Clinical Psychology PDF Past Paper

Paper 2: Applications of Psychology Clinical Psychology Fish Schizophrene (1986) by Bryan Charnley 1  PAGE CONTENTS NUMBER 5 Diagnosis of mental disorders. The 4 Ds....

Paper 2: Applications of Psychology Clinical Psychology Fish Schizophrene (1986) by Bryan Charnley 1  PAGE CONTENTS NUMBER 5 Diagnosis of mental disorders. The 4 Ds. 10 Classification systems: DSM-5 15 Classification systems: ICD-10 Schizophrenia: symptoms and features. The function of neurotransmitters as a theory/explanation for schizophrenia. One other biological theory/explanation for schizophrenia: Genetics. One non-biological theory/explanation for schizophrenia (Social explanation: Social Causation Hypothesis) One biological treatment for schizophrenia (antipsychotics). One psychological treatment for schizophrenia (Assertive Community Therapy). Describe symptoms and features of one other disorder: unipolar depression. One biological explanation for unipolar depression (The Monoamine Hypothesis). One non-biological explanation for unipolar depression (Beck’s cognitive model of depression). One biological treatment for unipolar depression (drug treatment) One psychological treatment for unipolar depression (CBT). Individual differences in mental health disorders and developmental psychology. Health and Care Professions Council (HCPC) guidelines for clinical practitioners. Researching mental health: Longitudinal, cross-sectional, cross-cultural methods, meta-analysis, and the use of primary and secondary data. The use of case studies, to include an example study: e.g. Tsang et al (1999) The use of interviews in clinical psychology, to include an example study: e.g. Kroenke et al (2008) Rosenhan (1973) On being sane in insane places. Carlsson et al (1999) Network interactions in schizophrenia – therapeutic implications. 2 Kroenke et al (2008) The PHQ-8 as a measure of current depression in the general population. Key question: What are the issues surrounding mental health in the workplace? Practical investigation: A summative content analysis that explores how attitudes to mental health have changed over time. Issues and debates specification checklist CLINICAL PSYCHOLOGY SECTION 5.1 CONTENT SPECIFICATION CHECKLIST 3 Subject Content What students need to learn: 5.1 Content 5.1.1 Diagnosis of mental disorders, including deviance, dysfunction, distress and danger. 5.1.2 Classification systems (DSM IVR or DSM V and ICD) for mental health, including reliability and validity of diagnoses. 5.1.3 Schizophrenia and one other disorder from anorexia nervosa, Obsessive-compulsive disorder (OCD) and unipolar depression. For schizophrenia: Description of symptoms and features, including thought insertion, hallucinations, delusions and disordered thinking. The function of neurotransmitters as a theory/explanation. One other biological theory/explanation. One non-biological theory/explanation. For the other disorder (unipolar depression) Description of the symptoms and features. Two explanations/theories: one biological theory/explanation and one non-biological theory/explanation. 5.1.4 For schizophrenia and the other disorder (unipolar depression), students should be familiar with two treatments for each disorder: one from biological and one from psychological. Two treatments for each disorder. The two for schizophrenia must come from different topic areas. The two for the other chosen disorder must come from different topic areas (these may be from the same topic areas as those used for schizophrenia). 5.1.5 Individual differences Cultural effects can lead to individual differences in mental health disorders, e.g. non-biological explanation for schizophrenia. 4  Cultural effects can lead to different diagnoses of mental health disorders affecting reliability and validity. 5.1.6 Developmental psychology Issues around genes and mental health, such as a genetic or biochemical explanation for schizophrenia, can affect development. DIAGNOSIS OF MENTAL DISORDERS (the four Ds) SPECIFICATION REQUIREMENTS 5.1.1 Diagnosis of mental disorders, including deviance, dysfunction, distress and danger. Clinical psychology considers how abnormality is defined and diagnosed. It is difficult to define what is meant by ‘normal’ and ‘abnormal’, and such concepts are dependent upon culture. What is normal in one culture may be deemed abnormal in another. Issues such as health and mental disorders are often said to be socially constructed meaning that they differ from society to society and are best understood within their social context. When defining abnormality and diagnosing mental disorders, the four Ds are referred to: deviance, distress, dysfunction, and danger. 1. Deviance This refers to behaviour and emotions that are not the norm in a society and deviate from cultural or statistical norms. Such behaviours are therefore viewed as unacceptable by society and may be classified as abnormal. Deviance from cultural norms 5  Every culture has certain standards and norms for acceptable behaviours and behaviour that deviates or differs markedly from these norms is considered abnormal. The concept of abnormality changes over time within the same society. For example, forty years ago, most Americans would have considered men wearing earrings as abnormal; but today it's considered as differences in lifestyle rather than as signs of abnormality. A further example of deviance is talking to oneself in public. Deviance from statistical norms Abnormal behaviour is statistically infrequent or deviant from the norm. Many characteristics such as height, weight and intelligence cover a range of values, when measured over an entire population. Most people for example fall within the middle range of height and few are abnormally tall or short. A person who is extremely intelligent or happy would be classified as abnormal using this definition, but clearly these are desirable behaviours. 2. Distress This refers to the negative feelings that someone with a disorder experiences. Distress alone is not a good indicator of abnormality as there may be an obvious cause such as bereavement. In some disorders such as schizophrenia, the patient is unaware of their problem. The patient themselves believe they are functioning adequately and do not experience distress. 3. Dysfunction 6 This refers to a person’s behaviour preventing them from carrying out everyday tasks and living their life in general. Examples of lack of functioning include insomnia, being unable to work, relationships being affected and a decrease in pleasure in many areas of the person’s life. No longer socialising and going out with friends would be considered dysfunctional as would only going out at night because this would limit the activities the individual could participate in. 4. Danger This refers to danger to others or to the individual themselves. A person may seem to be endangering himself by being least bothered about his diet and health or in extreme cases when having suicidal thoughts. Violent behaviour towards others would also signal danger. AO3 Useful application One strength of the 4Ds is that using all four helps avoid erroneous diagnosis. E.g. more factors than just deviance from statistical or cultural norms are considered. This avoids situations in which eccentric, but harmless people are seen as abnormal, and those with common but debilitating symptoms of depression are missed. This means the 4Ds is effective, as a valid system should be neither over or under inclusive. objective Another strength of the 4Ds is that by adopting self-report measures such as the WHODAS II it provides quantitative data in the form of a numerical score (from 0 to 48) for the level of dysfunction experienced by the client over the last 30 days. This means the 4Ds is effective if it adopts an objective measure of dysfunction, making it more valid. Qualitative and quantitative A further strength of the 4Ds is that it adopts both a qualitative and quantitative approach to defining abnormality. This means the 4Ds is effective, as both objective data from the statistical criteria (K10) and more in-depth and individualistic data is gained when considering aspects such as distress, dysfunction, and danger leading to a more valid diagnosis. Useful application A further strength of diagnosis using ‘danger’ is that an individual may be detained under the Mental Health Act (sectioned) if 3 professionals agree they are danger to themselves or others. This means the 4Ds is effective as a person can receive hospital treatment to prevent harm/protect them and members of society. A final strength is that the 4Ds provides a more holistic approach to diagnosis than previous definitions of abnormality. It combines several previous definitions such as failure to function adequately, social norms and deviation from the statistical norm. This means the 4Ds is effective as it provides a more complete definition of abnormality. Useful application One weakness is that there are no hard and fast rules about how to combine the 4Ds. For example, someone struggling to cope (signs of distress and dysfunction), 7 but with no signs of danger or deviance, may not require a diagnosis. This could be ineffective because it could be the situation causing the problem, so could not be resolved by treatment, which is the point of diagnosis. Another weakness is that adopting self-report measures such as WHODAS II which uses rating scales from ‘none, mild, moderate, severe to extreme (can’t do)’ for statements such as ‘how much difficulty did you have in maintaining a friendship?’ may not be answered truthfully or the options are too restrictive. This could reduce the effectiveness of the diagnosis due to the invalid nature of the responses. A further weakness is that the 4Ds compares the individual with others in society, the clinician will use their own subjective views/norms as the baseline. This means the 4Ds may not be effective in diagnosing disorders because the clinician is only using information about the individual and not their community/cultural norms. A further weakness is that the 4Ds creates labels. Such as ’deviant’ (from cultural norms) or ‘danger’ as a criterion for diagnosing mental disorder which leads people to equate mental illness with being ’disturbed’ or ‘dangerous’. This is ineffective because such attitudes may become distorted in the media and/or have the potential for social control and the abuse of power. A final weakness is that Davis (2009) suggested that the use of the 4Ds is insufficient and further concepts must be considered, such as the duration of the symptoms. Thus, the 4Ds are ineffective unless used by clinicians, in conjunction with classification systems (DSM-5 or ICD-10). 20 MARKER Assess the effectiveness of the 4 Ds as a means of diagnosing mental disorders. (20) The 4 Ds are used by clinicians to identify the point at which human behaviour changes from normal to abnormal and may be classified as a psychiatric disorder. The 4 Ds are deviance, dysfunction, distress, and danger. Deviance refers to behaviours which are unusual, undesirable, and bizarre or not the ‘norm’ in society. Cultural Norms exist which show how desirability of a behaviour depends on historical context, the culture, the situation, age and/or gender of the individual. Statistical Norms are used to measure the unusualness of any behaviour. Abnormal behaviour is statistically infrequent or deviant from the norm. One strength of the 4Ds is that using all four helps avoid erroneous diagnosis. E.g. more factors than just deviance from statistical or cultural norms are considered. This avoids situations in which eccentric, but harmless people are seen as abnormal, and those with common but debilitating symptoms of depression are missed. This means the 4Ds is effective, as a valid system should be neither over or under inclusive. However, a weakness is there are no hard and fast rules about how to combine the 4Ds. For example, someone struggling to cope (signs of distress and dysfunction), but with no signs of danger or deviance, may not require a diagnosis. This could be 8 ineffective because it could be the situation causing the problem, so could not be resolved by treatment, which is the point of diagnosis. Dysfunction refers to symptoms that distract, confuse, or interfere with ability to carry out roles/responsibilities. This includes trouble getting up in the morning, failure to complete tasks at work or college and problems participating in routine activities (e.g. socialising). Psychologists use a variety of self-report measures to assess everyday functioning. E.g. the WHODAS II questionnaire assesses a person's understanding of what is going on around them, communication, and deterioration in self-care. Another strength of the 4Ds is that by adopting self- report measures such as the WHODAS II it provides quantitative data in the form of a numerical score (from 0 to 48) for the level of dysfunction experienced by the client over the last 30 days. This means the 4Ds is effective if it adopts an objective measure of dysfunction, making it more valid. However, a weakness of adopting self-report measures such as WHODAS II which uses rating scales from ‘none, mild, moderate, severe to extreme (can’t do)’ for statements such as ‘how much difficulty did you have in maintaining a friendship?’ may not be answered truthfully or the options are too restrictive. This could reduce the effectiveness of the diagnosis due to the invalid nature of the responses. Distress refers to any symptoms which cause emotional pain and anxiety. A clinician considers the intensity or duration of the distress, individualistic features (job loss/bereavement), as well as a person’s level of functioning when making a diagnosis. A clinician may use the K10, a self-report scale to assess psychological over the last 4 weeks. A further strength of the 4Ds is that it adopts both a qualitative and quantitative approach to defining abnormality. This means the 4Ds is effective, as both objective data from the statistical criteria (K10) and more in- depth and individualistic data is gained when considering aspects such as distress, dysfunction, and danger. leading to a more valid diagnosis. However, a weakness is that the 4Ds compares the individual with others in society, thus the clinician will use their own subjective views/norms as the baseline. This means the 4Ds may not be effective in diagnosing disorders because the clinician is only using information about the individual and not their community/cultural norms. Danger refers to any careless, hostile, or hazardous behaviour which jeopardises the safety of the person and/or others. Violent behaviour towards others would signal danger. Danger may also be seen to in an individual who is less bothered about diet/health or having suicidal thoughts and may therefore be damaging their self. A further strength of diagnosis using ‘danger’ is that an individual may be detained under the Mental Health Act (sectioned) if 3 professionals agree they are danger to themselves or others. This means the 4Ds is effective as a person can receive hospital treatment to prevent harm/protect them and members of society. However, a weakness is the 4Ds creates labels. Such as ’deviant’ (from cultural norms) or ‘danger’ as a criterion for diagnosing mental disorder which leads people to equate mental illness with being ’disturbed’ or ‘dangerous’. This is 9 ineffective because such attitudes may become distorted in the media and/or have the potential for social control and the abuse of power. Overall, the 4Ds provides a more holistic approach to diagnosis than previous definitions of abnormality. It combines several previous definitions such as failure to function adequately, social norms and deviation from the statistical norm. This means the 4Ds is effective as it provides a more complete definition of abnormality. However, Davis (2009) suggested that the use of the 4Ds is insufficient and further concepts must be considered, such as the duration of the symptoms. Thus, the 4Ds are ineffective unless used by clinicians, in conjunction with classification systems (DSM-5 or ICD-10). CLASSIFICATION SYSTEMS SPECIFICATION REQUIREMENTS 5.1.2 Classification systems (DSM IVR or DSM V and ICD) for mental health, including reliability and validity of diagnoses. DSM-5 Classification systems are used by medical staff such as psychiatrists and clinical psychologists to diagnose mental disorders The Diagnostic and Statistical Manual of Statistical Disorders (DSM) is published by the American Psychiatric Association. The DSM was first published in 1952 and since then, there have been six revisions; the current version being DSM-5 which was published in 2013 (NOW THERE ARE 7 REVISIONS WITH THE DSM-5-TR BEING PUBLISHED IN 2022). The DSM contains descriptions, symptoms, and other criteria for diagnosing mental disorders and is used predominantly in the USA and other westernised countries. A diagnosis is valid if it leads to treatment that works and predicts the course of a mental disorder, because the DSM would be measuring what it claims to measure. Section I of DSM-5 describes the organisation of chapters in the manual and explains the way the DSM-5 has introduced some key changes compared to the previous version DSM-IV-TR such as moving away from a multi-axial system and introducing section III. Other changes have included removal of specific subtypes of schizophrenia, renaming gender identity disorder as gender dysphoria and the inclusion of hoarding disorder in the section about OCD. Section I also outlines the process of how the revisions were made including field trials by psychiatrists to investigate test-retest reliability. The reliability of the DSM depends upon whether one person’s set of symptoms would lead to a common diagnosis by different physicians. 10 Section II provides diagnostic criteria and codes. Chapters cover depressive disorders, schizophrenia spectrum and other psychotic disorders, anxiety disorders and others. Each chapter includes diagnostic features, culture-related diagnostic issues, prevalence, and prognosis. A structured interview is used to assess symptoms. The criteria provided are concise and explicit, intended to facilitate an objective assessment of symptoms. Section III relates to emerging measures and models and contains diagnostic categories that need more research before they are included in section II and recognised as a clinical disorder. One example is internet gaming disorder. It also contains information about being sensitive to cultural variations in diagnosis. DSM-5 now includes culture bound syndromes and recognises that some disorders are more likely to occur in specific cultures. AO3 One strength is that Kupfer (2013) claims that clinicians using DSM-5 are now required to obtain information from many different sources including the patient’s family history, their symptoms and how treatments affect them therefore increasing convergent validity. Another strength is that Stinchfield et al (2015) compared DSM-5 with DSM-IV as tools for diagnosing gambling disorder. Results showed significantly higher internal consistency in diagnosis when using DSM-5 therefore demonstrating good reliability. A further strength is that DSM-5 underwent field trials before publication, which included test-retest reliability where different clinicians independently evaluated the same patient using the criteria in section II therefore supporting the improvement of the reliability of the manual. A further strength is that the manual has updated its criteria to reflect cross-cultural differences in symptoms and more information about cultural concepts of distress therefore increasing the validity of diagnosis. A final strength is that the DSM has been continuously reviewed and updated since its creation in 1952, meaning that it has evolved to reflect changes and current trends in mental disorders; for example, the inclusion of hoarding as a disorder in DSM-5. One weakness is that the BPS has expressed concern about DSM-5 which requires social norms to be considered when making a diagnosis leaving the process open to some degree of subjectivity regarding the clinician’s judgements. This would subsequently challenge the validity of DSM-5. Another weakness is that research has found that the clinician’s experience and style of interviewing when using DSM-5 can significantly lower agreement rates between different clinicians assessing the same patient’s symptoms. This is 11 particularly evident when a shorter period is spent on the clinical interview. This would therefore challenge the reliability of DSM-5. A further weakness is that Cooper (2014) found a diagnosis of schizophrenia had a reliability estimate of 0.46 using DSM 5 compared to 0.81 in the DSM-III trial showing a significant reduction in the reliability of the manual. A further weakness is that the DSM-5 has also been criticised for being developed by a workforce consisting predominantly of male, westernised practitioners from similar cultural backgrounds. This would therefore challenge the validity of any diagnosis made due to cultural bias in the development of criteria. A final weakness is that critics of the manual have highlighted the fact that the psychiatric drug industry has unduly influenced the manual's content (around 68% of DSM-5 development members had ties to pharmaceutical companies) which could lead to bias in diagnosis, lowering internal validity. Reliability of the DSM5 8 MARKER Evaluate the reliability of the DSM classification system as a way of diagnosing mental disorders (8) The Diagnostic and Statistical Manual of Statistical Disorders (DSM) is a classification system published by the APA used by clinicians to diagnoses a patient’s symptoms. The DSM was first published in 1952 and since then, there have been seven revisions; the current version being DSM-5-TR which was published in 2022. The reliability of the DSM depends upon whether one patient’s set of symptoms would lead to a common diagnosis by different clinicians. Diagnosis can be affected by what the patient’s tell the psychiatrist so if a patient tells 2 psychiatrists two different things, this may affect the reliability of their diagnosis. One strength of the reliability of the DSM is from Stinchfield et al (2015) who found significantly higher internal consistency when diagnosing gambling disorder using the DSM-5 compared to DSM-IV. This is a strength as it shows that the most recent version of the DSM-5 is a more reliable tool for diagnosing gambling disorder than earlier versions. However, one weakness of the reliability of the DSM is from Maj et al (2000) who found a low Kappa score of 0.22 for schizoaffective disorder when using DSM-IV. This is a weakness because it suggests that the DSM-IV has a low level of reliability when diagnosing some disorders and this was believed to be due to ambiguity between clinicians in the duration of symptoms required for a diagnosis. Section I of the DSM outlines the process of how the revisions were made to the manual including field trials by clinicians to investigate inter-rater reliability where different clinicians conduct separate interviews to check their rate of agreement regarding a diagnosis. The level of reliability is measured using a Kappa score 12 which calculates the probability of agreement between raters; 1 is perfect reliability and the closer the Kappa score is to 1, the more reliable the diagnosis. Test-retest reliability is a measure of the consistency of a psychological diagnosis over time. A further strength is that DSM-5 uses a structured clinical interview called SCID-5 to standardise the questions asked to a patient. This is strength because different clinicians can carry out their clinical interviews in a consistent way with the same patient, meaning the reliability of their diagnosis can be checked. However, one weakness is that Cooper (2014) found a diagnosis of schizophrenia had a reliability estimate of 0.46 using DSM 5 compared to 0.81 in the DSM-III trial showing a significant reduction in the reliability of the manual.. This is a weakness because critics have argued that the specific wording in the DSM-5 diagnostic criterion has led to lower reliability in diagnosis. Overall, DSM-5 has been found to have high rates of reliability for many disorders including OCD and PTSD. This is a strength because receiving a reliable diagnosis where two clinicians are in agreement ensures that the patient will be given the correct treatment to help reduce their symptoms effectively. However, a final weakness is that the clinician’s experience and style of interviewing when using DSM-5 can significantly lower agreement rates between different clinicians assessing the same patient’s symptoms, particularly when a shorter time period is spent on the clinical interview. This is a weakness because it challenges the reliability of DSM-5. Validity of the DSM5 8 MARKER Evaluate the validity of the DSM classification system as a way of diagnosing mental disorders (8) The DSM-5 is a classification system that contains descriptions, symptoms, and other criteria for diagnosing mental disorders and is used predominantly in the USA and other westernised countries. A valid classification system includes symptoms that are operationalised and measurable such as people with schizophrenia having to have two or more symptoms over a month. There are different types of validity when considering diagnosis; predictive validity is established when we can accurately predict the outcomes for an individual for their diagnosis, e.g. their prognosis and reaction to treatment. Concurrent validity is established when a clinician uses more than one method or technique to reach a 13 diagnosis and both methods lead to the same diagnosis. One strength of the validity of DSM classification system comes from Kim-Cohen et al (2005) who found information obtained from interviews of children and their mothers; observations of the children’s anti-social behaviour; and questionnaires completed by the children’s teachers all led to the diagnosis of conduct disorder. This is a strength as it shows that the DSM-IV-TR has high concurrent validity as the methods used by the clinicians to reach a diagnosis, all lead to the same diagnosis for the children. However, one weakness is research from Kuyken (2008) who found that 75% of his participants stopped taking anti-depressants and more relapsed compared to CBT. This is a weakness because it shows that classification systems such as the DSM cannot predict who anti-depressants will work for therefore have poor predictive validity. Section III of DSM-5 relates to emerging measures and models and contains diagnostic categories that need more research before they are included in section II and recognised as a clinical disorder. One example is internet gaming disorder. It also contains information about being sensitive to cultural variations in diagnosis. DSM-5 now includes culture bound syndromes and recognises that some disorders are more likely to occur in specific cultures. When two people with the same diagnosis share similar causal factors, we can say the diagnosis has aetiological validity. One strength is that the DSM has been updated recently to improve the validity of diagnosis relating to schizophrenia; subtypes including paranoid and disorganised schizophrenia were removed in DSM-5 and replaced with a dimensional approach. This is a strength because it prevents clinicians from categorising patients and labelling their ‘type’ of schizophrenia which may have been too simplistic and did not lead to the correct treatment in older manuals. However, one weakness of the DSM is that different clinicians will use the criteria outlined in the manual differently depending upon their level of experience. This is a weakness because it may lead to a diagnosis being made that is not valid because it has been clouded by inexperience of younger clinicians or in the case of older clinicians, a reluctance to shift from their experience using the older classification systems. Overall, the DSM-5 now includes culture bound syndromes and recognises that some disorders are more likely to occur in specific cultures. This is a strength because reflecting cross-cultural differences in symptoms and more information about cultural concepts of distress will increase the validity when diagnosing patients from different cultures. However, a weakness is that the BPS has expressed concern about DSM-5 which requires social norms to be considered when making a diagnosis. This is a weakness because it leaves the process open to some degree of subjectivity regarding the clinician’s judgements and therefore challenges the validity of DSM-5. 14 ICD-10 The ICD is a classification system created by the World Health Organisation (WHO) and used worldwide by clinicians to diagnose all diseases, not just mental health disorders. The aim of the ICD is to improve healthcare across the world by allowing countries to share statistics on incidences of illness and mortality rates. The current version of the ICD is version 10 which was first published in 1995. It is available online (free) and is published in 43 different languages (multilingual). ICD-11 is currently in development and is due to replace version 10 in January 2022. ICD-10 contains 22 different sections addressing different categories of diseases. Section V refers to mental and behavioural disorders. Each section addresses both the mortality rates for the disease and the morbidity rates (number of people with this disease in the population). Section V details the classification of over 300 mental and behavioural disorders. It has been published following extensive field trials by more than 100 clinicians and research centred in 40 countries. Within section V clinical descriptions and diagnostic guidelines are provided which detail principle signs and symptoms of each disorder as well as comprehensive guidelines for their diagnosis. Within section V the ICD groups each disorder in a 'family'. E.g. Depression is part of the family of mood disorders (which is F3). It then uses different codes to identify the specific type of depression. E.g. F31 is bipolar disorder. In 2010 the UK government made a commitment to update ICD-10 every 3 years. The UK is currently using ICD- 10 (5th edition) which was published in 2016. Table to compare ICD-10 with DSM-5 ICD-10 DSM-5 Produced by WHO Produced by the APA Free and open resource Revenue source for the APA Multi-lingual English only Covers all diseases Only covers mental disorders AO3 One strength is that ICD-10 is used significantly more than DSM-5 by psychiatrists around the world (70% compared to 23% in a study by Reed et al, 2011) suggesting it is more user-friendly and accessible. This is likely due to the fact it is a free resource and is multi-lingual. Another strength is that Hiller et al (1992) gave case notes of 100 psychiatric patients with symptoms of schizophrenia to 4 different clinicians and asked for a 15 diagnosis. Found an 80% rate of agreement using the ICD-10 when diagnosing schizophrenia showing reliability for this manual. A further strength is that ICD-11 has a more sophisticated structure than the ICD-10. With around 55,000 codes that can be used to classify diseases, disorders, injuries, and causes of death, the ICD-11 offers a fine level of detail in coding these illnesses. A further strength is that Pihlajamaa et al (2008) found that when ICD-10 is used to diagnose schizophrenia the diagnosis matches a diagnosis using a different classification system, which suggests it is a valid diagnostic tool. A final strength is that ICD-10 is produced by a global health agency (WHO) and provides very specific detail for diagnosis of disorders which enables practitioners to do more research into the causes of mental illness and ultimately advances medical technology in helping to develop cures. This suggests the manual is useful in many countries for diagnosing disorders. One weakness is that when comparing classification systems, Andrews (1999) found only 68% agreement between clinicians when using ICD-10 and DSM-IV to diagnose the same symptoms in 1500 patients. This shows poor reliability between the two manuals. Another weakness is that Cheniaux et al (2009) found that schizophrenia was diagnosed more frequently when using ICD-10 than when DSM-IV was used which suggests a lack of reliability between the two systems. This difference may be due to the duration of symptoms – six months for DSM and one month for ICD. A further weakness is that ICD-10 CM (American version) has been criticised for including a long list of codes which are confusing and some for behaviours which are rarely seen. E.g. being struck by a cow and burns due to water skis on fire. This would make the manual less user-friendly. A further weakness is that Jansson et al (2002) studied the concurrent validity of ICD-9 and ICD-10. 155 patients in Copenhagen were assessed between 1998 and 2000.ICD-10 was found to be less valid than ICD-9 when diagnosing schizophrenia. Therefore, the newer version of the ICD is deemed as losing accuracy in diagnosis. A final weakness is that despite the fact the ICD has been reviewed and updated since its creation; this has not been done as frequently as DSM and for this reason, recent changes in mental disorders are not reflected in the categories. For example, ADHD is not in ICD-10 but is in DSM-5. This suggests that the manual is outdated and may not be an accurate system for producing accurate diagnosis of disorders. SCHIZOPHRENIA SPECIFICATION REQUIREMENTS 16  5.1.3 Describe symptoms and features, including thought insertion, hallucinations, delusions and disordered thinking. Schizophrenia is a mental illness that can affect the way someone thinks, speaks, or feels to such a degree that they lose their grip on reality. There are a number of symptoms and features of schizophrenia. Symptoms refer to things that characterise a disorder with regard to how the person thinks, feels, or behaves. Features refer to facts about the disorder such as statistics, how the illness develops and age and gender differences. Symptoms of schizophrenia Delusions are false beliefs and refer to an individual thinking their movements are being controlled by someone else. An individual experiencing paranoid delusions or delusions of persecution believes that someone is trying to mislead, manipulate or harm them. An individual experiencing delusions of grandeur believes that they are in a position of power or possess special powers. Other delusions may involve an individual thinking that unrelated things are intended to relate to them, e.g. a newspaper headline. Thought insertion is a specific example of a delusion whereby an individual believes that their thoughts have been implanted by some kind of external force over which they have no control. Hallucinations involve seeing, smelling, or hearing things that are not there. The most common type of hallucinations is auditory (hearing voices). For example, an individual may hear critical voices giving a commentary on what they are doing, or they may hear controlling voices telling them what to do. Disordered thinking results in an individual finding it difficult to put their thoughts into logical sense; thoughts are loosely connected, and this is reflected in the person’s speech. The individual will randomly skip from topic to topic during conversation and will answer questions with bizarre statements that do not seem to fit. Delusions, hallucinations, thought insertion and disordered thinking are all examples of positive symptoms which may be viewed as additions to behaviour. Examples of negative symptoms (the absence of something) include apathy and flatness of emotions. 17 Features of schizophrenia Schizophrenia is an example of a psychosis meaning that the individual has lost touch with reality. Schizophrenia is found in any nation at a rate of about 1% of the population. Of these individuals diagnosed with schizophrenia the breakdown is as follows: Schizophrenia 25% Continuous symptoms throughout life 25% One episode only and recovers 50% 25% Alternate periods of symptoms 25% and recovery 50% For males, the age of onset is typically late teens to early twenties whereas for females, this is in their late twenties. The life expectancy for individuals with schizophrenia is typically ten years less than average. When diagnosing schizophrenia using DSM-V, at least 2 of the 5 symptoms listed below must be present for at least one month. One of the symptoms must come from the first three on the list: 1. Delusions; 2. Hallucinations; 3. Disorganised symptoms; 18  4. Grossly disorganised or catatonic behaviour; 5. Negative symptoms. SPECIFICATION REQUIREMENTS 5.1.3 The function of neurotransmitters as a theory/explanation for schizophrenia. One biological explanation for schizophrenia is the function of neurotransmitters such as dopamine and glutamate. Dopamine is a neurotransmitter. It regulates how often synapses in the brain fire and this regulates the number of messages that the brain sends. The link between dopamine and schizophrenia was discovered when dopamine increasing drugs, like amphetamines, were found to produce schizophrenic symptoms. A high level of dopamine is called hyperdopaminergia. This causes too many synapses to fire resulting in too many messages been sent around the brain. This can cause schizophrenia symptoms. Along with this, hypodopaminergia is a lack of 19 dopamine that causes too little messages to be sent, which also causes schizophrenia symptoms. Positive symptoms of schizophrenia are thought to be caused by over-activity in the mesolimbic pathway. This involves the nucleus accumbens and the ventral tegmental area. Positive symptoms can include hallucinations, delusions, and disordered thinking. Negative and cognitive symptoms of schizophrenia are linked to under-activity of the mesocortical pathway. This involves the cortex and the VTA. These symptoms include memory loss and social withdrawal. Furthermore, glutamate seems to regulate the behaviour of dopamine; glutamate deficiency can result in elevated dopamine levels. AO3 One strength is that PET scans can be used to investigate the link between schizophrenia and neurotransmitters. People with schizophrenic symptoms can be scanned in order to see how many dopamine receptors are firing to establish a link. However, PET scans can be considered invasive as they involve the injection of a radioactive tracer. This could make them unsuitable for unstable schizophrenic patients. Another strength is that Seidman showed how hyperdopaminergia can be linked to schizophrenia through the post mortems of schizophrenic patients. He found they had more dopamine receptors in their brains thus supporting the explanation. Despite this though, the patients were dead, so it is impossible to see the dopamine receptors working in line with their symptoms, decreasing the validity of the test. A further strength is supporting evidence for the neurotransmitter explanation comes from the drug Levodopa. It is used to treat Parkinson’s patients by increasing dopamine levels. Through long term use, users of Levodopa experienced positive symptoms of schizophrenia. However, this proof can arguable only be generalised to Parkinson’s patients. A further strength of the neurotransmitter explanation is that it can be considered very scientific. This is because objective data can be obtained using brain scans to measure receptors. Objective, quantitative data is comparable. I&D Psychology in Society: A final strength is the development of a group of drugs called Phenothiazines in the 1950s which was important in reducing the use of controversial treatments such as ECT and lobotomies to treat schizophrenic patients. These drugs work by blocking dopamine receptors to prevent the effects of excess 20 dopamine. The effectiveness of these drugs in reducing the symptoms of schizophrenia supports the idea that excess dopamine is a cause of schizophrenia. A weakness of the explanation is that many tests on this hypothesis are conducted on animals. Experiments such as lesioning animal’s brains propose generalisation issues because of the differences between animal brains and humans. Animals may react differently when given more dopamine. However, it isn’t possible to lesion human brains due to ethical issues, so animal experiments are arguably the only practical option. Another weakness is that Carlsson refuted the idea that dopamine alone causes schizophrenia by claiming glutamate had a bigger role to play in the onset of schizophrenia. He stated glutamate regulates dopamine levels. Carlsson’s research is supported by the fact he complied a large amount of evidence from 33 studies in his review, creating a large sample. A further weakness is that the direction of effects is unclear. As neurotransmitters are only investigated at the onset of psychosis in schizophrenic patients, it is unclear if schizophrenia causes abnormal dopamine levels or if it’s the other way around. I&D Reductionism: A further weakness is that the neurotransmitter explanation may be criticised for being biologically reductionist, isolating a few specific neurotransmitters as the cause of schizophrenia. This ignores other biological factors which may be linked to the onset of schizophrenia, e.g. genes. Nature Nurture Debate: A final weakness is that this explanation only focuses on biological factors (neurotransmitters) which are due to nature and not nurture. The neurotransmitter explanation does not acknowledge environmental and social factors such as social class and urbanicity which may trigger the onset of schizophrenia. SPECIFICATION REQUIREMENTS 5.1.3 One other biological theory/explanation for schizophrenia (Genetics) 21  One other biological explanation for schizophrenia is genetics. This theory suggests that a person’s genetic makeup determines whether they develop schizophrenia or not. It is suggested that genes exist which predispose individuals to schizophrenia and such genes may run in families. Research using family studies has shown that schizophrenia has a very significant genetic component. These studies look at first, second and third degree relatives; first degree relatives share 50% of their genes, second degree 25% and third degree 12.5% For example, those who have a third degree relative such as a cousin with schizophrenia are twice as likely to develop schizophrenia as those in the general population (1%). This likelihood increases in line with the amount of genes shared with family members who have schizophrenia. Those with a second degree relative such as an uncle or aunt who has schizophrenia, have a several-fold higher incidence of schizophrenia than the general population. If an individual has a first degree relative with schizophrenia such as a parent or a sibling, they have a much higher chance of developing the disorder too (around 10% more than the general population) Another way of researching whether schizophrenia has a genetic component is by using twin studies. If one twin has schizophrenia and the condition is inherited, it would be expected that for MZ twins the other twin would be more likely to have the disorder too, but with DZ twins this would be less likely. This is supported by concordance rates whereby an identical (MZ) twin whose sibling has schizophrenia is between 50- 60% more likely to develop schizophrenia compared to the general population, whilst for DZ twins this is around 15% showing a correlation between the amount of genes shared and likelihood of developing the disorder. 22 Finally, the findings from adoption studies can also be useful in helping to establish whether schizophrenia has a genetic component. Such research is conducted by studying an adopted person who has developed schizophrenia and finding out if their biological parents also developed schizophrenia. AO3 One strength is that Heston (1966) studied individuals who were born between 1915 and 1945 to schizophrenic mothers and adopted from birth. The rate of schizophrenia in those born to schizophrenic mothers was 10.6% compared with 0% in those not born to schizophrenic individuals. This supports the concordance rate evidence for a first degree relative. Another strength is that Tsang et al (1999) conducted a case study of 12 adults who were first degree relatives of patients with schizophrenia. They were evaluated for negative symptoms and cognitive symptoms of schizophrenia. Tsang found that it was possible to both identify such symptoms and potentially reverse these using a drug called Risperidone. This supports the genetic component of schizophrenia in first-degree relatives. A further strength is that Gottesman et al. (1966) found a relationship between genetic similarity and the probability of two people both having schizophrenia. They identified a concordance rate of 42% for MZ twins and 9% for DZ twins. This is a strength because the greater rate for MZs shows that while schizophrenia is not entirely a genetic disorder, biology certainly plays a significant role. I&D 23 Psychology in Society: A further strength is that recognising the genetic aspect of schizophrenia is important for people with a history of schizophrenia in their families. It alerts them that they are at higher risk of developing the disorder themselves. Based on this information, they could avoid stressful occupations or drug use that might trigger the condition. If the symptoms of schizophrenia are recognised early enough (before a psychotic episode occurs), then the disorder can be managed much more effectively. Psychology as Science: A final strength is that the genetic explanation for schizophrenia is based upon objective data obtained from genetic testing and concordance rates. Such data removes subjectivity, therefore increasing the scientific credibility of this explanation. One weakness is that twin studies and adoption studies do not show 100% concordance in people with the same genes. This suggests that something non- biological is at work too, like the environment a person lives in. Genes may give a person a predisposition to develop schizophrenia but a trigger (such as stress) is needed to bring the symptoms out (this is Rosenthal's diathesis-stress model of schizophrenia). Another weakness is that Seidman showed how hyperdopaminergia can be linked to schizophrenia through the post-mortems of schizophrenic patients. He found they had more dopamine receptors in their brains therefore refuting the idea that schizophrenia is simply genetic in origin. A further weakness is that Cooper (2005) found that for single men the rate of schizophrenia in unskilled labourers was more than four times higher than those in managerial positions supporting the idea that social class is a feature in the onset of schizophrenia rather than genes. I&D Reductionism: A further weakness of pinpointing genes as an explanation for schizophrenia is that it is an example of genetic reductionism, focusing on parts rather than on the ‘whole’ characteristic in question. Such genetic explanations ignore environmental factors such as nurture and the role that parenting and stressors may play in the onset of schizophrenia. Nature-nurture debate: A final weakness is that studying individuals who live in the same environment and who share genes make it impossible to separate out the influence of nature and nurture upon the development of schizophrenia. For example, there are both shared genes and shared environmental experiences which may lead to schizophrenia and it is difficult to isolate either. 24  SPECIFICATION REQUIREMENTS 5.1.3 One non-biological theory/explanation for schizophrenia (Social explanation: Social Causation Hypothesis) One non-biological theory/explanation for schizophrenia (Social explanation: Social Causation Hypothesis) The human world (people around you) is a major cause of schizophrenia or a relapse into schizophrenia. Many environmental risk factors (stressors) contribute. People with a genetic pre-disposition to schizophrenia may develop schizophrenia as a result of the stressors acting as a trigger. Social causation hypothesis suggests that a possible biological vulnerability for schizophrenia only develops if social factors create stress. Furthermore, lower social class patients are more likely to be brought to get medical help by the police or social services and to become admitted as long-term schizophrenic patients. One example of this is social adversity (failure to meet needs, can be stressful), such as unemployment or poverty. Some children grow up in unfavourable environments; this makes them vulnerable to mental health disorders in the future. People from lower socioeconomic groups may not be able to access treatment, this makes their problems worse. Social isolation is where people with schizophrenia withdraw, as they find contact with others stressful. Self-imposed isolation cuts them off from feedback about what behaviours or thoughts are inappropriate and they begin to behave ‘strangely’ without this corrective feedback. Urbanicity is another factor linked to schizophrenia. High population density makes life more competitive, which may increase the experience of chronic social defeat (a stressor that occurs when a person is exposed to hostile confrontations). City life is more stressful than rural life with more noise, light pollution, criminality, faster pace, and anonymity. Long-term exposure may make a person more vulnerable to having an episode of schizophrenia. Immigration and minority status suggest that in many countries, first and second generation immigrants are at greater risk of schizophrenia. Minority status or marginalisation of out-groups may leave people vulnerable to schizophrenia. Second generation may be more at risk due to having a weaker cultural identity; they have learned to fit in with norms of indigenous society; beliefs and expectations are at 25 odds with parents and extended family leads to increased stress and increased vulnerability to schizophrenia. AO3 One strength is that Eaton (2000) found through a meta-analysis of 17 studies that the rate of schizophrenia is much higher in lower-class areas than in upper-class areas, therefore supporting the social explanation of schizophrenia. Another strength is that Cooper (2005) found that for single men the rate of schizophrenia in unskilled labourers was more than four times higher than those in managerial positions supporting the idea that social class is at least a feature in the onset of schizophrenia. A further strength is that Vassos et al (2012) analysed data from 4 studies (Sweden, Netherlands, Demark) to correlate location (urban to rural) with schizophrenia risk. The risk was 2.37 times higher for people living in the most urban environments compared with the most rural. I&D Holism: A further strength is that it has been noted that the social causation hypothesis of schizophrenia is a more holistic explanation because it takes into account both social and biological factors. For example, it suggests that individuals who already have a genetic predisposition to schizophrenia, through biology, and are exposed to environmental stress, through social aspects, are more likely to develop schizophrenia. Psychology in Society: A final strength is that treatments have been developed around this social explanation to tackle the issues with social adversity. For instance, care in the community is a way of allowing schizophrenic individuals to live in society whilst also taking their medication, therefore treating schizophrenia in both a social and biological way. One weakness is that Carlsson (2000) challenges the social causation hypothesis suggesting that schizophrenia is due to an imbalance of neurotransmitters whereby hypoglutamatergia consequently leads to hyperdopaminergia. This challenges the importance of social adversity factors. Another weakness is that Goldberg & Morrison (1963) found that the excess of patients with schizophrenia in the lower social classes was mainly attributable to 26 them drifting down the social classes at the onset of psychosis. This evidence therefore challenges the notion that social factors cause the onset of schizophrenia. A further weakness is that Gottesman and Shields (1966) supports a genetic explanation of schizophrenia with a concordance rate of 54% for MZ twins showing that social causation is not a complete explanation for schizophrenia. I&D Psychology as Science: A further weakness is that despite suggesting causation, it is not possible to determine that low social class does cause schizophrenia since many such individuals in the lower social classes do not have the disorder. Therefore, research is only correlational which challenges psychology as a science. Psychology as Science: A final weakness is that the neurotransmitter explanation may be viewed as more credible than the social causation hypothesis since it is based upon evidence from brain scans, animal and humans in laboratory experiments (i.e. Carlsson). Evidence for the social causation hypothesis may come from self-report data and meta-analysis which uses secondary data and may therefore lack validity. SPECIFICATION REQUIREMENTS 5.1.4 One biological treatment for schizophrenia (antipsychotics). Antipsychotics were initially developed in 1950 and were designed to replace biological therapies such as electroconvulsive therapy, insulin coma, frontal lobotomy, and simple sedation, causing an important revolution in psychiatric practice. The aim of antipsychotic medication is to help restore the balance of neurotransmitters such as dopamine, in the brain. This is achieved by prescribing the treatment as tablets or an injection (given every 2 to 4 weeks). The injection releases the medication slowly over this time and the effects are generally the same as medications taken by mouth. 27  Earlier antipsychotics were classified as ‘typical’ or first generation whilst more recent antipsychotics are classified as ‘atypical’ or second generation. First generation or typical antipsychotics were those first developed in the 1950s. The most common typical antipsychotic was Chlorpromazine which belongs to a category of drugs called Phenothiazines. Their mode of action is to block D2 receptors in the dopamine pathways of the brain. They are described as being ‘neuroleptics’ because they act at the neuron. These antipsychotics were more effective in reducing positive symptoms producing the maximum benefits within the first 6 months of treatment. Second generation or atypical antipsychotics first emerged in the 1980s. One of the most common atypical antipsychotics is Clozapine. Their mode of action is to Increase the release of dopamine but also work on serotonin, acetylcholine, and glutamate levels. Clozapine seems to be the most effective antipsychotic and has been found to reduce suicidal feelings in people with schizophrenia and causes hardly any of the stiffness, shakiness, or slowness that you can get with other antipsychotics. These antipsychotics were effective in reducing negative and cognitive symptoms. The recommendation is to try second generation antipsychotics first before resorting to first generation drugs as most people find the side effects less troublesome than those of the older medications. Most people take medication for 1 or 2 years after their first psychotic episode to prevent further acute schizophrenic episodes occurring, and for longer if the illness is recurrent. This is likely to be combined with a psychological therapy too such as CBT or family therapy. AO3 One strength is that antipsychotic drugs are viewed as both a cheaper and more ethical way of treating patients who may previously have been institutionalised or treated with electroconvulsive therapy. The drugs allow the patient to remain living in the community whilst accessing other therapies. Another strength is that Meltzer et al (2004) studied 481 patients who were divided into two groups: placebo or haloperidol (antipsychotic) for six weeks. He noted a 28 significant reduction in symptoms for those taking haloperidol compared to the placebo group showing the effectiveness of the antipsychotics. A further strength is that antipsychotic drugs have a rapid effect in comparison to other types of therapy such as counselling because patients can be relieved of some symptoms in a matter of weeks. Furthermore, antipsychotics are often more easily accessible from the NHS whereas psychological therapies may have extended waiting lists. A further strength is that Leucht et al (2018) conducted a meta-analysis consisting of over 6,000 patients with schizophrenia. He compared the rates of re- hospitalisation for those given antipsychotics (10%) with those given a placebo (26%) suggesting that medication was effective in reducing symptoms of schizophrenia. I&D Holism: A final strength is that the most effective approach to treating schizophrenia appears to be to take an ‘eclectic’ or more holistic approach by combining the medication to correct the levels of neurotransmitters, and counselling such as CBT or family therapy, to address the possible stressful triggers which may also be involved in the onset of symptoms. One weakness is that some people would argue that antipsychotics are palliative and not curative meaning that they do not address the cause of the patient’s schizophrenia, only masking the symptoms. This means that the treatment is not fully effective. Another weakness is that antipsychotics often produce unpleasant side effects which themselves often require further drug treatment. Side effects of antipsychotic drugs include, weight gain, shaking (Tardive Dyskinesia) and tiredness. Such side effects may make the patient feel physically unwell. This may subsequently explain the low compliance rates in patients taking antipsychotics. A further weakness is that Rosa et al (2004) found that only 50% of patients comply consistently with their medication regime for schizophrenia which can often lead to relapses and re-admittance to hospital. This may be due to forgetting, or a deliberate avoidance due to unpleasant side effects from the drugs. This therefore questions the effectiveness of antipsychotic medication as the best treatment for schizophrenia. I&D Social Control: A further weakness is that some people argue that antipsychotics are ‘chemical strait-jackets’ and believe that prescribing such medication is a form of 29 social control whereby doctors can enforce compliance to the medication regime through sanctions such as sectioning patients. This would therefore question the ethics surrounding the prescription of antipsychotic medication. Reductionism: A final weakness is that the use of antipsychotic medication as a treatment for schizophrenia may be challenged for being too simplistic and reductionist. Simply adjusting levels of neurotransmitters does not address other social factors which may play a role in the onset of schizophrenia, for example social isolation and social adversity. SPECIFICATION REQUIREMENTS 5.1.4 One psychological treatment for schizophrenia (Assertive Community Treatment). In the 1980s many patients were discharged from large psychiatric hospitals as a result of deinstitutionalisation and a move to care in the community (including programmes such as Assertive Community Therapy or ACT). The rationale behind this move, was to firstly reduce expenditure and secondly, to stop the issues associated with hospitalisation, such as isolation from society. This created a need to offer support and treatment for individuals with mental health disorders within the community. Care in the community is designed to encourage integration which will helps patients to adjust to the norms of the wider community and address any problems associated with social adversity e.g. lack of housing or access to amenities. ACT is used particularly to help patients with schizophrenia who experience frequent relapses and bouts of hospitalisation. Such patients may have difficulties socialising and living independently therefore ACT aims to help them to address these issues. The purpose of ACT is to treat patients in real-life settings with a commitment to spend as much time as necessary with each patient to support them with their individual requirements. The approach taken to treatment is multidisciplinary, with a team of professionals such as psychiatrists, nurses and social workers sharing the workload. Patients have access to care and support 24 hours a day and can access crisis intervention if needed. Each patient will have an individual care plan which is regularly reviewed, and care will remain in place for as long as is required. 30 Practical support would be provided such as making sure the patient attends medical appointments and takes their medication, assistance with shopping and help with organising their finances. This will make living independently easier for the patient. Emotional support is also provided in the form of group meetings and social events. Further interventions will also be integrated into ACT including social skills training and family therapy. AO3 One strength is that Leff (1997) found that symptoms/problems of institutionalisation tend to be reduced as a result of living and being treated in the community suggesting that ACT is an effective treatment. It is effective because patients are no longer isolated and restricted by strict routines. Another strength is that Bond (2002) found that ACT is effective across gender, age and culture. It is effective because only 11% of patients in surveys said they find their care restricting. A further strength is that Bond et al (2001) analysed 25 studies compared with standard community care ACT is highly effective. It is effective because it engages patients, prevents re-hospitalisation and increases housing stability. Furthermore, the use of a meta-analysis means access to a larger database leading to consistency in the findings. However, such data is secondary data and therefore the validity of the findings may be questionable. I&D Holism: A further strength is that ACT provides a holistic approach to treatment and involves the client in the decisions being made making it a more effective treatment. It is effective because it does not simply rely upon medication; it incorporates social support, practical help and family therapy. Furthermore, it attempts to tackle the root cause of schizophrenia, namely, the social adversity factors. Ethics: A final strength is that ACT removes the ethical issues associated with earlier, invasive treatments for schizophrenia given to patients in institutions; for example, lobotomies and electroconvulsive therapy. This makes ACT a more ethical approach to treating patients with schizophrenia and consequently, a more effective treatment. One weakness is that critics of ACT argue that these programs do not effectively encourage the patient to live independently, and, despite the patient not being hospitalised, they are still subject to strict routines and rules and may also develop a dependence on their carers. Furthermore, it might just be the regular one-to-one interaction with staff which leads to a reduction in symptoms. Once this is removed, the symptoms may worsen. They may be using the staff as a ‘crutch’ meaning that ACT is not effective. 31 Another weakness is that ACT programs are often underfunded, and private companies are often used for home care sometimes leading to high staff turnover reducing the effectiveness of ACT. It is less effective because consistency of care and positive interpersonal relationships between the client and career are essential for such vulnerable people. A further weakness is that ACT programs are expensive to run but are underfunded meaning the treatment is less effective. ACT programs are less effective because they are more common in urban areas, and funding in these areas may be even tighter. Others have criticised ACT programs for taking funding away from hospitals where the patients could ultimately end up if ACT fails. A further weakness is that ICT may be less effective as a treatment for schizophrenia because it does not have an effect on actual functioning such as reducing positive and negative symptoms of schizophrenia therefore there is still a need for antipsychotics. This is less effective because it may mean the patient still experiences side effects from the medication which may lead to poor compliance to their medication regime. I&D Social Control: A final weakness is that Gomory (2001) proposed that ACT patients are often forced to surrender all responsibility for making their own decisions and taking care of themselves making ACT a less effective treatment. It is less effective because it poses an ethical debate regarding a person having control over decisions about them and may be viewed a form of social control. UNIPOLAR DEPRESSION SPECIFICATION REQUIREMENTS 5.1.3 Describe symptoms and features of one other disorder (unipolar depression). Unipolar depression is now referred to as major depressive disorder. The word ‘unipolar’ is used to indicate a disorder with one aspect, namely persistent low mood. It is a mood disorder which makes daily activities difficult for the individual. There are a number of symptoms and features of unipolar depression. Symptoms refer to things that characterise a disorder with regard to how the person thinks, feels or behaves. Features refer to facts about the disorder such as statistics, how the illness develops and age and gender differences. 32 Symptoms of unipolar depression Psychological symptoms e.g. loss of interest and pleasure. Physical symptoms Cognitive symptoms Unipolar e.g. disturbances in e.g. pessimism. depression appetite. Social symptoms e.g. avoiding social activities. Psychological symptoms (feelings/emotions) Psychological symptoms include extreme lethargy, low mood and sadness, irritability, loss of interest and pleasure, anxiety, and feeling tearful. The individual may experience of a loss of interest and pleasure in everyday activities; things which they used to enjoy doing no longer appeal to them, for example hobbies, exercise and social interactions. In its most extreme form this is called anhedonia whereby the individual lacks motivation or desire to engage in activities which they previously found pleasurable. Physical symptoms Physical symptoms include headaches, disturbances in appetite, agitation or slowing and disturbed sleep. 33 Disturbances in appetite: depression tends to suppress most biological functions and drives; hunger being one of these. This means that the individual often has a decreased motivation to eat resulting in weight loss. However, sometimes a depressed individual will exhibit hyper appetite and craving for food resulting in overeating and weight gain. These symptoms are considered in a diagnosis of depression if the disturbances in appetite produce a significant (5% or more) weight change. Social symptoms Social symptoms include problems at work, avoiding social activities, avoiding friends and difficulties with family life. In avoiding social activities, the individual may neglect their hobbies and interests, and will also avoid social interactions with friends and family. Consequently, relationships may become strained resulting further avoidance of situations where the individual needs to interact with others. Cognitive symptoms (thoughts) Cognitive symptoms include difficulties with memory and concentration, thoughts of guilt and low self-esteem, pessimism, thoughts of hopelessness or helplessness, suicidal thoughts, and thoughts of self-harm. The individual may be prone to bouts of pessimism which is a tendency to dwell on the negative aspects of a situation and ignore the good parts. Linked to this are thoughts of guilt such as the individual thinking that they are to blame for anything which has gone wrong. Naturally, both of these tendencies contribute to the lowering of self-esteem. Features of unipolar depression Unipolar depression is an example of a mood disorder. The characteristics of mood disorders are disabling moods. Approximately 10% of people in England will experience some type of depression in their lifetime. Of these individuals diagnosed with unipolar depression the breakdown is as follows: 34  Unipolar depression Will experience at least one more episode after recovery 35% 35% Chronic 15% 50% Full recovery after one episode 50% 15% Depression is around twice as common in women than it is in men. The most common age of onset for both men and women is between the ages of 25-44 years. DSM-V Criteria for Unipolar Depression/Major Depressive Disorder (MDD) When diagnosing unipolar depression (major depressive disorder) the individual must display depressed mood or a loss of interest or pleasure in daily activities for more than two weeks. The individual will also display at least 5 of these 9 specific symptoms nearly every day: 1. Depressed mood or irritable most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful) 2. Decreased interest or pleasure in most activities, most of each day 3. Significant weight change (5%) or change in appetite 4. Change in sleep: Insomnia or hypersomnia 5. Change in activity: Psychomotor agitation or retardation 6. Fatigue or loss of energy 7. Guilt/worthlessness: Feelings of worthlessness or excessive or inappropriate guilt 8. Concentration: diminished ability to think or concentrate, or more indecisiveness 9. Suicidality: Thoughts of death or suicide, or has suicide plan The Psychiatrist must screen for conditions that may mimic or co-exist with Major Depressive Disorder: Substance abuse causing depressed mood (e.g. drugs, alcohol, medications) Medical illness causing depressed mood Bereavement SPECIFICATION REQUIREMENTS 5.1.3 One biological explanation for unipolar depression (The Monoamine Hypothesis). 35 Monoamines are a group of neurotransmitters that contain amino acid; they are important for emotions and cognition. One biological explanation for unipolar depression is the monoamine hypothesis which suggests that depression results from a decrease in monoamine neurotransmitters such as dopamine, norepinephrine (also known as noradrenaline) and serotonin in the central nervous system. A decrease in serotonin has been linked to depression. Serotonin receptors are found in different central nervous system cells, for example the raphe nuclei. This area is important in regulating behaviour such as moods, sleep, and appetite. Messages are sent around such areas in the central nervous system by serotonin being released from the presynaptic neuron into the synapse. Receptors on the postsynaptic neuron pick this serotonin up and the message is transmitted. However, sometimes a process called reuptake occurs where the serotonin is taken back up into the presynaptic neuron therefore preventing messages from being transmitted effectively due to a lack of serotonin in the synapses. The primary role of serotonin is to regulate other neurotransmitters; without regulation erratic brain functioning and thinking patterns occur. Low levels of serotonin (which are believed to be inherited) can lead to low levels of norepinephrine, which is thought to produce decreased energy and concentration, both of which are common symptoms of depression. Other symptoms of depression such as disruption of sleep patterns have been linked to deficiencies in monoamine neurotransmitters. Furthermore, regarding dopamine, low levels of this neurotransmitter have been linked to reduced motivation and inability to feel pleasure and reward; again, common symptoms of depression. 36 AO3 One strength is Drevets et al (1999) who demonstrated that serotonin levels were reduced in the raphe nuclei of unmedicated depressives compared to controls using PET scans. This supports the idea that individuals with depression have irregular levels of serotonin. Another strength is evidence that decreased levels of dopamine are linked to depression has been found in animals exhibiting ‘learned helplessness’ (depressive behaviour). Such animals were found to have dopamine depletion in the nucleus accumbens supporting the monoamine hypothesis. A further strength is that autopsy studies show that people who have experienced multiple depressive episodes have fewer norepinephrinergic neurons than people who have no depressive history supporting the monoamine hypothesis. A further strength is that post-mortem studies show that people who have experienced multiple depressive episodes have fewer norepinephrinergic neurons than people who have no depressive history. This evidence supports the monoamine hypothesis demonstrating that patients with depression have less norepinephrine receptors which would mean less of this neurotransmitter in their brain. However, the direction of effects is unclear here since the patients’ brains were only examined after they had already developed depression. I&D Psychology in Society: A final strength is the development of anti-depressants such as SSRIs which have been significant in treating patients with depression. Previously, such patients were either locked away or treated using more controversial techniques such as ECT. One weakness is that experiments with pharmacological agents that cause the depletion of monoamines have shown that this depletion does not cause depression in healthy people nor does it worsen the symptoms in depressed patients therefore refuting the monoamine hypothesis. Another weakness is that Thase et al (2002) found that depressed patients (especially those with severe depression) had increased levels of norepinephrine, which is the opposite of what would be expected, therefore refuting the monoamine hypothesis. A further weakness is that antidepressant drugs which increase the levels of biochemicals immediately can take weeks before they alleviate the depression, which further challenges a direct link between the neurotransmitters and depression and refutes the monoamine hypothesis. 37 A further weakness is the diathesis–stress model which shows how biological or genetic traits (diatheses) interact with environmental influences (stressors) to explain the onset of mental illness such as depression. A biological predisposition for depression may be triggered by an external factor such as losing one’s job. This model therefore refutes the idea that biological factors such as neurotransmitter levels are the sole cause of depression and challenges the monoamine hypothesis. I&D Reductionism: A final weakness is that the monoamine hypothesis may be viewed as biologically reductionist focusing specifically upon the levels of monoamines in the brain. This explanation therefore ignores other possible causes of depression which may interact with the chemistry of the brain such as stress. SPECIFICATION REQUIREMENTS 5.1.3 One non-biological explanation for unipolar depression (Beck’s cognitive model of depression). A cognitive explanation for depression focuses upon the idea that distorted thinking is a possible cause. Beck developed the cognitive model of depression which considers 3 aspects of thinking (cognitive triad, cognitive errors and schemata) as 38 shown in the model below. Cognitive triad: negative views of self, world and future Beck's cognitive model of Schemata: depression Cognitive patterns of errors: faulty maladaptive thinking with thoughts and negative and beliefs unrealistic ideas Cognitive triad A depressed individual will have negative thoughts of self (feeling inadequate and unworthy), the world (all of my experiences result in defeats or failures) and the future (believing that suffering will continue and the future is hopeless). Schemata Schemata are built from experiences and lead to positive and negative beliefs about the world. Negative schemata may develop during childhood as a result of unpleasant experiences such as the death of a parent, parental rejection and bullying. A depressed individual will possess many negative schemata producing maladaptive thoughts and beliefs. For example, behavioural schemata that lead to withdrawal and inactivity and motivational schemata that lead to helplessness and lack of direction. Cognitive errors Cognitive errors are inaccurate thoughts which are used to reinforce negative thinking and serve to keep us feeling bad about ourselves A depressed individual will display faulty thinking and negative ideas. 39 One example of a cognitive error is overgeneralisation whereby if something bad happens once, the individual expects it to happen again next time they are in the same situation. A further example is catastrophising where the depressed individual always assumes the worst and expects disaster to strike. Beck proposed a direct relationship between the amount and severity of an individual’s negative thoughts and the severity of their depressive symptoms. In other words, the more negative thoughts they experience, the more depressed they will become. Beck asserted that a depressed individual will pay selective attention to aspects of their environment that confirm their negative beliefs. For example, a depressed individual will focus on one negative comment in a conversation and ignore all of the other positive elements. AO3 One strength is that Alloy and Abramson (1999) conducted a longitudinal study of the thinking styles of young Americans in their early 20’s for 6 years. Their thinking style was tested, and they were placed in either the ‘positive thinking group’ or ‘negative thinking group’. After 6 years the researchers found that only 1% of the positive group developed depression compared to 17% of the ‘negative’ group. These results support the cognitive model and the idea of negative thinking as an explanation of depression. Another strength is that Beck et al (1967) investigated the cognitive distortions in patients with depression and demonstrated that a number of themes appeared in the depressed patients’ thoughts that did not appear in non-depressed patients. These included low self- esteem and self-blame which supports the cognitive model. I&D Psychology in Society: A further strength is that the explanation led to the development of Beck’s Depression Inventory. This is a self-report questionnaire consisting of 21 multi-choice items relating to symptoms of depression such as feelings of guilt, fatigue, and weight loss. This is a strength because it provides a way of collecting quantitative data/scores about each patient allowing the clinician to establish the severity of their depression. Psychology in Society: A further strength is that the development of Cognitive- Behavioural Therapy (CBT) has been found to be effective in treating depression by focusing upon issues around negative schemata and thoughts and changing these to more positive thoughts. Its success in reducing the symptoms of depression supports the link between negative thoughts and depression. 40 Holism: A final strength is that the cognitive model may be viewed as being more holistic in explaining depression than other theories taking into account both environmental and cognitive factors. The role of early experiences in the development of negative schemata is acknowledged by the model, predisposing the individual to developing depression as an adult. One weakness is that Kendler found that concordance rates for depression in mono- zygotic twins were 76% whereas the concordance rates for depression in di-zygotic twins were 19%. These findings do point to genes being an important factor in the development of depression rather than cognitive differences therefore challenging the cognitive model of depression. Another weakness is that there is strong, scientific evidence from genetic testing that genetic inheritance and biological differences are much more important in the development of depression than cognitive causes therefore challenging the cognitive model of depression. A further weakness is that it is difficult to establish the direction of effects with regard to negative thinking and depression. Negative thoughts seem to disappear when depression stops, which may suggest faulty thinking comes with depression rather than being a cause of it. I&D Psychology as a Science: A further weakness is that it is incredibly difficult to measure thoughts and therefore the assumptions being made are often based upon data collected via methods such as thought diaries which are prone to being subjective. This would not be viewed as having scientific credibility. Comparisons: A final weakness is that the monoamine hypothesis has provided objective evidence for the presence of decreased monoamines using methods such as brain scans whereas the cognitive model relies upon evidence collected from self- report methods. This is a weakness because the monoamine hypothesis is likely to be viewed as more credible and scientific because levels of neurotransmitters can be objectively measured whereas measuring cognitions relies upon inferences being made. SPECIFICATION REQUIREMENTS 5.1.4 One biological treatment for unipolar depression (drug treatment) Anti-depressants are a form of drug treatment usually recommended for moderate to severe depression. Most people need to take anti-depressants for at least six months 41 to benefit fully from their effect and for 24 months if the depression is long-term or keeps coming back. The most prescribed category of anti- depressants are called Selective Serotonin Re-uptake Inhibitors (SSRIs). One of the most common of these drugs is Fluoxetine (trade name Prozac). Depression is associated with a decrease in serotonin levels. A process called reuptake occurs where the serotonin is taken back up into the presynaptic neuron therefore preventing messages from being transmitted effectively due to a lack of serotonin in the synapses. SSRIs work by blocking the ‘reuptake’ of the brain chemical serotonin. In the brain, messages are passed between two nerve cells via a chemical synapse, a small gap between the cells. The cell that sends the information releases neurotransmitters (of which serotonin is one) into that gap. The neurotransmitters are then recognized by receptors on the surface of the recipient cell, which upon this stimulation, in turn, relays the signal. About 10% of the neurotransmitters are lost in this process; the other 90% are released from the receptors and taken up again by monoamine transporters into the sending cell (a process called reuptake). To stimulate the recipient cell, SSRIs inhibit the reuptake of serotonin. As a result, the serotonin stays in the synaptic gap longer than it normally would and may be recognized again (and again) by the receptors of the recipient cell, stimulating it. AO3 One strength is that Karp and Frank (1995) found that drug therapy alone is just as effective for treating depression as combined therapy therefore supporting the 42 effectiveness of anti-depressants. However, it is worth noting that they are only effective with serious depression. Another strength is that Pinquart (2006) reviewed studies of anti-depressants and psychological therapies used to treat depression and found that whilst psychological therapies were more effective, drugs were cheaper and can be provided immediately whereas there is a waiting list for psychological therapies therefore supporting the use of drugs to treat depression. A further strength is that Delgado (2000) claims that the use of drugs such as SSRIs (which specifically work to increase serotonin levels) are effective, resulting in a reduction of symptoms. This is a strength because it supports the effectiveness of SSRIs as demonstrated by a reduction in symptoms of depression. A further strength is that Drevets et al (1999) found that serotonin levels were reduced in the raphe nuclei of unmedicated patients with depression compared to controls using PET scans. This is a strength because it supports the idea that patients who have not taken their medication have reduced serotonin levels leading to depression demonstrating that SSRIs are effective when taken because they artificially raise serotonin levels. I&D Ethical Issues: A final strength is that antidepressants may be seen as both a cheaper and more ethical way of treating patients who may previously have been institutionalised or treated with electro-convulsive therapy. The drugs allow the patient to remain living in the community whilst accessing other therapies such as CBT therefore supporting the usefulness of antidepressants as a treatment for depression. One weakness is that Hollon et al. (2005) compared relapse rates for CBT and antidepressants and found that only 31% of CBT patients suffered a relapse compared to 76% of those treated with drugs. This is a weakness because it shows that drug therapy is only palliative whereas cognitive therapy offers a better cure for depression. Another weakness is that Kirsch et al (2008) reviewed 47 trials of patients with mild or severe depression who were prescribed SSRIs or a placebo and found that SSRIs weren't any better than placebos when it came to mild depression. This is a weakness because it shows that some of the effectiveness of these drugs is imagined (placebo effect). A further weakness is that unpleasant side effects can be caused by the drugs, for example SSRIs can cause nausea, insomnia, anxiety, dizziness, weight gain, nervousness and even depression. Furthermore, SSRIs can lead to withdrawal 43 symptoms such as insomnia, aches and pains therefore highlighting problems with prolonged use of anti-depressants. A further weakness is that SSRIs do not actually cure depression they merely ease the symptoms (palliative). Therefore, when a patient does stop taking the medication there is a strong possibility that they will relapse into depression highlighting the problems with using anti-depressants as a treatment. I&D Social Control: A final weakness is that Smith (2012) refers to ‘inappropriate prescribing’ of drugs such as SSRIs whereby using drug treatment seems to be the first choice but may not be the best choice. Drugs can be inexpensive for society and can control behaviours which society does not want; therefore drug therapy is a form of social control. Doctors are able to enforce compliance to the medication regime through sanctions such as sectioning patients and using their power to ensure that patients will accept the treatment. SPECIFICATION REQUIREMENTS 5.1.4 One psychological treatment for unipolar depression (CBT). Cognitive-behavioural therapy (CBT) comes under the umbrella term of psychotherapy. CBT deals with current problems, rather than focusing on issues from the past. It was developed from Beck’s cognitive model of depression and works upon the principles of replacing negative automatic thoughts with new ways of thinking. This change in thinking will in turn change the behaviour of the client. The client will be asked to initially commit to six session of CBT with each session lasting around 50 minutes. Sessions may be carried out individually, in a group with other people who may have similar problems or more recently through computer programmes e.g. ‘Beating the Blues’. For each session, the client is actively involved and will decide which issues they would like to raise with the therapist. Initially this will