have been used to look at excess dopamine receptors.
calcium voltagegated channel Ca
2+

calcium binds to vesicles

One suggestion is that development of receptors in one area of the brain might lead to the inhibition of dopamine synap their development in another area, so explaining why binds to Ca vesicles tic receptors containing 2+ there are different numbers of dopamine receptors in knob dopamine different parts of the brain. There also seems to be links between damage to the prefrontal cortex and schizophrenia. This area finishes developing in adolescence which is when the onset of schizophrenia may be observed. Much support for the dopamine hypothesis comes from drugs studies, in particular those involving amphetamines (speed), which are dopamine agonists and so prevent the breakdown of dopamine, leading to high levels. When amphetamines are given in large quantities, they lead to delusions and hallucinations, similar to those in schizophrenic patients, and symptoms get even worse when given to patients of schizophrenia.

dopamine released into gap

electrical impulse passed on

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The table below shows pieces of evidence for and against the hypothesis. These also serve as an evaluation of the dopamine hypothesis for schizophrenia. Evidence for the dopamine hypothesis Amphetamines give similar symptoms When given amphetamines, which in effect increase the levels of dopamine, delusions and hallucinations are common effects, which suggest that excess dopamine neurotransmitter action produces positive symptoms Schizophrenics are more sensitive to dopamine uptake PET scanning has shown that when given amphetamines, schizophrenics show greater release of dopamine than non-schizophrenics, suggesting those with schizophrenia are more sensitive to excess dopamine Biological factors influence dopamine sensitivity Brain differences have an effect, as the brains of those with schizophrenia seem to be different, such as differences in volume of grey matter, and such changes at an early age are linked with sensitivity to dopamine Blocking dopamine receptors reduces symptoms When given phenothiazines, drugs which block dopamine receptors, the positive symptoms of schizophrenic patients are alleviated, and since less dopamine is being taken up, this seems to support the hypothesis HOWEVER Evidence against the dopamine hypothesis Amphetamines only produce positive symptoms The effects of amphetamines are only those similar to positive symptoms of schizophrenia, which suggests that the dopamine hypothesis is not a completed explanation Other neurotransmitters might be involved Whilst this research shows schizophrenics to be more sensitive to dopamine, other chemicals such as glutamate have been shown to have similar psychotic effects, so perhaps dopamine is not the full explanation Social and environmental factors are also involved It cannot be said that the explanation is exclusively biological, as environmental and social factors seem also to be able to trigger schizophrenia perhaps stressful events trigger excess dopamine production Blocking receptors does not take immediate effect However, it is interesting that whilst a patient who takes anti-schizophrenic drugs has their dopamine receptor blocked immediately, the reduction in positive symptoms is not effective for at least a couple of days

Much of the evidence for the dopamine hypothesis comes from animal studies and PET scanning, but there is also incidental evidence from cases of those on drug treatment for conditions such as Parkinsons disease and the use of recreational drugs on behaviour. All of these research methods give the methodology triangulation which improves validity, another strength of the hypothesis. The methodology can also be said to be reliable, as there have been many repeated studies into dopamine levels and its effects. However, because so many animal studies are used in this evidence, the methodology can be criticised somewhat as the findings of animal research might not always be generalisable to humans. Whilst we are fairly certain schizophrenia is a disorder unique to humans, however, animals share many similarities in terms of nervous systems and biological models, and so the research is most likely appropriate. Another possible weakness of the hypothesis is that it may be something else to do with schizophrenia which causes the difference in levels of dopamine receptors, rather than having too many dopamine receptors results in the development of schizophrenia.

The environmental breeder hypothesis: a social explanation

Statistics show that the majority of schizophrenics in the UK come from lower classes, or from groups such as immigrants. Research suggests that social class is either a cause of schizophrenia, or at least somehow involved in its development, according to a second possible, explanation: the environmental breeder hypothesis. This comes from the social approach. In one meta-analysis of 17 studies, Eaton et al. (1988) showed that statistically there are more lower class schizophrenics and the disorder is more common proportionately in lower classes. Sufferers of a lower class also experience a different course of the illness and are treated differently. It was found that they are more likely to be taken by the police or social services for treatment than those of upper classes, and also more likely to become mandatorily committed or become long-term sufferers. Thus in the 1960s it was thought that being in a lower class was a causal factor of schizophrenia. This was known as the social causation hypothesis, or environmental breeder hypothesis. The ideas of social drift and social adversity offer two social explanations for schizophrenia, which are both outlined on the following page.

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HOWEVER

HOWEVER

HOWEVER

Social drift It has been suggested that sufferers of schizophrenia actually become lower class because of the difficulties that arise from having the disorder. One study took a sample of schizophrenic men and their fathers, and compared their social classes. It was found that the sufferers were all in the lower classes, whereas their fathers typically were not, providing evidence for social selection theory, which suggests just that. The theory argues social class isnt the causal factor but that schizophrenics drift downwards in terms of social class (this is known as social drift). Whilst social selection theory is now widely accepted by most, recently studies have suggested that there are actually environmental and social factors which can cause schizophrenia (or at least are involved in its development). Whilst social disadvantage may not be the main cause of such a disorder, it certainly appears to be a contributing factor to the development of schizophrenia. Social adversity Schizophrenia is certainly more common in urban communities (large towns and cities) rather than rural areas, so it is perhaps something about city life which leads to schizophrenia. In fact, schizophrenia tends to be almost exclusively found in cities, but there are many lower class people in rural places so the social drift hypothesis doesnt seem to fit here. Harrison et al. (2001) suggests being brought up in declining inner-city areas could lead to schizophrenia, as this is where the bulk of sufferers lie. Hjem et al. (2004) showed that social adversity (adverse being the opposite of favourable) in childhood has a correlation link with schizophrenia. The areas identified by Harrison et al. as where clusters of schizophrenics live support Hjems ideas, as the inner-city areas tend to be where the population groups of the lowest socioeconomic class are. It is therefore suggested that city life must have something which leads to development of schizophrenia. The sociogenic hypothesis (contrasting the social selection theory) suggests that it is stress factors which contribute to the disorder developing. These include the stress from poor education, unemployment, low rewards, low income and few opportunities, which have been suggested can lead to the disorder. Below is an evaluation of the environmental breeder hypothesis, suggesting social class is linked to schizophrenia: The ideas support the facts that there are more schizophrenics in inner-city areas and in lower classes, and both the social drift and social adversity ideas explain a possible link between the disorder and class Although not everyone who lives in environmental conditions suggested by these explanations develops schizophrenia, it is still highly likely that there are these environmental triggers (rather than strict causes), it is possible that there is a biological explanation also, which requires some environmental activation for the disorder to develop Since those in a lower socioeconomic group, with no jobs and living alone are more likely to be diagnosed, it suggests maybe a diagnosis problem, not an environmental problem It is hard to separate those factors which might be causing schizophrenia with those that are being caused by schizophrenia, it may be that lower social class, economic status and the lack of a job are all consequences of the disorder, not the other way around, as the social drift hypothesis suggests

Drug therapy: a biological treatment

Whilst there is no cure for schizophrenia, it is considered to be a highly treatable disorder. One treatment comes from the biological approach: drug therapy. Drug treatment, according to the NAMH of the USA, for schizophrenia is comparable to the success rate for drug treatment of heart disease. Drug therapy was an important step forward in the 1950s, allowing the movement of sufferers out of mental institutions by helping them to function normally. One of the biological explanations for schizophrenia suggests that the symptoms, such as hallucinations and delusions, are due to excess levels of dopamine receptors, leading to increased dopamine activity in the brain. Therefore, it only makes sense that drug treatment uses drugs which act to reduce dopamine action by blocking its receptors. For example, drugs such as phenothiazines can be used (e.g. chlorpromazine) which removes excess dopamine by blocking its receptors. This came about from French neurosurgeon Henri Laborit, who tried using anti-histamines to relax his patients before surgery, and when he saw the calming effects chlorpromazine had on his patients, he thought they might be useful in calming schizophrenic patients too. The results was spectacularly successful, and later it was discovered that the reason for this was that chlorpromazine blocked dopamine receptors.

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Drugs which are used to treat schizophrenia are called antipsychotic drugs. They work to suppress hallucinations and delusions, by correcting these chemical imbalances in the brain. Antipsychotic drugs are separated into two categories: typical drugs (which are older, and already well-established these have been in use for a long time) and atypical drugs (which are much more modern and in less use, although they are more experimental they do have fewer side effects, but act differently to typical antipsychotics). Common side effects of antipsychotic drugs include sleepiness and tiredness, shaking and muscle spasms, low blood pressure, problems with sex drive and weight gain. Other symptoms include dry mouth, constipation and blurred vision. A particularly nasty side effect, Tardive Dyskinesia affects older patients on the chemotherapy for schizophrenia, which causes involuntary spasms of the face and other areas of the body. These side effects are seen as a weakness. Meltzer et al. (2004) In 2004, Meltzer et al. conducted a study into the effectiveness of drug treatment for schizophrenia. He used 481 patients randomly assigned into groups, where some were given a placebo, some given a new investigative drug, and others an already established antipsychotic drug (haloperidol). They found that haloperidol and two of the new investigative drugs were effective at reducing the schizophrenics symptoms, more so than the placebo. This was seen as strong evidence that drug treatment works, at least to an extent. Drug therapy for schizophrenia is seen as much more ethical, and certainly more effective, than some of the pre-1950s treatments that there were, including lobotomies which would not be allowed nowadays The treatment is supported by strong evidence (such as Meltzer et al. 2004) and is based on a scientificallysound explanation of the disorder Drug treatment is a fairly easy and quick treatment, the drugs are easily prescribed and all patients have access to it, and it is also far cheaper than a person-based therapy, such as psychodynamic therapy, and so is the NHS therapy of choice for schizophrenia The drugs have many possible side effects which can be a problem, including damaging effects on the central nervous system and synaptic junctions becoming blocked, which are serious issues It is often criticised for only masking the problem, as drug therapy is by no means a cure for the illness, it is just alleviating the symptoms, possibly for the doctors convenience more than anything else? Patients often forget or purposefully stop taking their medication (if the latter, probably because they are worried about the side effects), possibly due to their disorder leading to problems with functioning

Cognitive-behavioural therapy: a cognitive treatment

This is currently the most popular form of psychological therapy for schizophrenia (drug treatment is chemotherapy, not psychotherapy, but drug treatment is the most commonly used), and it comes from the cognitive approach. It provides coping mechanisms, as it does not directly alleviate the symptoms of the disorder themselves. Cognitive-behavioural therapy (CBT) involves accepting the patients view of reality, and using that to help them learn to cope. A full course of cognitive-behavioural therapy lasts over a series of regular sessions, around 50 minutes to an hour in length each, with between five and twenty weeks worth of sessions (usually at one per week). Progress will normally be assessed at this stage of twenty weeks to see if further treatment is needed. An agreed agenda is established with the patient and the therapist tries to uncover their core beliefs (this is very much a person-centred therapy). This means not telling the patient their beliefs are wrong, but suggesting alternative thought patterns. The therapy may help the patient to normalise their experience of the disorder, allowing them to understand that its not just them, and that others have hallucinations and delusions too. The eventual aim is to improve the self-esteem of the patient and to develop their self-concept (getting them to see beyond their disorder, and see their positive features to focus on for example a particular area they are interested in or talented in, which they can build upon). Bradshaw (1998) An example of cognitive-behavioural therapy for schizophrenia in use comes from Bradshaw (1998). The aim was to look at how the therapy was used to treat a woman with schizophrenia (this was a case study), including its effectiveness. Until the time of the patients therapy, drug therapy had been the preferred treatment there was little done of this therapy.

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The patient was Carol, who was educated up until her first year of college. She had a perfectly normal life and seemed otherwise healthy, when during her first year at college she had auditory hallucinations and delusions and felt she was no good. She began acting in a bizarre manner, and was subsequently hospitalised. There had been no family history of psychiatric illness, and Carol was diagnosed with undifferentiated schizophrenia. The therapy began and it took about three months for a rapport to be built up. Self-disclosure was used to promote discussion of difficulties and to help build the rapport. Carol controlled a lot of the treatment: how often they met, how long the sessions were and roughly what they spoke about a common feature of CBT. A further two months were used to get Carol to understand the therapy. The course of the therapy was as follows: the first phase lasted a year and focused on managing stress and anxiety behavioural activities were worked out during the second phase with further stress control training, with another sixteen months of building cognitive strategies to cope with stressful situations finally, an ending phase of around three months where thoughts about the end of the treatment were focused on and plans to maintain the treatment without the therapists input were developed (e.g. strategies written on cue cards) It was shown that there was an improvement of psychosocial functioning after the treatment, as well as improvements in achievement of goals, and a reduction in symptoms and far fewer hospitalisations. Further analyses one year on showed more improvement as Carols social functioning improved yet again. There were considerable improvements in functioning in four measures after the three year course of therapy. It was therefore concluded that cognitivebehavioural therapy can be useful in the treatment of schizophrenia. Below is an evaluation for cognitive-behavioural therapy as a treatment for schizophrenia: There is a wide range of evidence to support the therapy for the disorder, such as Pfammater (2006) who did a meta-analysis finding CBT often reduced positive symptoms; Gould et al. (2004) who found a large reduction in symptoms and fewer dropout rates of drug treatment when patients also had CBT; and a study by NICE (2004) who, backed by government funding, studied courses of CBT finding a reduction overall in positive symptoms and negative symptoms, and concluded it should be made available publically for all schizophrenic sufferers The therapy uses cognitive shaping to develop strategies for stress management which has been shown to be effective in improving the daily lives of schizophrenics as they have new coping mechanisms Turkington et al. (2002) found that CBT was effective in increasing patients insights and awareness of the importance of taking medication, but with insights into themselves, their rates of depression increased, suggesting a link between CBT and depression CBT seems to be mainly effective when used alongside drug treatment, as it does not directly tackle to symptoms of the disorder, so drug treatment is usually required as well as a psychotherapy such as CBT Certain studies have actually shown other personcentred therapies to be more successful than CBT, although the government uses CBT as its therapy of choice for patients, presumably because it is cheaper and has been in use longer, although this may not be the best for patients

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3.6

Unipolar depression
Symptoms and features, two explanations and two treatments of unipolar depression

Symptoms and features of unipolar depression

Also known as clinical depression, or major depressive disorder, unipolar depression is a mood disorder, characterised by varying degrees of sadness, disappointment, loneliness, hopelessness and guilt. It is a relatively common mental health disorder, with an estimated 3.5 million sufferers in the UK. Unipolar disorder should be distinguished from bipolar disorder. Whereas unipolar depression is a mood disorder which is seen as a constant disturbance to mood, bipolar disorder involves fluctuations between moods of manic depression and mania, which is not the case with unipolar depression. Other than the depressive emotions listed above, common symptoms of unipolar depression are lethargy (lack of will or energy), permanent anxiety issues and problems with sleep (including waking early or continually through the night and difficulty getting to sleep). Some of the features of unipolar depression are listed below: Depression is twice as common in women as in men, although men are more likely to commit suicide Different people have different courses of the disorder, some are only affected once, for others it is chronic The peak time for depression is between the ages of 50 and 60, although it typically occurs between 30 and 40 People who suffer any form of depression usually live shorter lives, possibly due to a link between depression and heart disease and other stress-related illnesses There are as many as 3.5 million UK sufferers and 20 million American sufferers of unipolar depression One specific subtype of unipolar depression is postpartum depression, for which there is usually no obvious reason. This is a temporary form of unipolar depression which occurs, almost exclusively in women, but also sometimes in men, where distressed mothers suffer severe mood disorders. This is especially distressing for the mother when they have looked forward to having the baby for months. Feelings include guilt, and feeling unable to cope and as though you are a bad parent. Some women can go weeks or months without seeking treatment, and in some cases, even years! It is a very common disorder affecting as many as 1 in 10 new mothers.

The monoamine hypothesis: a biological explanation

One biological explanation for unipolar depression is the monoamine hypothesis. The monoamines are a group of neurotransmitters which include serotonin, noradrenaline and dopamine. You will recognise the latter, dopamine, from the biological offering of an explanation for schizophrenia. The monoamines are believed to regulate mood. One of the functions of serotonin is to regulate the other neurotransmitters. Without the regulation provided by serotonin, erratic brain functioning and thinking patterns occur. Low levels of serotonin produces low levels of noradrenaline (a neurotransmitter needed for alertness, energy, anxiety and attention to life). Evidence suggests that low levels of noradrenaline cause depression, and high levels cause mania, which suggests it is involved both in unipolar and bipolar depression. Dopamine is also related to feelings of alertness, motivation and attention, and so it is suggested low levels of dopamine similarly are linked to depression. Essentially the monoamine hypothesis suggests that low levels of dopamine and low levels of noradrenaline result in depressive moods, and low levels of serotonin mean low levels of noradrenaline. It can therefore be low levels of dopamine or noradrenaline that result in depression, or a mixture of both. The hypothesis is used to work with drug treatment, so that the correct drugs (antidepressants) can be prescribed based on the particular monoamine in question. In other words, when a clinician is presented with a patient, they will choose the correct drug that alleviates the presented symptoms of depression. Most antidepressants work by increasing levels of serotonin. It cannot be concluded that the explanation for depression is strictly biological. The diathesis-stress model explains how some mental disorders can have a biological underlying cause but require an environmental trigger to become active.

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Studies have indicated that there may be a genetic link for depression. Although the role of genes in depression is an alternative biological explanation, they share some similarities, and the genetic explanation also offers a diathesis-stress model. McGuffin (1996) studied 214 pairs of twins, where at least one of each twin pair was being treated for unipolar depression. It was found that 46% of the identical twins shared the disorder, and only 20% of fraternal non-identical twins shared the disorder. This indicates a genetic link. Whilst genetic makeup may predispose somebody to develop depression, a stressful life event might be needed to act as a trigger for that depression (diathesis-stress). An evaluation for the monoamine hypothesis for depression is shown below: There is much sound evidence to support the theory, particularly in treatment if the hypothesis suggests the symptoms are due to monoamine deficiencies and drugs which replace those monoamines alleviate the symptoms, there is evidence for the hypothesis Further evidence is seen from studies involving monoamine oxidase inhibitor enzymes, which prevent the inhibition of monoamines, so they can function properly which alleviates depression However, it could be argued that some drugs such as opipramol help relieve depression yet do not adjust monoamine imbalances, reducing the validity of the explanation Furthermore, in some studies, levels of monoamines have been deliberately depleted, which does not seem to reproduce the symptoms of depression Much of the research comes from animal studies, and we must take care when generalising from such data

Becks model of depression: a cognitive explanation

A different explanation for unipolar depression comes from the cognitive approach, from Aaron Beck, who is considered the father of cognitive therapy. There are three aspects to Becks cognitive model of depression: the cognitive triad three areas Beck considered suffered negative automatic thoughts the individuals cognitive errors faulty thought patterns and negative or unrealistic tasks the schemata patterns of maladaptive thoughts and beliefs Negative view of the self The cognitive triad The first part of Becks cognitive model of depression is the cognitive triad. This suggests three areas where there are negative automatic thoughts. The thoughts consist of negative views of the self (feeling inadequate and unworthy), negative views of the world (feeling defeated or deprived) and negative views of the future (believing that your suffering will continue). A sufferer of depression tends to think life will always be that way for them, and that nothing can improve: this comes from the future aspect.

Negative view of the world

Negative view of the future

The cognitive errors Cognitive errors mean that an individual gives selective attention to the negative side of a situation, and always ignore the positive aspects. Beck described this as the faulty thought patterns. The downside is overestimated so that the most negative conclusion possible is reached when in a situation. Schemata Schemata are built up through experiences of the world, and involve developing positive and negative beliefs and attitudes to interpret the world. A generalised negative belief pattern makes someone vulnerable to depression. A new situation is interpreted through the use of a persons relevant existing schemata, including a self-schemata (for example, if someone is regularly criticised by their parents, they are going to develop a negative set of beliefs about themselves). The way to overcome depression according to the cognitive model by Beck is to change the maladaptive thought interpretations by considering alternative thoughts and interpretations of events. If evidence is presented that there are other interpretations, an individual can change their cognitions. The likely schemata of a depressed person include: cognitive schemata lead a person to seeing actual or threatened loss affective schemata lead a person to feelings of sadness, loneliness and guilt physiological schemata (biological schemata) lead to feelings of tiredness, lack of energy and activity motivational schemata lead to helplessness and a lack of direction behavioural schemata lead to social withdrawal and inactivity

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The cognitive model is shown in the flow diagram to the right. There is some evidence which supports the cognitive model of depression. Koster et al. (2005) examined the role of attention to negative stimuli in depression. There were 15 depressed students and 15 non-depressed students in the participant sample, and they were each given a selective attention test on a computer screen, where they were presented with positive (e.g. powerful, successful), negative (e.g. loser, failure) and neutral (e.g. paper) words for one and a half seconds each. Half a second after the word disappeared, a square would appear onscreen on either the lefthand or right-hand side, and participants had to press q when it appeared on the left, and p when on the right. The time for them to react and press the right key was measured, and it was found that depressed people took an average of 12ms to disengage from negative words, compared to non-depressed students who only took 2ms. This supports Becks cognitive model as it shows depressed people respond to negative stimuli.

Early experiences and interactions with the real world

Core beliefs

Rules and assumptions (if then)

Trigger

Thoughts

Consequences

Feelings

Behaviour

Strengths of Becks cognitive explanation of depression: Research has shown that depressed people have negative thoughts and that the cognitive model is backed up both by self-report data and other test measures. The model is evidence-based, with many studies supporting Becks ideas, including Ingram (2001) who found that those with adverse childhood experiences had depression later in life, as the model suggests The theory takes into account other aspects, such as genes, development and early experiences and acknowledges that such developmental issues can lead to certain thinking patterns and core beliefs which lead to depression After treatment for depression, patients biased negative thought patterns seem to disappear, which seems to be evidence for the cognitive model for depression Weaknesses of Becks cognitive explanation of depression: Strict evidence that shows negative thinking precisely causes depression is hard to find whilst you could argue that since faulty thinking stops when depression disappears this must be in favour of the model, it might also be seen that perhaps faulty thinking and negative beliefs come with depression, rather than are the cause of depression It is difficult from a methodological point of view to distinguish between thinking which causes depression and thinking that is caused by depression, so objective measure is difficult Some studies, such as Dykman et al. (1991) have not shown the cognitive biases Beck suggests, observing that depressed people do not seem to have a distorted perception of their own abilities, and whilst perhaps still focusing on the negative parts of events, they do in fact understand the events accurately, against what the model suggests

Drug therapy: a biological treatment

Just as with schizophrenia, depression is treatable with the use of drug treatment, from the biological approach. Drug treatment for depression tends to happen in the community: rarely are depressed people hospitalised, unless they are at risk of endangering themselves or others. Antidepressants are used to treat depression, and these drugs usually work by increasing the levels of serotonin in the brain, since some of the symptoms of depression come about due to low levels of serotonin (leading to low levels of noradrenaline). This is how the well-known drug Prozac works, although this is not to say this is strict proof that the monoamine hypothesis is correct, it does provide some sound evidence. Such drugs used to treat depression are called SSRIs (selective serotonin reuptake inhibitors). The SSRIs include drugs like Prozac, and others such as Fluvoxamine and Citalopram, as well as some more modern and less-in-use atypical antidepressants (drugs which target individual monoamines, such as specifically noradrenaline).

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Another group of drug used to treat depression is the MAOIs (monoamine oxidase inhibitors), which work to prevent the breakdown of the monoamines (serotonin, noradrenaline and dopamine), so in effect achieving the same results: increased levels of the monoamines in the brain. As you would expect, no drug treatment comes without its potential side effects. Side effects of the SSRIs include nausea, insomnia, anxiety, dizziness, weight fluctuations, headaches, fatigue and blurred vision, and the MAOIs have more severe side effects and so are only used as a last resort if other drugs dont work; similarly, another group of drugs, the tricyclic antidepressants, are a subtype of SSRIs which are nowadays outdated, and also have more severe side effects. Treatment of depression with antidepressants has to be withdrawn gradually in order to avoid suffering withdrawal symptoms, which develop with what is known as antidepressant discontinuation syndrome and involve crying spells, insomnia, aches and pains and muscle spasms. Kuyken et al. (2008) In this study, Kuyken et al. compared drug treatment and a form of cognitive-behavioural therapy, finding that a group version of CBT was at least as successful as drug therapy. They divided 123 people with depression into two groups: one continued with their medication, and the other had the psychotherapy (with the option to remain on or come off of their drug treatment). Over 8 weeks, the therapy group met and carried out group exercises, such as how to focus on the present and not the past. About 47% of the CBT participants had a relapse rate over the 15 months after the course had ended, whilst those who had drug therapy alone had a relapse rate of 60% and so it was thought that the person-centred therapy gave the patients skills for life that drug therapy could not. This study showed that whilst drug treatment for depression can be effective, it is not as effective as it could be without having another type of therapy used as well. Antidepressants can be used to boost mood so that other therapies, such as CBT, can take place: without drug therapy these other treatments cannot happen Research is constantly undergoing to find more effective drugs with bigger success rates and fewer side effects (atypical antidepressants, for example, have far fewer side effects than the old tricyclic drugs) Drugs are easy, quick and cheap to prescribe and are the favoured treatment for the NHS The use of antidepressants is based on a scientific hypothesis, generally accepted by psychiatrists Although drugs are cheap and quick to prescribe and are readily available, it may be the case sometimes that doctors prescribe them over other treatments for their own convenience, rather than the good of the patient Drugs are often criticised for only masking the problem, they do not cure the disorder A common effect of discontinuation of drugs, especially with antidepressants, is withdrawal symptoms, which can prove troublesome and may need more drugs to treat the withdrawal symptoms, which is not ideal Patients may forget to take their drugs or purposefully choose not to take them to avoid the side effects

Cognitive-behavioural therapy: a cognitive treatment

A therapy from the cognitive approach, actually based around the work of Beck, cognitive-behavioural therapy (CBT) which you may have met from schizophrenia also is a person-centred form of psychotherapy used to work with the patient to try and overcome the symptoms of depression, rather than (or as well as) using chemotherapy. Usually it takes place once a week and consists of at least five-to-twenty sessions, progress is reviewed at around 20 sessions. The therapy works to try and help the patient identify negative and unhelpful thoughts and to try and change them. This may involve drawing diagrams for the patients to try and show them the links between their thinking, behaviour and emotions. The rationale of CBT is that our thoughts affect our feelings and behaviour, and so by changing our thoughts, we can make ourselves feel better. Some forms of CBT also focus directly on changing behaviour. The therapy is collaborative, the therapist and the patient will agree on what the patient wants to change. The therapist may then ask the patient to express their negative belief, for example, in relation to their social life. A depressed patient might believe that there is no point in going out as they wont enjoy it: the therapist will try and respond by convincing them that they should try it and will in fact enjoy going out.

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Stiles et al. (2006) This study looked at cognitive-behavioural therapy and other therapies (one person-centred therapy and psychodynamic therapy) over a three-year period, in 58 NHS settings around the UK. They found that no therapy stood out as being more successful than any of the others, but they were all very effective: there were reductions in relapse rates and improvements according to self-report data. Whilst this study did not show CBT to be any more effective than other psychotherapies, it did prove the therapy to be effective at treating depression. Below is an evaluation for the use of cognitive-behavioural therapy for treating unipolar depression: The individual is helped to recognise any problems and taught how to overcome difficulties, so solutions will be more lasting than therapies outside the patients control, such as token economy programmes Cognitive restructuring has been used successfully, for example in stress management by having a sense of control and coping mechanisms, a person is better able to deal with stressful situations in real life Studies such as Seligman et al. (1998) and Kuyken et al. (2008) have shown CBT to be particularly effective, especially when used alongside drug treatment The therapy relies on the assumption that the individual can change their own thought patterns and control their beliefs, so this isnt a treatment which everyone will get results from Whilst most studies support CBT as a treatment for depression, many studies have suggested a mix of therapies is more effective A weakness of Becks cognitive model is that it may be depression which causes negative thoughts, not the other way around and if this is the case, the therapy (based on the rationale changing thoughts changes behaviour) is not going to be effective

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3.7

Treatments and therapies

How to describe and evaluate one treatment from each of the five AS approaches

This unit requires that you know one treatment or therapy for each one of the five AS approaches. For both schizophrenia and depression, drug treatment (from the biological approach) and cognitive-behavioural therapy (from the cognitive approach) were used. This means you still need to know one treatment from the social approach, psychodynamic approach and learning approach. Although there are alternatives available, this document will discuss care in the community programmes (social), dream analysis (psychodynamic) and systematic desensitisation (learning), and will also cover drug therapy and CBT for comparison.

The social approach: care in the community programmes

This type of treatment arose during the social psychiatry movement, fronted by psychiatrist R. D. Laing who refuted the medical model of mental disorders, suggesting symptoms were treated first, patients second. He advocated a more humane method of treating those diagnosed with mental disorders, which treated them supposedly more so like human beings, much to the disdain of the medical community. Care in the community programmes (a treatment from the social approach) Rationale behind the treatment Care in the community programmes bear in mind that a mental disorder is not just biological, there are social aspects to the disorder too and the explanation works around the idea that there are environmental and social triggers and not just biological causes to mental illness Nowadays when these programmes are used, the NHS aims to provide a spectrum of care: sheltered accommodation with 24-hour care for those who cannot live by themselves employment opportunities in sheltered social firms and cooperative businesses specialist mental health outreach teams to provide long-term care and support in-patient hospital care if the patients condition worsens (those who do not need hospitalisation are administered to psychiatric wards, but the aim of the programme is to get the patients back out into the community as soon as possible) Programmes are aimed at a wide variety of mental disorders, including depression and schizophrenia, most people are eligible so long as they do not need institutionalisation By shutting down the old, large institutions to allow for community care, funds will be released which can be used to improve in-patient care and to fund the programme Research has shown that care in the community programmes can work, and have undoubted potential, but only when they are properly funded Care in the community programmes come from the social psychiatry movement and are a much more person-centred treatment they consider that patients are human beings and treat them accordingly, which is advantageous over other treatments, such as drug therapy, which can be just for the doctors convenience of reducing the symptoms of an individual Whilst regarded a much more ethical and person-friendly treatment, the monetary and time investment required for care in the community programmes is significant, and the NHS finds it difficult to sustain such programmes, especially given current budget cuts Care in the community programmes tend to be unsuccessful unless they are properly funded and the carers are expertly trained individuals it is difficult to provide out-patient care Leff (1997) showed that patients suffering from schizophrenia cared for in the community in long-term sheltered accommodation showed much lower symptom severity than hospitalised patients, especially for negative symptoms however, Leshner (1992) found that often communication was poor between different agencies, with no overall strategy for coordinating patient care and Shepherd (1998) saw that most care in the community programmes in this country are severely under-funded although Margaret Thatchers closure of the large psychiatric hospitals saved 2,000m for her deinstitutionalisation scheme, none of this money was reinvested in community care

Process of the treatment

Disorders treated

Strengths

Weaknesses

Evidence and studies

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The cognitive approach: cognitive-behavioural therapy

Cognitive-behavioural therapy stemmed from the ideas of psychologist Beck, who put forward his cognitive model for depression, and it remains one of the most popular forms of psychotherapy as a treatment for disorders today. It can be used for a variety of disorders, and is often praised as it works with the patient, allowing them to move at their own pace. Cognitive-behavioural therapy (a treatment from the cognitive approach) Rationale behind the treatment This treatment is based around the idea that people develop maladaptive thoughts, emotions and behaviours, and suggests that by training the individual to change those maladaptive thoughts, their negative feelings, emotions and in turn, behaviours, too, will be changed respectively agree the agenda agree with the client what the aims and the agenda are build a rapport CBT cannot work if the client and therapist do not build a rapport, and this part alone can take a few months before any real work can begin assess core beliefs discover the patients core beliefs, and rather than telling them theyre wrong and this is what you should think, suggest alternative thinking patterns self-esteem as the patient is trained to rethink differently, build their self-esteem: their view of themselves and their view of the world around them CBT can be used to treat a variety of disorders, it is most commonly used for treating non-severe unipolar depression, but can be used to treat bipolar depression, some other anxiety disorders and certain mental health disorders, including schizophrenia Unlike drug therapy, CBT does not just mask the symptoms, it attempts to address the cause of the problem and treat accordingly, also possibly looking at the environmental and social causes (which not all therapies do) There is a strong evidence base for CBT, including for schizophrenia and unipolar depression as you will have seen The therapy is funded healthily by the government and is the NHS preferred choice of psychotherapy, it is seen as successful and relatively cheap, and made available to many When used as a treatment for depression, increasing the patients insights into their disorder can actually make them more depressed It is difficult to distinguish between what is causing the depression and what the depression is causing, which makes treatment difficult The therapy can not usually be used without drug treatment as well (e.g. schizophrenia) Pfammater (2006) conducted a meta-analysis and found CBT to be effective in reducing the positive symptoms of schizophrenia also, case studies such as Bradshaw (1998) have shown CBT to be successful although Turkington et al. (2002) suggested the link between CBT and depression, as the therapy course made patients more aware of their disorder and importance of medication and whilst Stiles et al. (2006) showed the treatment to be successful, it was not found to be any more successful than other therapies, so perhaps a cheaper therapy should be used

Process of the treatment

Disorders treated

Strengths

Weaknesses

Evidence and studies

The psychodynamic approach: dream analysis

Freud is considered the father of the psychodynamic approach, and one of the founders of psychoanalysis, another type of psychotherapy still in use today, although the treatment has changed radically since its introduction to society. The rationale, theory and method behind psychoanalysis remains questionable still, and dream analysis (one of Freuds original therapies which spawned from psychoanalysis) is one of those controversial treatments: both its success and rationale are considered debatable. Dream analysis (a treatment from the psychodynamic approach) Rationale behind the treatment Freuds personality theory suggests that our actions are governed by the thoughts of our unconscious, which are not normally accessible, but dream analysis aims to uncover the unconscious wishes by analysing the content of our dreams

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Process of the treatment

The therapy involves frequent visits to a psychoanalyst, which can be expensive as lasts usually a number of years. Traditionally, the psychoanalyst sits behind the analysand to allow them to fully concentrate, and so that the focus is on them. The material for discussion is the consciouslyremembered dream: the manifest content is the actual content of the dream produced, which is analysed to discover the latent content (the underlying meaning of the dream). Patients defence mechanisms are confronted, and transference (when the analysand transfers feelings onto the analyst, such as love or hate to be expected as part of the release of the unconscious wishes and fears) is dealt with Dream analysis can be used to treat non-severe depression and some anxiety disorders Dream analysis seems to be an effective way of uncovering unconscious thoughts, and although the theory cannot be objectively tested, Freud questioned whether a strictly scientific approach should be used to try and understand human individuals anyway Freuds work on dream analysis (and other psychoanalytical therapies) has led to the development and use of other therapies, such as cognitive-behavioural therapy, humanisticcentred therapy and conflict resolution Freuds work is based on case studies of unique individuals such as Little Hans and himself, so it is not necessarily a generalisable theory Research has shown dream analysis is not a hugely successful treatment Ethical issues may be raised regarding dream analysis It is frequently suggested that the therapy is highly subjective, and the success of the treatment is questioned, seeing as if the same patient were to visit two different psychoanalysts they would receive entirely different interpretations Shapiro (1991) suggests that psychodynamic therapies are only occasionally successful for depression, possible as depressed people are not motivated enough to participate in this slow process involving a great deal of concentration and personal-analysis Storr (1987) also criticised the psychoanalysts as they use much subjectivity: the therapy relies heavily on personal interpretation and so cannot be described as scientific famously, Masson (1989) argued against psychodynamic therapies, claiming psychoanalysts have too much power over their analysand clients (e.g. case study of Beth Rutherford)

Disorders treated

Strengths

Weaknesses

Evidence and studies

The biological approach: drug therapy

Biological psychology is a very much scientific approach to psychology: it considers the biological root causes of problems, such as those to do with gender development and mental disorders. Drug therapies come about from scientific research into biological causes for medical disorders: the drugs prescribed try and reverse the suggested issues. Drug therapy (a treatment from the biological approach) Rationale behind the treatment The rationale behind drug therapy is that disorders have biological causes, and a chemotherapeutic approach is able to correct the biochemical problem, alleviating symptoms The process is operationalised and always follows the same staged routine: 1 diagnosis: the disorder in question is identified and its cause discovered 2 prescription: decide on the drugs to use (for example, to correct the chemical imbalance) 3 course: let the patient take the prescribed drugs over a period of time 4 amend dosage: over time the drug will be removed (phased out to reduce withdrawal) Any disorder which has a biochemical cause which is reversible or treatable with the use of drugs, for example, due to a chemical imbalance or improper functioning of a neurotransmitter Very scientific approach, based on a biological explanation and evidence Biological treatment is constantly undergoing further research to discover more effective drugs, with higher treatment rates and fewer side effects, which is an advantage Patients who are on drug therapy are able to participate in other, more personal, therapies, such as cognitive-behavioural therapy, which certain patients would not otherwise be able to

Process of the treatment

Disorders treated

Strengths

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Weaknesses

Patients may forget to take their drugs, or choose not to so they can avoid the side effects People can become drug-dependent, or suffer withdrawal symptoms when drugs are stopped The therapy is often criticised for not addressing the root cause and curing the disorder, it simply corrects chemical imbalances to remove the symptoms of the disorder Meltzer et al. (2004) gave schizophrenic patients either haloperidol (an established antipsychotic), one of three new investigative atypical drugs, or a placebo, and found that two of the new drugs and haloperidol were successful in reducing symptoms, the placebo was not however, Kane et al. (1988) found that between 10% and 20% of patients on chemotherapy for schizophrenia do not improve Kuyken et al. (2008) saw that whilst drugs do improve patients generally, they are less effective than when they are used as well as a person-centred therapy, such as CBT

Evidence and studies

The learning approach: systematic desensitisation

The learning approach uses the principles of classical conditioning, operant conditioning and social learning theory to address treatment. One is systematic desensitisation, which is based on the principles of classical conditioning, and can be used to help individuals overcome fears in a way which is seen as more ethical than others, such as flooding. Systematic desensitisation (a treatment from the learning approach) Rationale behind the treatment The treatment is based on the principle of incompatible responses using the principles of classical conditioning: it suggests one response can be replaced with another after treatment functional analysis: the therapist decides on the triggers and the strength of the phobia anxiety hierarchy: a series of steps is decided, from the least-to-most stressful, based on a hierarchy of fears, which the patient can work their way up as the therapy progresses relaxation training: choosing methods of relaxation whilst coping (e.g. listening to music, meditation, hypnosis, and sometimes but less often drugs, such as valium) graduated exposure: slowly introduce the phobia and work your way up the hierarchy Effective for phobias and some anxiety disorders, but not used at all for other mental disorders It has been shown as very effective for treating phobias such as those of a particular species, such as spiders The therapy is ethical as the individual is involved throughout, as they devise the hierarchy and learn to relax in their own way As the goals are clearly specified, the therapeutic outcomes are easy to measure: this means that data on the effectiveness of the treatment is easily compiled, providing scientific measure for the therapy To work, the individual has to be able to relax and get involved in the whole process, which is more difficult for some than others Although it may be useful for treating phobias and anxiety disorders, it is not useful for a large number of other clinical disorders, such as psychoses The treatment only focuses on observable symptoms, rather than any underlying issues and as such makes little or no attempt to address the root cause of the problem Classical conditioning principles come mainly from animal studies, so there may be problems with generalisability to humans as a treatment McGrath et al. (1990) found that 75% of patients with specific phobias showed clinically significant improvements with their phobias following treatment similarly, Brosnan and Thorpe (2006) used a ten week desensitisation programme to help 16 students who were technophobic, on an ICT course, and compared to a control group, their anxiety levels were considerably lower by the end of the course on the other hand, some studies have shown it to be less successful, one where between 60% and 80% of patients showed slight improvement following treatment, but the difference was minimal and many completely relapsed after six months Craske and Barlow (1993)

Process of the treatment

Disorders treated

Strengths

Weaknesses

Evidence and studies

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3.8
Aims

Rosenhan (1973)
Study in detail: Rosenhans 1973 study On being sane in insane places

David Rosenhan was interested in the difficulty of defining abnormality. The aim of his study was to illustrate experimentally the problems involved in determining normality and abnormality, in particular, the poor reliability of the diagnostic classification system for mental disorder at the time (as well as general doubts over its validity); and the negative consequences of being diagnosed as abnormal and the effects of institutionalisation.

Procedure
The sample involve eight pseudo-patients (three women and five men), who were clinically sane, but were sent by Rosenhan to a mental health institution (twelve hospitals in total were used, Rosenhan wanted different settings to generalise the findings) with fake names and occupations, reporting one symptom: they were hearing voices each patient would report hearing one word repeatedly, either empty, hollow or thud. Apart from this one pseudosymptom and the fake names and jobs, each pseudo-patient did not change the rest of their behaviour. The pseudo-patients called the hospitals to arrange appointments, and arrived at the admissions offices saying that they were hearing this voice. It was unclear and always of the same sex as the patient. One of the pseudo-patients was Rosenhan himself (where his research was conducted, the hospital administrator and chief psychologist knew about his research, but the other seven patients were secret). After being admitted, the pseudo-patients stopped simulating any symptoms immediately, and responded normally to all instructions except they did not swallow the medications they were given. They all reported they were fine and told staff their symptoms had gone. Their tasks then were to: seek release from the psychiatric hospital by convincing the members of staff that they were sane, and all but one of the pseudo-patients were very motivated to do this observe and record the experience of the institutionalised mentally disordered patient each was to record notes about patient life and how they were treated, based on their experience, and at first they recorded their experiences covertly (although this was not specified as necessary by Rosenhan)

Findings
Admission All of the pseudo-patients except for one were admitted to the wards with a diagnosis of schizophrenia in remission, but all eight were admitted with some diagnosis to every hospital. None of the staff were doubtful of the pseudo-patients, in fact Rosenhan stated that once given the label of schizophrenia it seemed very hard to shake. He noted that more of the actual patients on the ward, 35 of the 118 from the first three hospitalisations, were suspicious of the pseudo-patients, suggesting things like Youre not crazy, youre a journalist or a professor (due to the note-taking). It should be noted that the hospitals were considered good or excellent and were not to blame for the failure to recognise the patients sanity, and also that prior to admission, the pseudo-patients were not carefully observed: so it was not full observation of their behaviour which led to the label of schizophrenia. Release The length of stay ranged from 7 days to 52 days (with an average stay of 19 days). All except the one had the diagnosis of schizophrenia in remission (meaning schizophrenia, but being able to be discharged, so non-severe), supporting the view that they had never been detected as sane. There were no records of any suspicion among the staff members. Observations of pseudo-patients lack of monitoring there was very little contact with doctors, and a strong sense of segregation between the staff and the patients was noted powerlessness and depersonalisation the pseudo-patients noted that powerlessness and depersonalisation was produced in the institution through the lack of rights, constructive activity and privacy, plus there were frequent verbal and even physical abuse from the attendants

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 distortion of behaviour all normal behaviour become interpreted in the light of the schizophrenic label the pseudopatients were given, for example: a note-taking pseudo-patients were never asked why they were taking notes, but it was recorded by nurses as patient engages in writing behaviour implying that it was a symptom of their disorder b pacing the corridors this was done out of boredom, and was noted by the nurses as a sign of nervousness, again implying that this was a symptom of their supposed disorder c waiting outside the cafeteria before lunchtime this was interpreted as showing the oral-acquisitive nature of the syndrome by a psychiatrist, rather than just waiting outside in preparation for lunch lack of normal interaction for example, pseudo-patients courteously asked a staff member Pardon me, doctor, could you tell me when I will be presented at the staff meeting? or When am I likely to be discharged? and they found mostly a brief and not always relevant answer was given, on the move, without even a normal turn of the head or any eye contact (psychiatrists were recorded as stopping to answer the questions a mere 4% of the time)

Follow-up
After Rosenhan published the results of his study, On being sane in insane places, to check the poor reliability of diagnosis, and to see if the insane could be distinguished from the sane, a later study was conducted where a teaching hospital, who had been informed of Rosenhans initial studies, was told to expect at least one more pseudo-patient over a three month period. During that time, the teaching hospital rated 193 incoming patients for how likely they were suspected to be pseudo-patients, and in total 41 patients were suspected of being pseudo-patients (19 of whom had been suspected as so by both a psychiatrist and another staff member). Rosenhan had in fact sent no more pseudopatients, and so the 41 patients identified by the teaching hospital as fake were in fact real (as far as Rosenhan knew).

Analysis
Rosenhan claims that the study demonstrates that psychiatrists cannot reliably tell the difference between people who are sane and those who are insane. The main experiment illustrated a failure to detect sanity, and the follow-up study (above) demonstrated a failure to detect insanity. Rosenhan explains that psychiatric labels tend to stick in a way that medical labels do not, and that everything a patient does once admitted is interpreted in accordance with the diagnostic label once it has been applied. He suggested that instead of labelling a person as insane, we should focus on the individuals specific problems and behaviours. The study demonstrates both the limitations of diagnostic classification and importantly the appalling conditions in many psychiatric hospitals. This has stimulated much further research and has led to many institutions improving their philosophy of care. Rosenhan, like other anti-psychiatrists, is arguing that mental illness is a social phenomenon. It is simply a consequence of labelling. This is a very persuasive argument, although many people who suffer from a mental illness might disagree and say that mental illness is a very real problem.

Evaluation Strengths
The hospitals used were varied (new and old, private and public, and different locations) allowing for generalisation, and since twelve hospitals were used this strengthens the findings further again allowing for generalisation There was validity to the study in that the pseudo-patients behaved as themselves except for the voices which were only mentioned in the admissions stage: this validity could be seen in that other patients questioned their diagnosis Using eight people in twelve hospitals meant that the study was replicated and, as the same results were found, this gives the study reliability

Weaknesses
The study involved telling the staff that they were hearing voices, which was a classic symptom of schizophrenia, so perhaps it was hardly surprising they were diagnosed accordingly, similarly it might not be surprising that the teaching hospital identified some people they thought to be pseudo-patients: the validity is compromised Since the study was carried out 30 years ago, methods of care and diagnosis has improved, and there is more emphasis on care in the community, and so it might be wrong to say that there is still a problem with diagnosis

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3.9
Procedure

Goldstein (1988)
Study in detail: Schizophrenia in women and men, and the reliability of the DSM

Goldstein (1988) is a study which comprises a number of parts. Primarily, Goldstein was interested in comparing the experiences of schizophrenia in men and women. However, her study also used two measures which looked at the reliability of the DSM in diagnosing schizophrenia.

This was a longitudinal study, the main part of which followed 90 patients who had been hospitalised, and were followed for ten years. They were chosen based on being diagnosed with schizophrenia using DSM-II, being aged between 18 and 45 and having no other mental health issues (or general conditions such as drug or alcohol abuse). They had all been hospitalised for less than six months before returning to their families. Rediagnosis and testing reliability of the rediagnosis Firstly, in order to test for reliability of the DSM, Goldstein re-diagnosed 199 patients who had been diagnosed with schizophrenia using DSM-II. The criteria for the disorder from DSM-III were used, and it was found that 169 of the patients were re-diagnosed with schizophrenia. Such a proportion of the 199 sample suggests that the DSM is a reliable tool for diagnosis of schizophrenia. In order to test the reliability of Goldsteins re-diagnoses, she used a small sample of these patients and asked an independent expert to diagnose the patients again to see if the diagnoses matched (below) One of the parts of the study involved choosing 8 of the participants at random to be re-diagnosed using DSM-III to test for reliability. Four males and four females were chosen to be diagnosed by experts (including Goldstein). The experts were given case studies, including the patients names, but no other details: it was a single-blind technique as only Goldstein knew the hypothesis, the experts did not. There was a 0.80 agreement, and only one case where they disagreed with Goldsteins diagnosis (she diagnosed schizoaffective disorder and the experts diagnosed schizophrenia). Overall, it was thought that the diagnoses were reliable, even though there was this one disagreement Information about the patients in terms of symptoms, premorbid functioning (how the patients functioned before the onset of the disorder), social functioning (how the patients function post-diagnosis) and the course of the illness: information about symptoms was gathered by trained interviewers using specially-developed questions, focusing on hallucinations, formal thought disorders, paranoia, isolation, withdrawal and anxiety, as well as depression information about premorbid functioning was measured by a questionnaire dealing with isolation, peer relationships and interests the patients had when younger, also taking into account marital status and employment information about social functioning was measured using details about the patients after they received their diagnosis, including marital status and employment information about course of the illness was operationalised in two ways: counting the number of re-hospitalisations experienced and the duration of stay in the hospitals, data for which was taken from hospital records both five years after diagnosis and ten years after diagnosis

Findings
Goldstein was interested to see if men experienced a more severe course of schizophrenia than women, and this was measured by seeing if they had longer stays when admitted to hospitals, and also more frequent hospitalisations. It turned out men did. Women had a significantly lower average number of admissions and lengths of stay than men when comparing the two over a ten year period (as the results table shows). The findings were found to be statistically significant in all cases. Further statistical testing was carried out to explain the gender differences in the courses of the disorder. Researchers could use these tests to look at other factors (including premorbid functioning, social functioning and the diagnosis) to see how they affected findings. 0 to 5 years Male Female 0 to 10 years Male Female 0 to 5 years Male Female 0 to 10 years Male Female

Mean 1.40 0.59

Number of rehospitalisations

2.24 1.12

Length of stay in hospital (days)

267 130

418 207

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It was found that 13% of gender effect on re-hospitalisations was due to premorbid functioning, but only 4.3% was down to social functioning. It was also found that 11.3% of gender effect on length of stay was due to social functioning and only 4.2% was due to premorbid functioning. Goldstein therefore concluded that the number of re-hospitalisations was largely affected by premorbid functioning, whereas the length of stay was affected more by social functioning.

Conclusions
Goldstein concluded that her study had reinforced what other studies had found, supporting her hypothesis that women had a less severe experience with schizophrenia than men. This was backed up in her study by the fact that men had more hospitalisations and longer stays on average. She also found that the DSM-III was a reliable tool for diagnosis, but noted that there were some diagnostic differences (169 of the 199 patients were re-diagnosed with the same disorder). She concluded that premorbid functioning and social functioning are important factors in the development of schizophrenia.

Evaluation Strengths
The secondary data (based on number of re-hospitalisations and average length of stay) are quantifiable and so scientific conclusions can be drawn (and are also both valid as they come from real hospital records, and objective because they require no individual interpretation) Goldstein could show that her schizophrenia diagnoses were reliable, as they were supported by two experts who found the same diagnoses as her (despite one small disagreement of the eight cases) By using interviews, she was able to gather rich and detailed qualitative data (as well as the quantitative data), so all the information about premorbid history and social functioning among other factors was detailed to enhance the conclusions and ensure validity

Weaknesses
Of women who are diagnosed with schizophrenia in the country, only 9% are over the age of 45, and yet no women aged 45 or above were included in the sample, which may have affected the results (and conclusions) because women over 45 tend to experience a more severe course of the disorder than those under 45 (so the findings may not be as valid as previously thought, as the statistics for men cannot be applied to women) Goldstein used mainly white, middle-class people from one area within the USA, and the sample size of 90 was fairly small, so the findings may not be generalisable to all populations and all schizophrenics There may have been interviewer bias when Goldstein conducted the interviews

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3.10
Aims

Gottesman and Shields (1966)

Study in detail: To test if there is a genetic basis to schizophrenia

The main aim of this study was to see if whether schizophrenia had a genetic basis. Using a twin study methodology, Gottesman and Shields planned to test different twin pairs to investigate the concordance rates of schizophrenia in twins. They also wanted to replicate other studies that had indicated a genetic basis to the disorder, to find if their findings would be similar (to test for reliability).

Procedure
Researchers looked at patient records from a short-stay psychiatric hospital with a large outpatients department. The records covered a sixteen year history from 1948 to 1964. Over that time, 392 patients were seen who said that they had a twin of the same sex, and of those 68 had a diagnoses of schizophrenia or a related psychosis although six patients were discounted either because their twin counterparts were overseas or it was unclear whether they were monozygotic (MZ) or dizygotic (DZ) twins. This left 62 patients: and 5 twin pairs were both on the register, leaving 57 study pairs. The other 52 patients twin counterparts were tracked down to participate in the study. Monozygotic Female Male Total 11 13 24 Dizygotic 16 17 33 Total 27 30 57 Of the 62 patients in the participant sample, exactly half were male, and half were female. Their ages ranged from 19 to 64 when they were last assessed, with the average patient age being 32. Zygocity was determined using three methods: fingerprint testing, blood testing and resemblance assessments (this was done before DNA testing was around).

Multiple data collection methods were used, involving both primary and secondary resources. These included: hospital notes case histories based on self-report questionnaires and interviews with the twins and their parents tape-recorded 30 minute samples of verbal behaviour from semi-structured interviews personality testing testing to measure disordered thinking, conducted both on the twin sets and their respective parents The researchers wanted to look at concordance rates. If the one twin had been diagnosed with schizophrenia, they wanted to know how often their counterpart twin would also be diagnosed with schizophrenia, or a related psychosis. The patient who had been admitted to the psychiatric hospital initially first coming to attention was called the proband. The data was analysed between each proband and their twin, with twin pairs being categorised in four ways.

Findings
The tables below display the main results from Gottesman and Shields study. The four categories were: category 1 both the proband and co-twin had been hospitalised and diagnosed with schizophrenia category 2 both had hospitalisation, but the co-twin had been given another diagnosis related to schizophrenia category 3 the co-twin had some psychiatric abnormality, but nothing related to schizophrenia category 4 proband had schizophrenia, but the co-twin was diagnosed as clinically normal Monozygotic twins Category: 1 1 and 2 1, 2 and 3 4 Total: Number 10 13 19 5 24 %age 42 54 79 21 100 Dizygotic twins Number 3 6 15 18 33 %age 9 18 45 55 100 Concordance rates: Severe schizophrenia Mild schizophrenia MZ 75% 17% DZ 22% 0% Categories 1, 2 & 3: Males Females MZ 69% 91% DZ 29% 62% It is recommended that you learn those figures highlighted in red, as learning them all is not realistic Note: severe means having longer than two years hospitalisation, mild means less than two years

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In summary, the results showed: There was a significant difference found between MZ and DZ twins in all measures MZ twins were always more similar in diagnosis than DZ twins in each case where the co-twin had some diagnosis Similarity was greater between female twins compared to male twins (for both MZ and DZ twins) Concordance rates were higher for both MZ and DZ twins for severe schizophrenia compared to mild schizophrenia

Conclusions
The findings suggested that the closer the genetic relationship between two people, the greater the likelihood that if one of them is diagnosed with schizophrenia , the co-twin is also going to develop schizophrenia or a related psychotic disorder. The study also suggested that this relationship was more prevalent among females than males. However, as twins in the monozygotic twin pairs did not have 100% concordance rates, the implication is that schizophrenia is not caused entirely by genes. Instead, the results led Gottesman and Shields to believe that genetic factors do predispose someone to schizophrenia, by lowering their threshold for coping with stress, but environmental triggers may also be needed to actually start the development of the disorder. They said the diathesis-stress model best fit this explanation, taking on board a biological and environmental explanation. Gottesman and Shields also looked at 11 other studies, and concluded that their results did support each other, although they thought there were some methodological issues, such as with the sampling techniques. This is how they concluded their results were reliable, and that there is a genetic element to schizophrenia.

Evaluation Strengths
The results are supported and backed up by other studies which have produced similar findings, such as Inouye (1961) who found a 74% concordance rate of twins with a progressive chronic schizophrenia disorder, and a 39% concordance rate for mild schizophrenia One of the findings of their analysis of the other studies was that the sampling techniques were questionable, but a strength of Gottesman and Shields study is that the sampling was carefully controlled using multiple measures to make sure that twins were correctly allocated either MZ or DZ twin status, and a lot of data was gathered using multiple research methods to check the diagnoses were correct

Weaknesses
It would have been useful to know more about what related psychosis meant when describing the schizophrenia scale to take into account the related disorders, as they failed to make this clear Gottesman and Shields suggested that there are different types of schizophrenia and some might be caused by life events (so environmental stimuli), such as being a prisoner of war, and it was hard to distinguish between such types in the results of the study

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3.11
Aims

Brown et al. (1986)

Study in detail: Browns 1986 study on Social support, self-esteem and depression

Brown et al. looked at factors involved in depression, and considered only women. They used interviewing techniques to find out how self-esteem and social support factors affected the development of depression. The aims were: to see whether crisis support protects against the onset of depression, even if there is low self-esteem and a lack of general support to see if a lack of support and low self-esteem are vulnerability factors for depression to see if support from a husband, partner or close relationship reduces the risk of depression

Procedure
The study took place in Islington, North London. The study used a prospective design this means that it was a longitudinal study that started when the participants were not affected by the condition of interest, in this case depression. This allows risk factors to be studied. If someone with depression is interviewed once they are depressed, then the depression may affect answers given concerning events that led up to the depression. This would make it difficult to investigate the causation factors. Women whose husbands worked in manual occupations, had at least one child aged 18 or under living at home, and were themselves aged between 18 and 50, were sent a letter by their GP asking if they were willing to take part. Women who fit the criteria and all single mothers (since depression is frequent among single mothers) were put into the sample. In total, 435 women were found, and a number of them were randomly selected to participate: 91% of the initial response (so 395 women in total) were used in the first stage of the study. The study had two phases: at first contact measures of self-esteem and personal ties were measured, and psychiatric history collected the second phase, one year later, collected data about any onset of psychiatric disorder in the twelve months following first contact, and measures of live-event stress and social support were also taken the measures were carried out carefully and by experienced interviewers; there were tests for reliability, with 60 women being interviewed intensively and 21 used in a reliability study: of these 21, eleven were seen by two interviewers and ten were rated by a second person using tapes of the original interviews, and satisfactory inter-rater reliability was found In this study, fifty participants who were found to be depressed when first contacted were excluded from the follow-up study one year later, as the researchers were only interested in new cases of depression to find causation factors.

Findings
In all, 353 women agreed to the follow-up interview one year on (89% of the original sample interviewed), although 50 of those were the initially depressed, and so the study excluded their data and analysed the cases of 303 women. About half of those women (150) had experienced a severe event or major difficulty at some point in the twelve months between first contact and the follow-up, and 32 of the women had the onset of depression. Life events and onset of depression Of the women who had developed depression in those twelve months, 29 of the 32 had experienced some major life event (involving a loss, failure or disappointment) six months prior to developing depression thats 91% of all those who were depressed. This compared to only 23% of the women without depression who had experienced such an event. Self-esteem and the onset of depression Of those who had a life event, Did they have negative Did the women have a provoking agent? 33% of those who developed evaluation of self? Yes (% of those with onset) No (% of those with onset) depression had negative Yes 33% (18 out of 54) 4% (1 out of 27) No 13% (12 out of 96) 1% (1 out of 126) evaluation of the self and 13% did not. The table shows the relationship between provoking agents (life events) and negative self-esteem.

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Social support The majority of women with core crisis support (85 of 92) saw it as helpful, and there was no difference in their perception of support being helpful whether they had developed depression or not. It is interesting that where a woman had said she had confided in a close tie (core support) at first contact, but not at crisis support and so felt let down, 42% developed depression. Of those who had no support either at first contact or at crisis, 44% (or 4 of the 9) developed depression. Note: core support refers to the support of a husband, partner or other close relation, whereas crisis support refers to (professional) support at the time of a provoking agent (life event) which may possibly lead to depression

Conclusions
- In general, those who had a husband or other close tie had a lower chance of the onset of depression - However, those women who were married and confided in their husbands (core support) but were let down by a lack of such support at crisis (crisis support) had an increased risk of developing depression - Low self-esteem is implicated in the onset of depression after a provoking agent - A provoking agent seemed to be necessary for the development of depression in most cases

Evaluation Strengths
Both the first contact and follow-up interviews gave the in-depth and detailed data that were required for the analysis of such complex inter-related concepts such as self-esteem, core social support and major life events There was strong inter-rater reliability, which strengthens the findings which come from the data The data were likely to be valid as they were gathered carefully by trained and experienced interviewers using a semistructured interview technique, allowing detailed information to be gathered and explored Sampling was carefully carried out by contacting all eligible women and then carrying out random sampling this meant that all the women had equal chances of being chosen, which removes a source of bias

Weaknesses
It was hard to separate out the concepts that were scored as numbers and then percentages because qualitative data were in some cases reduced to quantitative data for example, the presence or lack of support from a husband or partner at crisis point seemed easy to access, but then it was shown that such lack of support meant, at least in some cases, that the husband was part of the situation, rather than a bystander This was a study of working-class women with at least one child still at home the sample was quite precise, and therefore generalising the findings to all women might not be possible

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