Clinical Theory Flashcards
what is clinical psychology?
Clinical Psychology is about diagnosing, explaining & treating mental illness. A range of psychological difficulties are dealt with including anxiety, depression, relationship problems, child & family problems & other serious mental health problems. We will be specifically focusing on schizophrenia & OCD (Obsessive Compulsive Disorder) which are both common mental health disorders in the UK today.
diagnosis explanation in terms of clinical psychology?
To assess a client, a clinical psychologist may undertake a clinical assessment using a variety of methods including psychological tests, interviews & direct observation of behaviour. Assessment may lead to therapy, counselling &/or advice.
Diagnosing a mental disorder is complex & can be both unreliable & invalid. Often there is no physical evidence & diagnosis relies on a list of symptoms & features that have to be present (E.g. To diagnose a phobia, there needs to be an intense & irrational fear, not just a fear. A fear becomes a phobia when it stops the person living their life successfully). These diagnoses are also often subjective, such as looking at how long the patient has been suffering, this adds to the complexity of diagnosis.
how do we explain mental health issues
Explanations for mental disorders are often not fixed or definite and there is often more than one explanation for a particular disorder. It could be argued that if there is more than one explanation, then this indicates more than one disorder. Perhaps there is a label attached to certain symptoms that are then thought of as one disorder (E.g. Schizophrenia can be caused by a single bad experience, this is called reactive schizophrenia. However, schizophrenia can be genetic, as there can be many cases of schizophrenia in one family. Also, the dopamine hypothesis suggests that schizophrenia is caused by the presence of excess dopamine).
how do we treat disorders
There are lots of ways of treating mental disorders including drugs, ECT (Electro Convulsive Therapy), psychotherapy, CBT (Cognitive Behavioural Therapy) & systematic desensitisation amongst many others. Some are used on their own & others are combined together to give the most effective treatment.
strengths and weaknesses of deviation from a statistical norm
Strengths:
- Patterns & trends of a mental health disorder can be plotted to see if certain disorders are getting more or less common in society. This gives a scientific & objective measure of a mental health issue or disorder based on a quantitative statistical norm value meaning that it can be compared over time.
Weaknesses:
- Deviations from the statistical norm that are above average are as uncommon as those below average. However, we would not always call someone ‘abnormal’ if
they scored high on a scale, therefore the term ‘abnormal’ is associated with negative stereotypes & may have a significant effect on those who are labelled ‘abnormal’.
- Some mental disorders are not statistically rare enough to be defined as ‘abnormal’ (E.g. Phobias). However, just because lots of people suffer from them this does not mean they are less important or that those suffering from them should be given less care.
explain deviation from a statistical norm
Abnormality can be defined as a ‘deviation from a statistical norm’. This provides a statistical (numerical) point of view where abnormality is any substantial deviation from the statistically calculated average. This is commonly seen with dyslexia, where ‘scores’ can be plotted & statistical deviations from the mean score can then lead to determinants of abnormality.
explain deviation from a social norm
Norms are expected ways of behaving in society according to the majority. Those members of society who do not think & behave like everyone else break these norms & are often defined as ‘abnormal’. The deviation from the social norm is built from these principles & is a socially based definition. Abnormal behaviour is seen as vivid & unpredictable, it causing observer discomfort & violates moral or ideal standards because this differs from what most people do. It is a process of comparing a person to others in their social world.
This suggests that mental illness can be considered socially constructed. Meaning that it differs from society to society & may change over time (E.g. Homosexuality was once considered to be a mental health disorder, but over time, as the norms of society have changed, it is no longer considered to be a disorder).
strengths and weaknesses of deviations from the social norm
Strengths:
- The idea that abnormality is a deviation from the social norm is appealing to clinicians, as that is how we think of abnormality. It fits in with human logic regarding illness because if people are behaving ‘strangely’ we think of them as abnormal, as they are not doing what we expect.
- Social norms are culturally specific & can differ from generation to generation, ethnic group, region & socio-economic group (E.g. A modern rave or the punk movement would have been seen as abnormal in the 19th century). This means that an objective measure across different cultures & generations is impossible.
Weaknesses:
- Luhrmann Et Al (2015) carried out a study of hallucinations & found that in some cultures hearing voices was considered a negative experience, whilst in others it was seen as a positive experience. Therefore, the social norms of a culture or community may determine not only your diagnosis, but your actual experiences of a mental health disorder.
- One issue with the deviation from social norms definition of abnormality is the idea of cultural relativism. Social norms differ between cultures & what is considered normal in one culture may be abnormal in another (E.g. As of 2024, there are 64 countries in the world, in which homosexuality is still illegal & therefore considered abnormal. However, in the rest of the world it is considered normal). The result of this is that there is no global standard for defining behaviour as abnormal & therefore abnormality is not standardised.
explain failure to function adequately and strengths
Failure to Function Adequately:
The failure to function adequately definition considers a person to be abnormal if they are unable to cope with the demands of everyday life. They may be unable to perform the behaviours that are necessary for day-to-day living (E.g. Self-care, holding down a job & interacting appropriately with others). Rosenhan & Seligman (1989) suggest the following characteristics that define failing to function adequately:
- Suffering.
- Maladaptiveness (Being a danger to themselves).
- Unpredictability & loss of control.
- Irrationality & Incomprehensibility.
- Causes observer discomfort.
- Violates moral & social standards.
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Many people engage in behaviour that is harmful or threatening to themselves, but we don’t class them as abnormal (E.g. People that smoke, drink alcohol or partake in adrenaline sports). One way of defining if someone is abnormal, is by seeing whether they can function to a reasonable standard & asking whether they are able to do the basic things that are needed to function in day-to-day life (E.g. Someone might be considered abnormal if they are so paranoid, that they can’t leave they homes. This would be considered as functioning inadequately & so they may have a mental abnormality. However, a person may be paranoid, but this doesn’t prevent them from living a reasonably normal life as they may still be able to do the things that are necessary for everyday living, so this definition would say that they are functioning normally).
Strengths:
- The failure to function adequately explanation helps to explain why different cultures have alternative ideas about what is abnormal behaviour & it takes into account that there is no universal rule about what is ‘abnormal’. This helps to increase the validity of diagnosing patients accurately.
strengths and weaknesses of deviation from ideal mental health
Strengths:
- Jahoda’s definition takes a positive & holistic stance in general. The definition focuses on positive & desirable behaviours, rather than focusing on negative & undesirable behaviours. Also, the definition considers the whole person, taking into account multiple factors that may affect their health & well-being. Therefore, the definition is comprehensible & covers a broad range of criteria.
Weaknesses:
- One weakness of the deviation from ideal mental health definition of abnormality is that the criteria proposed by Jahoda is unrealistic. There are times in everybody’s life when they will experience stress & negativity (E.g. When grieving the death of a loved one). However, according to this
definition, these people would be classed as abnormal as they circumstances are not taken into account, even if they are out of the individuals control. The standards set by the criteria are very high & it would need to be questioned how many of the criteria need to be absent for diagnosis.
- An issue with Jahoda’s definition of abnormality is cultural relativism as some of the criteria that is used when determining ideal mental health could be considered normal in the West (E.g. Emphasis on personal growth & development may be considered self-centred in collectivist cultures that favour community rather than individualism. Also, independence is not a sought after trait in collectivist cultures which means that it could be considered culture-bound).
explain the 4 d’s
Deviance – Behavior that significantly differs from societal or cultural norms.
Distress – Psychological suffering (e.g., anxiety, depression) experienced by the individual.
Dysfunction – Impairment in daily life, work, or relationships due to mental health issues.
Danger – Risk of harm to oneself or others.
explain deviation from ideal mental health
Jahoda (1958) suggested that abnormal behaviour should be defined by the absence of particular (ideal) characteristics. These are behaviours that deviate from ideal mental health. This is similar to the approach taken by medical professions when measuring physical health (E.g. Checking that blood pressure is within the normal range). She proposed six principles of ideal mental health:
- Having a positive view of yourself with a strong sense of identity (Having high self-esteem).
- Being capable of personal group & self-actualisation.
- Being independent of others & self-regulating (Having autonomy).
- Having a realistic & accurate view of reality.
- Being able to integrate within society & resist stress.
- Being able to master your environment (Juggling love, friendships, work & leisure).
Therefore, if an individual doesn’t demonstrate one or more of the criteria, they would be classified as abnormal according to Jahoda’s definition (E.g. Somebody who suffers from depression may have a negative view of themselves & would therefore be classed as abnormal.
strengths of evaluating diagnoses
- work for professionals + has a practical application as all features are recognisable and measured without a lot of training and using them alongside the DSM classification system.
(Davis 2009)
supports the validity of the DSM system in that various diagnosis are shown to focus on specific D’s showing each has value.
weaknesses evaluating diagnoses
The 4D’s causes subjectivity to occur as clinicians are interpreting what patients say during the clinical interview. This raises issues of the reliability of the diagnosis as two different clinicians may reach different conclusions.
Deviance dimensions = restricting human rights as social norms change over time e.g. homosexuality was viewed as a mental disorder but now its not.
describe the dsm and dsm-v
The DSM:
The Diagnostic & Statistical Manual of Mental Disorder (DSM) produced by the American Psychiatric Association (APA), provides criteria from which a mental health disorder can be diagnosed. It was first published in 1952 & has been revised numerous times. The DSM-IV was published in 1994 & the DSM-IV-TR was updated in 2000, containing over 200 new mental disorders. The DSM-V was. Released in May 2013.
The DSM was created in response to the need for a census of mental health disorders. The USA army had collated many descriptions & classifications of symptoms such as neurosis & psychosis, which later pulled together a list of symptoms, gradually developing to create the first DSM. This created a central system for diagnosing those with mental health problems in a more accurate, reliable & valid way.
For each disorder included in the DSM, a set of diagnostic criteria indicates symptoms that must be present & for how long, as well as a list of other symptoms, disorders & conditions that must be ruled out first to qualify for a particular diagnosis. These criteria help increase doctor reliability (The likelihood that 2 doctors would come up with the same diagnosis for a patient) when using the DSM.
The DSM-V:
Work on the DSM-V started in 1999, with 3 planning conferences held by the APA & the National Institute of Mental Health (NIMH). Trustees approved the final DSM-V criteria in December 2012 & it was released in May 2013.
The 5th edition of the DSM represents the latest scientific thinking in the criteria content & organisational structure of mental health disorders. As well as the refinement of the diagnostic criteria for disorders, the organisation of the manual was also changed. The manual contains a table of contents, which signals how various conditions relate to each other, as well as the occurrence of mental disorders across a person’s lifespan. Both of these features can influence the care of the patient. The primary goals for the new framework of the manual were to help clinicians make a more accurate & consistent diagnosis & to help researchers better study how disorders relate to one another, which can lead to better treatment for patients.
20 Disorder Chapters:
Whilst the actual number of disorders has not significantly changed, 3 additional chapters were added to the DSM-V to better classify the disorders based on known similarities to one another. Certain disorders come under more representative & comprehensive chapter headings (E.g. Neurodevelopmental Disorders is a new heading that includes autistic spectrum disorders, intellectual developmental disorder, attention deficit disorder (ADD) & tic disorders). The chapter on substance-related disorders is now titles ‘Substance Use & Addictive Disorders’ & includes gambling disorder as the only behavioural addiction.
Other groupings of disorders have been moved around based on new scientific understanding of their principal features (E.g. Recent studies have shown that obsessive compulsive disorder (OCD) involves distinct neurocircuits, meaning that it & other related disorders are now found in their own chapter, rather than in the chapter on anxiety disorders. Mood disorders have now been divided into 2 chapters – Bipolar & Related Disorders & Depressive Disorders).
describe disorders on a spectrum
Disorders on a Spectrum:
Whilst all disorders in the DSM-V remain in specific categories, measuring indicating the degree of acuteness of the disorders has been added to several diagnoses. Autistic Spectrum Disorder (ASD) combines 4 different categorical disorders & conceptualises them as occurring along a single spectrum focused on dysfunctional social communication & restricted, repetitive behaviours or interests. Under the DSM-IV, patients with these symptoms could be diagnosed with autism, Asperger’s disorder, childhood disintegrative disorder or as a general pervasive developmental disorder that is not specified. However, the diagnoses were not consistently applied across clinicians due to the large overlap of shared characteristics. Researchers determined that these separate disorders are actually related conditions that lie on a single continuum. With ASD, some individuals show mild symptoms & others have much more severe symptoms, the spectrum allows clinicians to account for the variations amongst patients.
describe the ICD
The International Statistical Classification of the Causes of Diseases & Related Health Problems (ICD) was produced by the World Health Organisation (WHO) & is used in certain parts of the world. The same diagnostic codes are used as the DSM & the 2 systems are developing together. The ICD is now in its eleventh edition (The ICD-11).
The ICD includes general health & disease, along with mental health & behavioural issues. It is used to monitor the number of incidents & frequency of a disease or disorder & also the mortality & morbidity information (Number of deaths & number of diseases).
describe accounting for culture
Accounting for Culture:
Cultural background can greatly influence how an individual perceives & presents with psychiatric symptoms; it also impacts their diagnosis & treatment. Section III of the DSM-V addresses this important issue through cultural concepts of distress, which detail the ways that different cultures perceive different symptoms & syndromes. To help clinicians to gauge these factors, a cultural formation interview guide is provided to them, with questions to ask patients about their race, ethnicity, language, religion, social culture, customs & geographical origin. This interview provides an opportunity for individuals to define their distress in their own words & then clinicians can relate this to how others, who do not share their culture, see their problems. This gives the clinician a more comprehensive foundation on what their diagnosis may be & the care they will receive.
Throughout the DSM-V development process, they put a large amount of effort in to modify culturally determined criteria so that they would be more equivalent across different cultures. In Section II, specific diagnostic criteria were changed to better apply across diverse cultures (E.g. The criteria for social anxiety disorder now includes the fear of ‘Offending Others’ to reflect the Japanese belief that avoiding harm to others is more important than causing harm to oneself).
The newest manual also addresses cultural concepts of distress, which detail ways in which different cultures describe new symptoms. In the Appendix, they are described through cultural syndromes, signs of distress & explanations for their symptoms. These concepts assist clinicians in recognising how people in different cultures think & talk about their psychological problems.
describe conditions for further study
Conditions for Further Study:
Section III of the DSM-V introduces emerging measures & models to assist clinicians in their evaluation of patients. This area of the manual includes assessment measures, guidance on cultural formation, an alternative method for diagnosing personality disorders & conditions for further study. In previous editions of the DSM, content from this area of the manual was contained in the Appendix. By bringing this content into the main body of the manual, the APA hoped to bring greater awareness & attention to these tools.
Some proposed conditions had clear merit but were judged to need further research before they could be considered as formal disorders. The inclusion of Section III was subject to the amount of empirical evidence available on a diagnosis, diagnostic reliability or validity, a clear clinical need & the potential benefit to advancing research. Additional research may result in new information & data that can guide decisions in future DSM’s.
New conditions that have been included in the DSM-V’s Section III include:
- Caffeine Use Disorder – Relating to the potential addictive behaviour caused by excessive, sustained use of caffeine.
- Depressive Episodes with Short-Duration Hypomania – Exhibiting bipolar behaviour characterised by a hypomanic episode that lasts less than 4 days.
- Internet Gaming Disorder – This deals with the compulsive preoccupation some people develop in playing online games.
- Non-Suicidal Self Injury – Self-harm without the intention of suicide. This condition is regarded as a major problem on university campuses & a public health issue that needs to be better understood.
Whilst the conditions included in Section III are not intended for routine clinical use, clinicians can note the possible presence of certain disorders by designating patients as ‘Other Specified’ (E.g. ‘Other Specified Bipolar & Related Disorder’ would be the official diagnosis for a patient, but a clinical could refer to Section III for depressive episodes with short-duration hypomania by indicating that this condition is present when recording the diagnosis). This will allow clinicians to provide richer diagnoses for patients whose symptoms don’t completely fit within other named disorders.
pros and cons of getting a diagnoses
✅ Self-Understanding – Helps you understand your experiences and emotions.
✅ Access to Treatment – Opens doors to therapy, medication, and support.
✅ Validation – Confirms that your struggles are real and not just “in your head.”
✅ Community Support – Connects you with others who share similar challenges.
✅ Legal & Workplace Accommodations – May provide protections under disability laws.
Cons:
❌ Stigma – Some people may judge or misunderstand.
❌ Self-Doubt – You might internalize the diagnosis negatively.
❌ Medication Side Effects – If treatment includes medication, side effects may occur.
❌ Labeling – Can feel like being put in a box rather than seeing the full picture of yourself.
❌ Insurance & Costs – Treatment can be expensive or difficult to access.
differences between DSM and ICD
Authority & Organization
DSM: Published by the American Psychiatric Association (APA), primarily used in the U.S. and some other countries.
ICD: Published by the World Health Organization (WHO), used internationally for both physical and mental disorders.
Scope
DSM: Focuses solely on mental health disorders.
ICD: Covers both physical and mental health conditions.
Purpose & Use
DSM: Primarily used for psychiatric diagnosis, research, and clinical practice in mental health.
ICD: Used for global epidemiology, insurance billing, and medical record coding for all diseases, including mental disorders.
Revisions & Updates
DSM: More frequently revised with in-depth discussions on diagnostic criteria (e.g., DSM-5, DSM-5-TR).
ICD: Updated less frequently but provides a broader international perspective (e.g., ICD-10, ICD-11).
Coding Differences
ICD codes are used for insurance and global health statistics.
DSM includes ICD codes but provides additional diagnostic details relevant to mental health professionals.
reliability of the DSM and ICD
Reliability rests on the question of whether one person’s set of symptoms would lead to a common diagnosis by different physicians. So, if different doctors give different diagnoses for the same set of symptoms, then the diagnoses are not reliable & the treatment may not work.
How do we Maximise Reliability?
Gelder (1999) proposed that any classification will be of little value unless psychiatrists can agree on one set of criteria, only then can reliability be applied accurately, as it can be used over & over again getting similar results.
One measure to see whether a test is reliable is to use inter-rate reliability, which involves more than one person classifying the mental illness. In addition, the test-retest reliability method can be used, which looks at replicating & comparing the results. Reliability is often presented numerically. There are 2 common measures or reliability that both use the test-retest technique:
- The PPV (Positive Predictive Value).
- Cohen’s Kappa.
The PPV (Positive Predictive Value) is simply the proportion of people that keep the same diagnosis over time. It is usually expressed as a percentage. If depression has a PPV of 80, this means that 80% of people with a diagnosis of depression received a subsequent diagnosis of depression when re-assessed.
Cohen’s Kappa is slightly more complex. It is the correlation between the results of 2 rounds of diagnosis in a group of patients. Like all correlation coefficients, it is a number between 0 & 1. A Kappa of 1 would indicate complete agreement in 2 rounds of diagnosis of the same patients, which is an excellent reliability. A Kappa of 0 would indicate no agreement & very poor reliability.
is the dsm reliable
is the icd reliable
strengths of the validity of DSM and ICD
- The validity of the DSM & ICD systems has increased with each new version. The ICD-11 & the DSM-V are more valid that previous versions (E.g. Culture bound syndromes have now been added).
- The evidence regarding the validity of the DSM indicates that the DSM is valid in its diagnosis. It is likely that symptoms for disorders such as alcohol abuse, dependence, cocaine abuse, pathological gambling & ADHS are well established given the work & revision that have happened over the years.
weaknesses of the validity of the DSM and ICD
- Valid diagnosis for mental disorders is more difficult than physical disorders. This is due to the lack of objective signs of disorder (E.g. Temperature & Blood).
- It has been said, that co-morbidity (Having more than one mental disorder) is hard to diagnose using the DSM. The system relies on the user choosing the disorder closest to the symptoms, this could prove invalid is the diagnosis is incorrect.
- It could be claimed that splitting a mental disorder into symptoms & features is reductionist & that a holistic approach may be more valid (E.g. In a counselling situation, symptoms are treated as aspects of the whole person & mental health is the focus, not the mental disorder. In counselling, a diagnosis is not as important as treating the individual).
explain the types of validity
Even though the DSM has taken into account personal & social factors, as well as how the person is functioning, these may not actually be part of the mental disorder that the patient has been linked to (E.g. If someone is suffering from depression & is not functioning well within society, it may not be because of the depression but for other reasons such as unemployment). So, a diagnosis of depression would not be valid in that
case.
Concurrent Validity: This is when the result of a study or test matches a result from another study or set of data done at the same time. For results to have concurrent validity, the second diagnosis has to match a first diagnosis or result that has been shown to be valid. So, if a diagnosis using the DSM comes up with the same disorder than another diagnosis has given at the same time, then the new diagnosis is likely to have concurrent validity.
Predictive Validity: This means that if the diagnosis is correct, we should be able to predict the outcome of the disorder (E.g. People with manic depression should respond favourable to being given lithium). This is the same as concurrent validity, but the result can be obtained at another time. However, not all patients react in the same way when given drugs, so predictive validity is difficult to prove.
Convergent Validity: When a test result converges on (Gets close to) another test result that measures the same thing it has convergent validity. A correlation test is carried out. If 2 scales measure the same construct, the a person’s score on one should converge with their score on the other. The difference between convergent & concurrent/predictive validity is that in convergent validity the 2 measures should measure exactly the same thing, whereas in the others there can be a different way of measuring in each case.
validity of the dsm and icd
If the DSM was not reliable, it wouldn’t be valid either. If a diagnosis was repeated & this time the DSM provided a different diagnosis, then it would not be a valid diagnosis (It wouldn’t be measuring what it set out to measure). In the case of diagnostic manuals, reliability & validity go together. A diagnosis is valid if it predicts the course of a disorder & the treatment suggested is useful.
For classification systems to be valid it should meaningfully classify a real pattern of symptoms, which result from a real underlying cause, which can, therefore lead to a suitable treatment & prognosis.
Validity means that something measures what it is supposed to measure (Whether it is telling the truth). In this context, a valid classification system means that a particular diagnosis actually represents a disorder (It has to be the correct diagnosis to be valid).
If the DSM is to be successful in defining mental disorders, it needs to be able to operationalise the illnesses. However, operationalising a concept like depression is very difficult as we cannot always determine the nature of why a person is suffering, therefore the DSM is not a valid tool. There is a lack of construct validity as ideas that are drawn up to represent depression may not be representative enough because it has been chunked down into measuring blocks & therefore not seen as a whole illness. Unfortunately, this is what happens when mental illness is diagnosed.
strengths and weaknesses of the 4 d’s
Deviance – Behavior that differs from societal norms.
✅ Strength: Helps recognize unusual behavior that may need intervention.
❌ Weakness: Social norms change over time and across cultures.
Dysfunction – When behavior interferes with daily life.
✅ Strength: Focuses on how a disorder affects a person’s ability to function.
❌ Weakness: Some people with disorders can still function well.
Distress – When a person experiences emotional suffering.
✅ Strength: Considers the person’s subjective experience.
❌ Weakness: Some disorders (e.g., psychopathy) may not cause personal distress.
Danger – Risk of harm to self or others.
✅ Strength: Helps identify those who need urgent intervention.
❌ Weakness: Not all people with mental disorders are dangerous.
summary of HCPC guidelines:
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Here’s a concise summary of the HCPC (2016) guidelines for clinical practitioners:
Promote and Protect Interests: Respect service users and carers as individuals, maintain their privacy, work collaboratively, obtain consent, challenge discrimination, and maintain professional boundaries.
Communicate Effectively: Be polite and considerate, listen actively, provide clear and accessible information, address language and communication needs, collaborate with colleagues, and use social media responsibly.
Work Within Limits: Stay within your scope of practice, refer cases when needed, continually update your knowledge, comply with relevant laws and guidance, and use feedback for improvement.
Delegate Appropriately: Assign tasks only to qualified individuals and provide supervision.
Respect Confidentiality: Protect user information and only disclose it when necessary under specific conditions (e.g., legal requirements or safety concerns).
Manage Risk: Minimize risks to users and colleagues, and adjust or stop work if health issues compromise safety.
Report Safety Concerns: Promptly report and address safety concerns, follow up if necessary, and ensure user well-being takes precedence.
Be Open About Mistakes: Be transparent about errors, apologize, take corrective actions, and provide explanations to users.
Be Honest and Trustworthy: Uphold public trust through integrity, transparency about qualifications, and accurate communication while avoiding conflicts of interest.
describe what culture is:
Culture is a self of beliefs, values and practices that characterises a group of people and varies between people from different parts of the world, between different ethnic and religious groups living in the same region, between socio-economic groups, between men and women and even between families. Most research has focused on differences between different national and ethnic groups.
describe whether culture does affect diagnosis because it is a ‘spiritual model’
It has often been argued that the DSM classification system reflects Western culture and so does not accurately assess people from other cultures ie, it is ethnocentric (spiritual model).
A clinician from one culture must be aware that a patient from another culture is guided by their own frame of reference.
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.
describe whether culture doesn’t affect mental disorders because they are ‘scientific’
The DSM was developed in America 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 schools of thought suggests means disorders are scientifically defined illnesses that are explained in a scientific way and therefore cultures do not affect diagnosis as it should be the same cross-culturally.
For example, Lee 2006 conducted his study in Korea deliberately to see if the DSM-IV-TR was valid in a non-Western society and it was found it was for ADHD.
describe ethnocentrism and cultural relativism
ethnocentrism - the view that your own culture is the standard against which other cultures can be judged right or wrong
cultural relativism - a view that judges other cultures not by standards of the observers culture but by the standards of the other culture itself
give Example of cultural influences on mental health diagnosis: schizophrenia
It does seem to be the case that for mental disorders like schizophrenia there are cultural differences. It was reported that catatonic schizophrenia is in the decline because of health measures that prevent it from occurring.
CHANDRASENA (1986) reported more incidences of catatonia in Sri Lanka 21% compared with 5% amongst British white people. HOWEVER, it was found that in Sri Lanka it was less likely that patients had received early interventions with drug treatments; this was not therefore a cultural difference in attitude to the mental disorder, but a difference in treatment available.
Auditory hallucinations were reported to doctors by patents more in Mexican-born Americans than in non-Mexican-born Americans. The study by 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, for example so culture had led to the difference.
White Americans were reported (using patient records) as showing more “grandiosity” as a symptom of schizophrenia compared with Americans of Mexican origin, again showing cultural differences. It is important to look at individual symptoms if looking for cultural differences in symptoms of mental disorders. The DSM looks at a set of cultural differences therefore differences would not be found.
LIN (1996) summarised schizophrenia in other cultures and noted that it is found in all cultures that have been studied, and the prevalence seems similar across all cultures. With regard to symptoms, similarities outweigh the differences. Good outcomes appear more likely in developed countries.
So, just because the symptoms seem the same and symptoms under the heading schizophrenia occur in all cultures as far as it is known, it does not mean that “schizophrenia” in all cultures is in fact the same thing, with the same cause and the same course through the illness, which is what the DSM and ICD tend to assume.
describe linguistic differences for individual differences
Language Barriers: Differences in language can make it harder for service users to explain their symptoms or understand the treatment. Miscommunication can lead to misdiagnosis or inadequate care.
Cultural Variations: Linguistic differences often reflect cultural variations, which may shape how mental health symptoms are expressed (e.g., somatic vs. emotional symptoms).
Clinical Implications: Clinicians must address linguistic differences by using interpreters, culturally sensitive assessments, or adapting therapy techniques to ensure inclusivity.
Ethical Practice: Recognizing and accommodating linguistic differences aligns with ethical guidelines, ensuring that service users receive equitable and respectful care.
describe fear of being misunderstood for individual differences
Reluctance to Share: Service users may withhold information about their symptoms or feelings due to fear that clinicians will misinterpret them, leading to incomplete or inaccurate diagnoses.
Cultural and Linguistic Factors: Fear of misunderstanding is more pronounced in individuals from different cultural or linguistic backgrounds, where communication styles or expressions of distress might differ from the clinician’s norms.
Therapeutic Alliance: A strong, trusting relationship between clinician and service user can reduce fear of misunderstanding, encouraging open communication and better outcomes.
Clinical Implications: Clinicians must use active listening, validate emotions, and demonstrate empathy to reassure service users and address their fears.
describe cultural links with specific disorders for individual differences
Cultural Expressions of Disorders: Certain disorders are more prevalent or uniquely expressed in specific cultures. For example, Koro (fear of genital retraction) is seen in Southeast Asia, while Anorexia Nervosa is more common in Western societies due to cultural beauty standards.
Cultural Beliefs and Stigma: Cultural attitudes toward mental health can affect whether individuals seek help, how symptoms are reported, or how disorders are understood (e.g., attributing symptoms to spiritual causes in some cultures).
Diagnosis and Bias: Clinicians must be aware of cultural factors to avoid misdiagnosing conditions due to differing norms in symptom presentation.
Clinical Implications: Therapy must be culturally sensitive, incorporating an understanding of cultural values and practices to ensure effective treatment.
describe cultural bias in diagnosis in individual differences
Misinterpretation of Symptoms: Cultural expressions of distress, such as somatic complaints or spiritual explanations, may be misunderstood or pathologized by clinicians unfamiliar with those cultural norms.
Over- or Under-Diagnosis: Cultural bias can lead to over-diagnosis in minority groups (e.g., higher schizophrenia diagnoses among Black individuals) or under-diagnosis due to stereotypes or unfamiliarity with cultural expressions.
Ethnocentric Approaches: Diagnostic tools, like the DSM or ICD, are often developed in Western contexts, potentially neglecting cultural variations in symptom presentation.
Clinical Implications: Training clinicians in cultural competence, using culturally sensitive assessments, and involving interpreters or cultural consultants can reduce bias.
describe symptoms and features in relation to schizophrenia
SYMPTOMS are what the person presents to the doctor i.e., delusions, hallucinations.
FEATURES are wider, for instance that there are different types of schizophrenia or that schizophrenia is found in all countries, certain genders etc.… where research has been carried out.
One FEATURE of schizophrenia is that there are different TYPES.
describe the types of schizophrenia
- PARANOID SCHIZOPHRENIA is characterised by someone being suspicious of others and having delusions of grandeur. There are often hallucinations as well.
- DISORGANISED SCHIZOPHRENIA is characterised by speech being disorganised and hard to follow, as well as the person having inappropriate moods for the situation. There are no hallucinations.
- CATATONIC SCHIZOPHRENIA is when someone is very withdrawn and isolated and has little physical movement.
- UNDIFFERENTIATED SCHIZOPHRENIA is when the person does not fit the other types.
describe the symptoms of schizophrneia
SYMPTOMS OF SCHIZOPHRENIA
There are a number of ways of characterising schizophrenia, including giving first- and second-rank symptoms or positive, negative and cognitive symptoms.
First-rank symptoms include hearing voices and ideas about being guided by others. For example – these are positive symptoms such as hallucinations and delusions, they are added to the patient’s behaviour as they were not there before the disorder became active.
Second-rank symptoms include flattened emotions. These 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.
describe the positive and negative symptoms of schizophrenia
Positive symptoms
Are additions to behaviour and actual symptoms that can be noted. They include first-rank symptoms. Positive symptoms are about changes in the person.
HALLUCINATIONS such as seeing or hearing things that are not there. Hearing voices in some cultures is not seen as a sign of mental disorder, but of a personal spiritual capability. In these cases the voices are often kind and positive, whereas with schizophrenia the voices are harsh and critical. Critical voices provide a running commentary on what the person is doing. Controlling voices tell the person what to do, usually uncharacteristic
acts.
DELUSIONS (false beliefs), such as someone thinking their movements are being controlled by someone else. A common form of delusion is the paranoid delusion; the sufferer believes that someone is trying to mislead, manipulate or even kill them. Someone suffers from delusions of grandeur when they think they are in a prominent position of power, such as a king, or that they possess special power, such as to cure cancer. Delusions can also take the form of the person thinking that unrelated things are in fact intended to relate to them; they may feel that a newspaper headline carries a secret message for them. Delusions can lead to strange behaviour, such as covering windows to shut out the sound of the voice of God.
THOUGHT DISORDERS which make someone’s speech hard to follow. They might also lose concentration at work or complain of having muddled thinking. The person may become disorganised thoughts. Further developments of thought disorders are “thought insertion” (a person thinks their own thoughts are put there by someone else), or “thought broadcasting” (thinking others can hear their thoughts).
Negative symptoms
Are where normal functioning is not present, there is something missing. Negative symptoms often start before positive ones, sometimes years before schizophrenia is diagnosed. This is known as the PRODROMAL period.
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.
AFFECTIVE FLATTENING – a reduction in range and intensity of emotional expression, including eye contact, voice tone, body language and facial expression - all become dull.
LOSS OF SENSE OF SELF which includes not looking after appearance or self and not adhering to expectations with regards preserving a sense of self.
ALOGIA, where the patient uses as few words as possible and fluency deteriorates.
evaluation of positive and negative symptoms of schizophrenia
EVALUATION - Positive symptoms tend to have greater weight when diagnosing schizophrenia but, they are affected by cultural differences so perhaps should not be weighted as strongly as negative symptoms, which might be more
objectively measured.
EVALUATION - Negative symptoms are less affected by cultural factors and it has been suggested that they can be more objectively measured. Hearing voices, for example is hard if not impossible to measure. Lack of energy, flatness of emotions or social withdrawal might be more easily monitored. Prodromal features have been found to be present in many adolescents and cannot be taken to indicate the onset of schizophrenia on their own.
describe the cognitive symptoms of schizophrenia
Cognitive symptoms in schizophrenia include difficulty in concentrating and paying attention, problems with working memory and difficulty with executive functioning (understanding information and making decisions).
For some people, the cognitive symptoms of schizophrenia are subtle, but for others, they are more severe and patients may notice changes in their memory or other aspects of thinking. Similar to negative symptoms, cognitive symptoms may be difficult to recognize as part of the disorder. Often, they are detected only when specific tests are performed. Poor cognition is related to an increased likelihood of unemployment and poor social outcomes and can be distressing to individuals with schizophrenia.
describe dopamine
Dopamine affects your brain processes that control movement of your body, emotional response, and your ability to experience pain and pleasure. Dopamine also plays an essential role in your mental and physical health. Dopamine works by attaching itself to specific proteins called receptors, and the binding of dopamine molecule with a receptor initiates a cascade of biochemical events inside the cell. It helps in the effective transmission of messages from one nerve cell to the next. It helps one cell talk to the next. Individuals with Parkinson’s disease have decreased amounts of dopamine in two structures deep in the brain, the basal ganglia and substantia nigra. This becomes important as dopamine coordinates our movements, both balance and walking.
What dopamine does once it’s released is not fully understood. Scientists used to believe that it alone was responsible for the joy and pleasure that comes with rewarding behaviours. That belief stemmed from studies that linked the amount of dopamine released with the degree of the high that drugs produced. It now appears, however, that dopamine has a much more sophisticated role. While dopamine in the brain might coincide with pleasure, it does not necessarily produce pleasure. Studies of the neural effects of nicotine show, for example, that nicotine causes a surge of dopamine but does not produce euphoria that smokers would consider a high. Meanwhile, events that are unpleasant and stressful also prompt the release of dopamine in the nucleus accumbens. Consequently, dopamine cannot simply be the brain’s pleasure switch, though it clearly has an important role in pleasure.
describe the dopamine hypothesis
The “Dopamine Hypothesis” proposes that schizophrenia is linked to over activity of dopamine at certain receptors in the brain.
It is generally believed that this over activity is not due to too much dopamine being produced but because the dopamine receptor sites are too sensitive or there are too many receptor sites.
Another possibility is that there is a faulty regulation of the re-uptake mechanism by which dopamine returns to and is stored by ventricles in the pre-synaptic neuron.
evidence supporting the dopamine hypothesis
Wonget al.(1986)carried out PET scans on living schizophrenicsprior to medicationand found evidence for a more than twofold increase in (dopamine receptors compared to controls.
However, Fardeet al.(1990)carried out PET scans in the same way, and found not significant differences between schizophrenics and controls. So research methodology may differ between studies so results may not be reliable.
Iverson (1979) found that post-mortems conducted on schizophrenic patients show high levels of dopamine in the brain
Falkai et al. (1998) examinations of brains from dead schizophrenic patients show that there is an excess of dopamine in the left amygdala
However, it is difficult to determine if increases in dopamine found in brain regions are the result of schizophrenia or the cause of it.
Research investigating the role of L-dopa, a dopamine releasing drug, has shown it can cause schizophrenic symptoms in non-psychotic people.
LINDSTROEM ET AL (1999) found L-DOPA was taken up more quickly in the patients with schizophrenia, suggesting that more dopamine was needed or more was taken up in schizophrenic patients.
However, L-dopa tends to affect positive symptoms of schizophrenia, but not negative symptoms, suggesting that all of the symptoms of schizophrenia may not be directly related to dopamine.
LSD and amphetamines increase dopamine activity and have been noted to induce positive schizophrenic symptoms.
Drugs to increase dopamine production in sufferers from Parkinson’s disease give psychotic symptoms. People given Levodopa (which adds to dopamine production) for Parkinson’s disease can experience symptoms similar to schizophrenia.
However, excess dopamine can also have a stimulant effect such as overconfidence and high alertness, which relate to symptoms of mania more than schizophrenia.
Supporting this has been evidence that Phenothiazines (which inhibit dopamine activity) can reduce the symptoms of schizophrenia.
If the receptors are blocked, then less dopamine will be taken up so that the effects of excess dopamine are avoided.
However, Clozapine is effective in treating schizophrenia, but this changes levels in serotonin and not dopamine.
evidence against the dopamine hypothesis
anti-psychotic drugs don’t work on 1/3 of patients therefore not only is it an incomplete explanation of schizophrenic causes
difficult to determine cause and effect, excessive dopamine activity may be the result of having schizophrenia
reductionist, it ignores other possibilities, Fox (1990) suggested it is likely that factors associated with living in poorer conditions e.g. stress, may trigger the onset of schizophrenia.
blocking dopamine receptors does not always remove the symptoms of schizophrenia in patients who had had schizophrenia for 10 years or more, even if the block was 90% effective.
It is also interesting that anti-schizophrenic drugs block the dopamine receptors almost immediately but any calming effect is not noticed for several days.
Another neurotransmitter, glutamate, is also thought to cause psychotic symptoms if its production is blocked. Again, this shows up in those who take recreational drugs, such as PCP (also known as ‘angel dust’). So perhaps dopamine is not the only neurotransmitter involved in the development of schizophrenia.
describe glutamate
Glutamate is also a neurotransmitter.
It’s a chemical that is in the brain that is secreted into synapses and facilitates nerve impulses.
Its role is to EXCITE receptors-that is, it stimulates them rather than calms them.
Glutamate is the principle neurotransmitter of cells that communicate across long distances in the brain, such as across cortical regions and from the cortex down into the spinal cord or out into the rest of your body.
There are at least three major types of glutamate receptors: the AMPA receptor, the NMDA receptor, and the kainate receptor.
It is the NMDA receptor that evidence suggests is involved in the psychotic symptoms associated with schizophrenia.
Therefore, too little glutamate at the NMDA receptor results in too little excitation in the pre-frontal cortex, inducing schizophrenic symptoms.
Also, most of the genes that have been found that relate to schizophrenia, seem to impact on the function of glutamate in the brain.
So glutamate might be a common link between the biological risk factors that translate into the kind of behaviour and brain function we see in schizophrenia.
Based on observations of the effects of a recreational drug called PCP, phencyclidine, or ‘angel dust’ it was found that when people take this, it induces symptoms of schizophrenia
Not just a psychotic state but also change in cognitive function, change in the ability to pay attention, distraction which have certain features of schizophrenia.
This was the start of the research into the glutamate hypothesis of schizophrenia.
describe glutamate and PCP (‘angel dust’)
It was found that PCP acts at one of the receptors that glutamate stimulates (NMDA receptor) to block the effects of glutamate (PCP is an antagonist).
Therefore, it is suggested that people with schizophrenia have a deficiency or a defect in this NMDA receptor and the receptor cannot be properly stimulated by glutamate
Animal studies have shown that in animals treated with an NMDA antagonist, this led to a lack of glutamate but did not always lead to an increase in dopamine.
If NMDA antagonists are psychostimulants and lead to psychosis-like symptoms and they inhibit dopamine, then this does not support the idea that excess dopamine causes schizophrenia.
It seems that there is more to schizophrenia and psychotic behaviour than excess dopamine, so glutamate seems also to have a role.
glutamate evidence
Evidence reviewed by Carlsson et al. does support the dopamine hypothesis, so accept that schizophrenia-like symptoms link to excess dopamine in the brain, however they investigate whether this is due ‘just’ to excess dopamine or whether there is more to it – like glutamate.
strengths of the glutamate hypothesis
Carlsson et al (1999) explain that the glutamate hypothesis works with the dopamine hypothesis and expands on it rather than replacing it.
This is a strength as it means evidence for the dopamine hypothesis, which is strong evidence, can be incorporated into the glutamate hypothesis.
The idea that glutamate has a role as well as dopamine adds to the original hypothesis, enabling a body of knowledge to be built and adding to its scientific credibility.
Waters et al (1996) researched the effects of blocking NMDA receptors in rats and mice.
Finding that there was an increase in psychotic behaviours in the rats and mice was not as a result in excessive dopamine, but from antagonising NMDA receptors and reducing glutamate uptake.
Therefore supporting the hypothesis that reduced glutamate uptake induces schizophrenic symptoms.
weaknesses of the glutamate hypothesis
Supporting evidence such as Waters et al (1996) research into blocking NMDA receptors in rats, are used to explain human behaviour, questions are asked about generalisability of the findings.
Perhaps especially when looking at areas of human functioning like psychoses, which has mental roots even if manifested in behaviours.
Additional, using findings from animal studies like Waters et al (1996) about the effects of NMDA on rats to explain human brain functions and psychosis, lacks construct validity.
What seems like erratic behaviour and is seen as a psychosis in these rats might not relate to psychotic behaviour in humans as claimed, so researchers may not be testing what they set out to test.
Studies using volunteers to undertake recreational drug trials, such as Lahti et al (1991), could be considered unethical.
Although participants must give informed consent to take part in clinical drug trials, the potential risk or harm to a person is not fully known and could breach ethical guidelines for protection.
carlsson aim, iv and dv
Aim
This isn’t a investigative study, like an experiment or an observation. It’s a review - summing up the research so far and suggesting where it should go next.
The aim is to present the current (in 1999, but it’s not changed much since) view of the relationship between schizophrenia and dopaminergic dysfunction (problems relating to dopamine). Another aim is to explore a rival theory, that of glutamatergic deficiency or hypoglutamatergia (too little of a neurotransmitter called glutamate).
IV
This isn’t an experiment so there’s no IV.
DV
This isn’t a piece of empirical research so there’s no DV. However, Carlsson et al. describe the findings of a number of earlier studies..
sample and procedure of carlsson et al
Sample
Carlsson et al. aren’t carrying out empirical research and they don’t have a sample of their own. However, they refer to a number of earlier studies that do have samples of patients with schizophrenia.
Procedure
Carlsson et al. aren’t carrying out empirical research so they don’t have a procedure. However, they refer to a number of studies that use positron emission tomography (PET).
PET is a brain imaging technique which injects the participant with a radioactive tracer that dissolves in the blood stream. The tracer is carried by the blood to the brain, where it concentrates around brain structures that are particularly active. A PET scan detects the radioactivity and converts it into a digital image of the brain, highlighting the active areas in yellow and red.
Some PET tracers are designed to bind to receptors on neurons in the brain. They won’t be able to do this if certain neurotransmitters are over-active in the brain. Therefore, on a PET scan, these areas will show up as lacking in radioactivity, coloured green or blue. On the other hand, if these neurotransmitters are under-active in the brain, the tracers will bind themselves to lots of receptors and show up on the PET scan as yellow and red areas.
results of carlsson…
Carlsson revisits the Dopamine Hypothesis of schizophrenia, showing PET/SPECT evidence that schizophrenic patients have increased dopamine activity, especially in the basal ganglia. However, Laruelle et al. (1999) found that patients in remission have normal dopamine levels, suggesting antipsychotic drugs might cause hypodopaminergia, leading to side effects.
Carlsson explores the role of glutamate, noting that drugs like PCP and ketamine induce psychotic symptoms by affecting NMDA receptors, not dopamine directly. Glutamate helps regulate dopamine, acting as an “accelerator” or “brake.” Studies show blocking NMDA receptors increases dopamine, while boosting glutamate can reduce psychotic symptoms.
He links low glutamate (hypoglutamatergia) in different brain areas to schizophrenia symptoms: in the basal ganglia, it causes positive symptoms, while in the cerebral cortex, it leads to negative symptoms. His “thalamic filter” theory suggests that dopamine and glutamate imbalances affect pathways through the thalamus, either overstimulating or starving the cerebral cortex.
Carlsson contrasts the hyperdopaminergia and hypoglutamatergia models of schizophrenia, suggesting treatment-resistant patients may have glutamatergic dysfunction. Clozapine, an atypical antipsychotic targeting serotonin, may be more effective for them.
Despite new insights into glutamate, Carlsson sees potential in dopamine-based treatments. He supports research into drugs that regulate dopamine at the pre-synapse, avoiding harmful side effects.
Ultimately, he argues schizophrenia may involve different biological subtypes, some driven by glutamate rather than dopamine. Future research should explore other neurotransmitters like GABA, acetylcholine, and neuropeptides.
aim and iv,dv of rosenhans
Aim
Rosenhan wanted to test the reliability of mental health diagnosis, to see if medical professionals could tell the sane from the insane in a clinical setting. He also wanted to investigate the effect of labeling on medical diagnosis.
In particular, Rosenhan investigated whether healthy pseudopatients would be given a diagnosis of mental illness and whether their imposture would be recognised by medical staff and other patients. Later, he investigated whether genuine patients would be identified as pseudopatients by suspicious staff.
IV & DV
This is an observation, not an experiment, so there is no IV or DV.
sample and procedure of rosenhans
Sample
A common mistake students make is to write about the pseudopatients as if they were the participants in the study. The pseudopatients were the observers, not the participants (although Rosenhan does make some observations about the effect the study had on them).
The participants were the staff and patients in 12 psychiatric hospitals (mental asylums) in the United States.
The hospitals were in 5 different states, on the East and West coasts of the country.
Procedure
The pseudopatients went to clinical interviews and reported their symptoms.
Rosenhan approached the head of the hospital he went to and informed him of the deception, but the other pseudopatients weren’t known to anyone on the staff. Rosenhan also briefed lawyers to get the pseudopatients out if anything went wrong.
When they were admitted to a hospital, they started behaving normally and stopped reporting hearing voices. They took a notepad and pen along with them to record what they heard and saw (unstructured observation). They tried to do this covertly, but if the staff detected them they carried on recording things overtly.
As soon as they were admitted, the pseudopatients requested to be discharged. They secretly disposed of any medication they were given (eg they flushed pills down the toilet) but otherwise they were friendly and polite and did everything that was asked of them - Rosenhan instructed them to be “paragons of cooperation”.
Structured observations: Rosenhan carried out two structured observations during the study:
In 3 hospitals, a record was kept of how many patients voiced suspicions about the pseudopatients and how much time the staff spent on the ward, interacting with the patients
In 4 hospitals, the pseudopatient approached staff with a scripted question: “Pardon me, Mr [or Dr or Mrs] X, could you tell me when I will be eligible for grounds privileges?” (or “ . . . when I will be presented at the staff meeting?” or “. . . when I am likely to be discharged?”). The member of staff’s answer and body language were recorded.
Follow-on study: After the main study ended, Rosenhan contacted his own hospital and revealed the results. The hospital agreed to a second study, but this time they would be aware that new pseudopatients would be seeking admission over the next 3 months. Staff were issued with a questionnaire to rate each new patient on a 10-point scale: 9-10 meant high confidence that the patient was really ill but 1-2 meant a strong suspicion that this was a pseudopatient.
results of rosenhans
Results
All 12 hospitals diagnosed the pseudopatients as mentally ill. 11 hospitals diagnosed schizophrenia, 1 hospital (the private hospital) diagnosed manic-depression (bipolar disorder). The pseudopatients went to hospitals that had diagnosed them with schizophrenia.
None of the staff recognised that the pseudopatients were healthy. It took between 7 and 52 days for the pseudopatients to be discharged; the mean length of stay was 19 days.
Who was the person stuck in a mental hospital for 52 days? Why, that was Rosenhan himself! The irony!
The pseudopatients were discharged with a diagnoses of “schizophrenia - in remission” (meaning the person has schizophrenia but the symptoms appear to have stopped) in 7 cases; 1 pseudopatient was discharged with a diagnosis of “schizophrenia” on their medical record.
The pseudopatients observed many disturbing things while in the hospitals.
Staff abusing patients: The pseudopatients were well-behaved and none of them were harmed in any way, but they observed other patients being verbally or physically abused by staff. Rosenhan reports that patients were awakened in the morning by an attendant shouting “Come on you m—- f—-s, out of bed!” and one patient was beaten for saying to an attendant “I like you”.
Patients refusing medication: The pseudopatients disposed of their pills but when they went to flush them down the toilet, they often observed that other patients had done the same thing
Depersonalisation & powerlessness: The patients weren’t treated as persons. There were no doors on toilet cubicles and staff would inspect their medical records and personal belongings without asking permission. Staff would not make eye contact with patients. Staff would discuss patients within earshot, as if the patients could not hear them. Attendants would abuse patients while other patients were watching, but not when doctors were present.
Rosenhan describes feeling as if he were invisible and offers one memorable example of this:
A nurse unbuttoned her uniform to adjust her brassiere in the presence of an entire ward of viewing men. One did not have the sense that she was being seductive. Rather, she didn’t notice us - David Rosenhan
Structured observations: Rosenhan carried out two structured observations during the study:
Although staff were not suspicious of the pseudopatients, other patients were. 35 out of 118 patients accused the pseudopatients of not being genuinely ill.
You’re not crazy. You’re a journalist, or a professor You’re checking up on the hospital - anonymous patient
The staff spent most of their time in a secure area with glass windows (“the cage”) and little time on the ward. On average, staff spent only 11.3% of their time outside “the cage” and much of this was doing chores rather than interacting with patients. Doctors only came onto the ward on average 6.7 times per day. Rosenhan observes that the staff behaved as if mental illness were “catching” (contagious).
Follow-on study: Rosenhan sent NO pseudopatients in the follow-on study, so ALL the patients seeking admission were genuine. 193 patients arrived at the hospital: 41 were rated as pseudopatients by at least one member of staff, 23 were rated as pseudopatients by at least one psychiatrist and 19 were rated as pseudopatients by a psychiatrist AND a staff member.
evaluate rosenhan
Generalisability
Rosenhan used a variety of psychiatric hospitals, but his small sample of 12 may not represent the entire USA. Changes in mental health care since the 1970s, including DSM-5’s stricter diagnostic criteria, mean the findings may not apply today. However, psychiatrists misused DSM-II, so errors in diagnosis could still occur.
Reliability
Pseudopatients did not follow standardized procedures, affecting consistency. Some revealed their psychology backgrounds, and one engaged in a romantic relationship. Slater (2004) tried to replicate the study but got different results, which Spitzer et al. (2005) challenged, questioning the reliability of such findings.
Application
The study significantly impacted mental health care, leading to reforms in hospital procedures and diagnostic criteria (DSM-III onward). It contributed to reducing reliance on medication and improving psychiatric training.
Validity
Critics like Kety (1974) argued that faking symptoms means the study lacks ecological validity. However, Rosenhan countered that some patients might feign symptoms to avoid prosecution. Spitzer (1976) noted that the unusual “Schizophrenia - in Remission” diagnosis indicated psychiatrists recognized something was off rather than proving unreliability.
Ethics
Deception was used without staff or patient consent. The study may have harmed public trust in psychiatry, potentially deterring those in need from seeking help. Pseudopatients faced stress, but Rosenhan arranged legal support for their safety. Confidentiality was maintained as no hospitals or staff were named.
Overall, Rosenhan’s study revealed flaws in psychiatric diagnosis, leading to reforms, but it had methodological weaknesses and ethical concerns.
evaluation of carlsson
Generalisation
Carlsson et al.’s study is a review, so it does not have a sample group, meaning generalisability does not apply in the usual way. However, Carlsson, a leading expert in dopamine and schizophrenia, reviewed 33 studies (14 of which he contributed to), making his selection highly representative of the research at the time (2000).
The study may be “time-locked” since nearly two decades have passed, and research has progressed. However, rather than being refuted, Carlsson’s ideas have been expanded upon, suggesting continued relevance despite being from 1999.
Reliability
The studies cited by Carlsson et al. were mainly lab experiments using PET or SPECT brain imaging, which are standardised and replicable, making the research reliable. However, one study (Laruelle et al.) was unpublished at the time and had not been peer-reviewed, which may raise concerns about its reliability.
Application
Carlsson’s study has been instrumental in the development of new antipsychotic drugs, particularly those targeting dopamine pathways more precisely and exploring neurotransmitters like glutamate and serotonin. Glutamatergic antipsychotics are still in development, offering hope for patients who do not respond to traditional drugs. Despite ongoing research into “smart” antipsychotics, none have yet become widely prescribed, suggesting Carlsson’s study remains relevant rather than outdated.
Validity
Carlsson questioned the validity of the Dopamine Hypothesis, which he helped establish, by highlighting evidence supporting alternative theories. For example, atypical antipsychotics like Clopazine reduce psychotic symptoms without primarily targeting dopamine. He proposed that both the Dopamine and Glutamate Hypotheses may be valid, and research should continue on both, a position that has been widely accepted by later scientists.
Ethics
As a review study, Carlsson et al. did not conduct new experiments, meaning there are no direct ethical concerns. However, some cited studies involved ethical issues, such as:
Animal research in which lab mice were given drugs to induce psychotic symptoms.
Human studies where participants (some with schizophrenia) were given amphetamines or PCP to increase psychotic symptoms, often without knowing if they received the real drug or a placebo (raising concerns about deception and risk).
While these ethical concerns exist, Carlsson et al. were only reporting on these studies, not conducting them.
describe genetics as an explanation, inc. adoption studies and twin family studies for schiz
There is evidence from twin and family studies for a genetic factor in schizophrenia. If identical twins are more likely to both have schizophrenia than non-identical twins, this suggests a genetic explanation, at least in part, for schizophrenia. If a family has more members with schizophrenia than might be expected in the general population, this too can be evidence for a genetic explanation for schizophrenia.
ADOPTION STUDIES
These look at the incidence of schizophrenia when a child is born to parents of whom one or both are schizophrenic and whom are adopted early in life into non-schizophrenic families. If schizophrenia is genetic, we would expect a higher rate of the disorder in those who are adopted but have biological parents with schizophrenia compared to those who are adopted where their biological parents do not have schizophrenia.
HESTON (1966) Compared adopted children whose natural mother had schizophrenia and 47 adopted children whose natural mothers didn’t have a mental disorder. Of the children with schizophrenic mothers, 10% went on to develop it, whilst none of the other group did, suggesting it is genetically passed down from parent to child.
FINNISH ADOPTION STUDY (1969) comprised of 112 babies who were adopted away from their schizophrenic mothers with a matched control group of 135 babies adopted away from their non-schizophrenic mothers. By 1987, only 1.5% of the control group have developed schizophrenia compared to 7% of the experimental group with schizophrenic biological mothers, again suggesting a genetic link.
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TWIN (FAMILY) STUDIES
Twin studies investigate the concordance rate for schizophrenia in identical twins that have been reared apart. If pairs of twins are both diagnosed with schizophrenia they are said to be concordant (in agreement for schizophrenia). Monozygotic (MZ) twins have the same genetic makeup, but if they are reared apart they have different environments. If there is a high concordance rate for MZ twins reared apart, this suggests that genes have an influence – this helps provide evidence in the nature-nurture debates surrounding mental illness. Studies have found a high concordance rate, with the average rate for MZ twins being 48% (including those who have been reared apart).
KENDLER ET AL (1985) have shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population at getting schizophrenia, which indicates a genetic link.
Gottesman and Shields (1966) conducted a twin study on schizophrenia to investigate the genetic basis of the disorder. They analyzed medical records of 57 twin pairs (both identical [MZ] and fraternal [DZ]) where at least one twin had been diagnosed with schizophrenia. Their findings showed a higher concordance rate for schizophrenia in MZ twins (42%) compared to DZ twins (9%), suggesting a strong genetic component. However, since the concordance was not 100%, environmental factors also play a role. This study provided key evidence for the hereditary nature of schizophrenia while acknowledging the influence of environmental factors.
what does the genetic explanation show for schiz
The data shows that schizophrenia can only be in part genetic, if it were entirely genetic MZ twins would show a 100% risk, as they are genetically identical. The 48% shows that other factors must be involved, so genetic factors do not cause schizophrenia, BUT provide a PREDISPOSITION to developing it.
Many of the genes that have been found that relate to schizophrenia seem to impact on the function of the brain. So genetic predisposition might be the link between the risk and neurotransmitter dysfunctions that result in schizophrenia, such as glutamate.
Family studies have been criticised as they do not remove environmental influences. Members of the same family share a similar environment and so the higher risk for close family members could reflect elements of a common environment such as psychosocial stress or social learning rather than genetic factors.
Genetic factors can also explain schizophrenia in families when there is not family history of the condition. This is because of MUTATIONS which are changes in cells, resulting from copying errors during cell division or exposure to radiation, poison or viruses.
evaluate the genetic explanation of schiz
HOWEVER, there are only fairly small statistical relationship between variations in particular genes and the development of schizophrenia. This suggests that either several genes are involved, or that genes work in conjunction with particular environmental conditions that make some individuals particularly vulnerable to schizophrenia.
Fewer than one third of people with schizophrenia have a family history of schizophrenia, which suggests that there is complexity in the genes in question. More direct genetic influence should have been found if schizophrenia came through the family line, but for many, that is not the case.
Chromosomal abnormalities found by SHERRINGTON (1988) linked schizophrenia to an abnormality on chromosome 5, although these findings have not been replicated, other evidence has made chromosomal connections to schizophrenia, for example patients with a section of 22q11 missing (known as ‘22q11 deletion’) do show psychotic symptoms similar to the symptoms of schizophrenia and the frequency of these symptoms for those with ‘22q11 deletion’ is 18%, greater than the 1% frequency for schizophrenia in the general population.
The International Schizophrenia Consortium (2008) found that schizophrenics are more likely to have structural changes to their genes. The abnormalities were found in chromosome 22, chromosome 1 and chromosome 15, all of which had missing DNA when compared to non-schizophrenics.
Genetic explanations can take into account other factors in schizophrenia that come from the environment. These include maternal infection affecting the foetus, taking cannabis and epigenetic modification, where genes not only act on the organism at the start of its development but continue to affect the organism’s development. This is a DIATHESIS STRESS MODEL. Environmental factors can affect body mechanisms that are driven by genes, such as stress (cortisol) and hormones. To understand genetic factors there is a need to study such environmental factors as possible triggers as well. This is a more holistic view of the biological causes of schizophrenia, and can account for differences in concordance rates in familial groups, especially MZ twins reared in different environments.
Another strength is in the many different ways genes and variations are studied. Family studies can help to identify gene issues, such as deletion in a section of 22q11, which shows symptoms of psychosis. Twin studies suggest a high likelihood that genes explain schizophrenia. DNA pooling is used to compare the DNA of those with schizophrenia against controls to look for gene variants and differences. Having many methods can help if the same findings are uncovered as this increases the reliability of the findings.
A final criticism of studying genes in relation to schizophrenia is that it is reductionist, focusing on parts rather than on the ‘whole’ characteristic in question. There is room for environmental factors either to ‘cause’ schizophrenia or to lead to epigenetic modification. It is likely that both environmental stressors and genetic features are what lead to schizophrenia.
describe the social explanation of schiz for social class
SOCIAL CLASS
There is evidence that people in the lowest social classes and groups such as immigrants have a higher incidence of
schizophrenia than others in the UK. It appears therefore that social class might either be a cause of schizophrenia
or at least be involved in its development. In the UK an incidence of about 4 people per 1,000 has been found, both
in the lowest social class in the white population and in black immigrant groups. This is a lot higher than the 1% that is generally accepted as the rate of schizophrenia in the general population. Studies regularly show that schizophrenia is found more in the lower social classes, among the unemployed and those living in deprived city areas.
Several characteristics associated with urban living (social deprivation, unemployment, poor housing, crowding, low social status) may provide a high level of psychological stress, leading to schizophrenic breakdown in people who are vulnerable.
Cooper (2005) suggests that for single men the rate of schizophrenia in social class 5 (unskilled labourers) was 4.1 times as high as in social class 1 (higher managerial), which is evidence that social class is at least a feature in schizophrenia. Lower social class is a risk factor for schizophrenia, as it involves social adversity.
Complete Social Drift is an explanation that those with schizophrenia become lower class because of the difficulties that arise from having schizophrenia.
“Social Drift” suggests that when suffering with schizophrenia, coping skills are poor, individuals who suffer from schizophrenia have difficulty completing their education and getting a decent job.
They gradually drift downward in society and become part of the lower classes, which has nothing really to do with the development of schizophrenia; it is linked to life circumstances that they are in this situation.
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describe social adversity for a social exp. for schiz.
SOCIAL ADVERSITY
Schizophrenia is found more in cities than rural areas, so it might be that city life leads to schizophrenia. Schizophrenia shows clustering in declining inner city areas, so perhaps being brought up in a poor and declining city area leads to schizophrenia and not just being in the city.
Hjem et al. (2004) showed that ‘social adversity’ in childhood relates to the development of schizophrenia later in life. Pressures in childhood and adolescence (social adversity) link to being in a lower social class and also link to schizophrenia.
Features in the environment that might affect the development of schizophrenia include:
“Sociogenetic Hypothesis” claims that living under conditions of poverty may create enough additional stressors to precipitate schizophrenia, particularly in individuals who are already genetically predisposed to develop the disorder. Stressors associated with poverty include higher crime rate, poor housing and lack of employment opportunities and therefore it is these factors that cause or help promote the onset of the illness.
The idea helps to explain the fact that although there are more people with schizophrenia in the lower classes, they are concentrated in inner-city areas, and that black immigrants are more likely to be diagnosed with schizophrenia than white lower-class groups. Social adversity helps to explain these two pieces of evidence better than social drift.
There are problems in claiming that social adversity, including poverty, unemployment, social isolation and living in inner-city areas, is responsible for someone developing schizophrenia. A tendency to schizophrenia seems to come from what happens to someone in childhood and the early stages of their lives, rather than developing because of lower socioeconomic status and related issues (Cooper, 2005). Therefore, the link between schizophrenia and low
socioeconomic status might come from children living in these circumstances as much as from the social status of an adult.
Stressful life events, rather than social class or adversity, may trigger schizophrenia. Brown and Birley (1968) found that 50% of patients with schizophrenia had experienced at least one major life event in the 3 weeks beforehand; only 12% had experienced a life event in the preceding 9 weeks; very few healthy controls reported any life events over the same 12-week period.
describe immigration as a social explanation for immigration for schiz.
IMMIGRATION
In the UK, census data have consistently shown a higher incidence of schizophrenia in African-Caribbean immigrant populations (Census 1991 and 2001), It is estimated that there are four times as many incidences of schizophrenia in these populations as in the white indigenous population, HOWEVER, it is not thought that there is a genetic reason for higher levels of schizophrenia in black immigrants, this points to social situations as a possible causal factor.
The evidence supporting the social class and adversity affecting schizophrenia within immigrant populations includes:
HOWEVER, social factors may act with other factors particular to the individual (such as their early experiences or genes) in such a way that either trigger, or perhaps not prevent, schizophrenia. White people in the lowest socioeconomic groups do not show the increased risk of having mental disorders that black immigrants to the UK do. This suggests that there is more to this than simply social adversity and lower class status.
ALSO, there could be a cultural bias in diagnosis, and any differences in incidence of schizophrenia across social class and ethnic groups may be better explained by bias in diagnosis than social causation. However, there is no conclusive evidence for this as in retrospect it is nearly impossible to know if a patients’ diagnosis is due to their social or ethnic group or because they presented with clear symptoms of the disorder.
evaluation of the social exp. for schiz
Evaluation of social explanation
STRENGTHS
Not everyone with certain environmental circumstances develops schizophrenia although there might be environmental triggers. Other causes are possible such as genetic and neurotransmitter functioning i.e., dopamine receptors being faulty. It is possible that both explanations are right and so they should complement one another in helping the schizophrenic patient rather that going for a reductionist stronghold.
The diathesis-stress model considers that stressors in the environment work with an individual’s biological features such as genes when considering issues like schizophrenia. A strength of the social causation hypothesis is that it helps to explain the environmental part of the interaction between biology and environment in the cause of schizophrenia.
There is a strong of supporting evidence for social factors, for example Mortensen et al. (1999) in Denmark, who found a two-fold increase of risk of developing schizophrenia for those born in the capital compared with those born in a rural region; and Eaton et al. (2000), who also found that there was more schizophrenia in urban settings than in rural settings. These findings support one another and suggest reliability in the claim that social factors at least affect
whether schizophrenia develops, even if they are not the actual cause of it.
WEAKNESSES
It might be that poverty, unemployment and lack of social support are stressors and it is this stress that causes the schizophrenia, not the environment itself. Myin-Germeys et al. (2003) found patients with schizophrenia showed more intense negative emotional reactions to daily hassles. This suggests that these emotional reactions make patients with stressful life events more vulnerable.
Hemsley (1993) suggests there is a substantial breakdown in the relationship between memory and perception in schizophrenics. As a result, people with schizophrenia are often unable to predict what will happen next, their concentration is poor, and they attend to unimportant or irrelevant aspects of the environment. Their poor integration of memory and perception leads to disorganised thinking and behaviour. Therefore, schizophrenia could be a cognitive dysfunction and not social or biological in its roots.
It is hard to separate environmental factors to see if they cause schizophrenia, as they could be the result of schizophrenia, as the social drift hypothesis suggests. It is plausible that those with schizophrenia drift into the lower social classes and into adversity because of the disorder, such as not being able to work, and also through symptoms of the disorder, such as difficulty with personal care.
In urban regions crowded living conditions can lead to toxins in the environment, such as leaded fuel, and there are other risk factors, such as not having social support, instability among communities leading to social isolation, and difficulties in communication, but it is hard to know which social factors are involved in the development of schizophrenia.
describe individual differences for schiz.
The document discusses various explanations for schizophrenia, including individual, social, developmental, and psychodynamic perspectives:
Cultural & Social Factors: Cultural differences affect the experience, diagnosis, and risk factors of schizophrenia. Social adversity in childhood (e.g., poverty) may increase the risk of developing schizophrenia later in life.
Family Communication: Some theories suggest that maladaptive family interactions, like double-bind communication (sending mixed messages), contribute to schizophrenia. However, studies show this may not be a definitive cause.
Psychosexual Development: A psychodynamic perspective suggests schizophrenia results from unresolved childhood trauma, causing regression to an early developmental stage.
Neurodevelopmental Model: The most widely supported theory states that schizophrenia originates from brain development issues in early life (prenatal or infancy), which later manifest as symptoms during adolescence or adulthood.
The document emphasizes evaluating different explanations while recognizing that biological factors play a crucial role in schizophrenia’s development.
describe and evaluate developmental psych for schiz
5.1.6 Developmental Psychology
Genetic and Developmental Factors: Schizophrenia may arise due to genetic influences affecting brain development.
Social Adversity: Hjem et al. (2004) found that difficult childhood environments, such as poverty or stress, contribute to the risk of schizophrenia.
Family Communication Issues:
Double-Bind Theory (Bateson et al., 1956): Schizophrenia may result from receiving conflicting messages from parents (e.g., saying “I love you” in a harsh tone). This confusion may lead to disorganized thinking.
Ringuette & Kennedy (1966): Clinicians analyzed letters from parents to hospitalized children. They found no significant difference in double-bind communication between schizophrenic patients and those with other disorders, challenging the theory’s validity.
Psychodynamic Explanation:
Trauma and unresolved conflict between the id, ego, and superego can cause regression to an earlier psychosexual stage.
Schizophrenia is linked to primary narcissism, where the ego has not fully developed, leading to a loss of contact with reality.
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Evaluation of the Psychodynamic Explanation
✅ Strengths:
Highlights early childhood experiences as a potential factor in schizophrenia development.
Explains why symptoms such as disorganized thinking and withdrawal may occur due to regression to an earlier stage of development.
Emphasizes the role of family dynamics, which can be explored in therapy.
❌ Weaknesses:
Lack of empirical evidence: The theory is based on subjective interpretations rather than scientific studies.
Ignores biological factors: The majority of research supports a neurodevelopmental model, which links schizophrenia to brain abnormalities rather than early psychosexual conflicts.
Limited explanatory power: If early trauma caused schizophrenia, we would expect a much higher number of cases among those with difficult childhoods. However, not all individuals with childhood trauma develop schizophrenia.
Ringuette & Kennedy (1966) study contradicts the double-bind theory, showing that schizophrenic patients did not receive significantly more contradictory messages than those with other disorders.
describe and explain drug therapy for schiz.
Summary of Drug Therapy for Schizophrenia
Introduction:
Drug therapy emerged in the 1950s as a breakthrough, allowing many patients to function normally.
Since schizophrenia is linked to neurotransmitter imbalances, drugs aim to correct these imbalances.
Chlorpromazine (first used in 1952) is a dopamine antagonist that blocks dopamine receptors to stabilize symptoms.
Types of Antipsychotic Drugs
Typical (First-Generation) Antipsychotics
Includes chlorpromazine and haloperidol
Blocks dopamine receptors to reduce symptoms
Well-established but has more side effects
Atypical (Second-Generation) Antipsychotics
Includes clozapine, risperidone, olanzapine
Fewer side effects and works differently than typical antipsychotics
Some mechanisms remain unknown
Antipsychotics can be taken as tablets, syrups, or injections (for those at risk of stopping medication).
Some patients may stop after a course, while others require lifelong medication.
Effectiveness of Drug Therapy
✅ Strengths:
Meltzer et al. (2004) tested 481 schizophrenia patients using different drugs, a placebo, and haloperidol (a well-known antipsychotic).
Haloperidol significantly improved symptoms compared to the placebo.
Some new drugs also improved symptoms, proving that drug treatment is effective to some extent.
❌ Weaknesses (Side Effects):
Typical antipsychotics (e.g., chlorpromazine, haloperidol) cause:
Sleepiness, muscle spasms, low blood pressure, weight gain, dry mouth, and motor restlessness.
Atypical antipsychotics (e.g., risperidone, olanzapine) also have similar side effects.
evaluate drug treatments
Evaluation of Drug Treatments for Schizophrenia
✅ Strengths of Drug Therapy
More Ethical & Effective: Compared to pre-1950s treatments, antipsychotic drugs allow patients to live in society rather than being permanently institutionalized.
Scientific Basis: Drug treatments are backed by strong biological evidence, making them reliable and effective.
Pickar et al. (1992): Found clozapine to be the most effective in treating schizophrenia, even in patients resistant to previous drugs. Placebo was the least effective.
Emsley (2008): Studied early risperidone injections, finding 84% of patients had at least a 50% symptom reduction, and 64% went into remission.
Schooler et al. (2005): Compared first-generation (haloperidol) and second-generation (risperidone) drugs in 555 patients. Both reduced symptoms in 75% of cases, but risperidone had fewer side effects and a lower relapse rate (42% vs. 55%).
❌ Weaknesses of Drug Therapy
Non-Adherence: Around 50% of patients do not take their medication consistently due to forgetfulness, lack of awareness, or side effects.
Ethical Concerns: Drugs are sometimes criticized as a “chemical straitjacket,” raising concerns about forced medication.
Limited Effectiveness: Even with medication, 50% of patients still experience distressing symptoms (Rosa et al.).
Side Effects:
Short-term: Sleepiness, muscle spasms, weight gain, and sexual dysfunction.
Serious Risks:
Neuroleptic Malignant Syndrome (NMS): A rare but life-threatening condition (0.05% of cases) causing nausea, high blood pressure, confusion, coma, and even death (Adityanji & Kaizad, 2005).
Tardive Dyskinesia: Involuntary facial and limb movements, though less common with second-generation drugs.
Doesn’t Address Social/Environmental Factors: Drugs don’t resolve issues like housing, employment, or social support, which impact relapse and hospitalization rates. Assertive community programs provide a more holistic approach.
describe and explain act therpay and evaluate
Assertive Community Therapy (A.C.T.) for Schizophrenia
Overview of A.C.T.
A.C.T. is designed for schizophrenic patients who frequently relapse and require hospitalization.
It helps individuals with social and independent living difficulties.
Developed by Stein & Test in Madison, Wisconsin, originally called the Madison Project.
Became essential in the 1970s after mass hospital discharges, requiring strong community-based support.
Characteristics of A.C.T.
Focuses on community mental health services.
Helps with social skills, friendships, and independent living.
Reduces hospitalization rates by providing continuous support.
Often used with other psychosocial treatments like family therapy and social skills training.
Evidence for A.C.T.
Dixon (2000), Bond et al. (2001), Mueser et al. (1998), Bustillo et al. (2001), and Zygmunt (2002) provide supporting research.
Studies show reduced hospitalization and improved patient stability.
Ethical Concerns & Counterarguments
Gomory (2001) argues A.C.T. is paternalistic and coercive, as 11% of clients feel forced into treatment.
Case managers exert control over clients with severe symptoms, arrests, or substance abuse.
Bond (2002) counters, stating A.C.T. increases freedom by preventing hospitalization and promoting community living.
Conclusion
A.C.T. is widely used in Australia, Canada, the UK, and the USA.
It is combined with other treatments like social skills and family therapy for better rehabilitation.
It has been extended to other mental illnesses beyond schizophrenia.
✅ Strengths of A.C.T.
Effective for frequent relapsers, providing social skills training and family therapy.
Bond (2002) found A.C.T. beneficial across age, gender, and culture, and only 11% of clients find it restrictive.
Helps patients integrate into society, preventing long-term hospitalization.
❌ Weaknesses of A.C.T.
Doesn’t improve symptoms directly (positive/negative symptoms or employment prospects).
Best suited for urban areas with high schizophrenia cases, as it requires intensive staffing.
Gomory (2001) criticizes the lack of patient choice, as clients lose decision-making responsibility.
describe ocd and features
Features of OCD:
The illness affects as many as 12 in every 1000 people (1.2% of the population) from young children to adults, regardless of gender or social or cultural background. In fact, it can be so debilitating and disabling that the World Health Organisation (WHO) has actually ranked OCD in the top ten of the most disabling illnesses of any kind, in terms of lost earnings and diminished quality of life.
The ratio of men to women suffering with the disorder is 1:1, although, more specifically, the disorder’s onset is reported to occur earlier in men than women.
Based on current estimates for the UK population, there are potentially around 741,504 people living with OCD at any one time.
Studies have demonstrated that at least a third of all adult sufferers have reported onset of OCD as occurring during childhood or adolescence.
Obsessions
Obsessions are unwelcome and intrusive thoughts, images, urges or doubts that repeatedly appear in someone’s thoughts; for example, thinking that they have been contaminated by dirt and germs, or experiencing a sudden urge to hurt someone.
These obsessions are often frightening or seem so horrible that they cannot share them with others. The obsession interrupts their other thoughts and make them feel very anxious.
Compulsions
Compulsions are repetitive activities that someone with OCD will feel they have to do.
This could be something like repeatedly checking a door to make sure it is locked or repeating a specific phrase in their head to prevent harm coming to a loved one.
The aim of a compulsion is to try and deal with the distress caused by the obsessive thoughts and relieve the anxiety they are feeling. However, the process of repeating these compulsions is often distressing and any relief is often short-lived.
Classification
At present (2016) the European International Classification of Diseases (ICD) currently lists OCD in its own subcategory under the category of Neurotic, Stress-related and Somatoform Disorders (F40-F48), although within the same larger category as other anxiety disorders. With regard to the essential features of OCD, the ICD-10 and DSM-IV-TR manuals state several diagnostic criteria for Obsessive-Compulsive Disorder.
describe one biological theory/exp. of ocd
Neural Explanations of OCD
Brain Structures Involved
Prefrontal Cortex (PFC): Controls decision-making and regulates primitive behaviors.
In OCD, overactivation of the PFC leads to exaggerated control over primal impulses.
Example: Handwashing compulsion—an overactive PFC does not switch off after the action is completed, leading to repetitive behavior.
However, this does not fully explain socio-territorial concerns, such as obsessing over locked doors.
Orbitofrontal Cortex (OFC): Located in the prefrontal cortex, responsible for impulse control and response inhibition.
Converts sensory information into actions.
PET scans show increased activity in OCD patients, leading to excessive compulsions.
The heightened activity also prevents patients from stopping their compulsive behaviors.
Neurotransmitter Involvement
Serotonin & Dopamine abnormalities are linked to OCD.
These neurotransmitters affect impulse control, compulsions, and anxiety regulation.
Socio-Territorial Concerns
Unlike primal survival instincts, obsessions with checking locks do not seem necessary for survival.
Saxena & Rauch (2000) suggest further research is needed to determine whether such concerns are instinctive or learned behaviors.
The basal ganglia, a brain structure involved in motor control, inhibition, and facilitation of movement, is also linked to habitual behavior, emotion, and cognition. Research suggests its involvement in disorders such as Tourette’s syndrome, schizophrenia, and OCD. Evidence for its role in OCD includes cases where head injuries in this region lead to OCD-like symptoms. Additionally, Max et al. (1994) found that disconnecting the basal ganglia from the frontal cortex during surgery reduced OCD symptoms, further supporting its significance in the disorder.
describe adler and kim and lee for ocd
Adler et al. (2000) used fMRI scanning to provide neurological evidence, likely identifying brain regions associated with a particular cognitive function or psychological condition. Their study contributed to understanding how specific areas of the brain are activated during certain tasks or experiences.
Kim and Lee (2002), on the other hand, conducted a case study, offering a detailed examination of an individual or a small group. This method allowed for an in-depth exploration of unique or rare conditions, providing qualitative insights that complement broader experimental findings. While fMRI studies offer generalizable neural patterns, case studies help illustrate real-world applications and individual variability.
dler et al. (2000) used fMRI scanning to provide neurological evidence, likely identifying brain regions associated with a particular cognitive function or psychological condition. Their study contributed to understanding how specific areas of the brain are activated during certain tasks or experiences.
Kim and Lee (2002), on the other hand, conducted a case study, offering a detailed examination of an individual or a small group. This method allowed for an in-depth exploration of unique or rare conditions, providing qualitative insights that complement broader experimental findings. While fMRI studies offer generalizable neural patterns, case studies help illustrate real-world applications and individual variability.
evaluate brain structure as an explanation for ocd
Neuroimaging studies provide reliable and objective data, consistently showing hyperactivity in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and caudate nucleus in OCD patients. However, these findings are correlational, meaning brain activity abnormalities may be a consequence rather than a cause of OCD.
Chamberlain et al. (2005) suggest that OCD symptoms arise from deficient inhibitory control, supporting the involvement of the orbitofrontal cortex and basal ganglia. However, most studies focus on adults with long-standing OCD, whereas the disorder often begins in childhood. This raises concerns that structural brain differences may result from prolonged OCD behaviors rather than causing them.
Neurotransmitters like serotonin and dopamine are also linked to OCD. SSRI antidepressants, which increase serotonin, effectively treat OCD, suggesting neurotransmitter involvement. However, the treatment aetiology fallacy warns that just because SSRIs help does not mean serotonin deficiency causes OCD—similar to how aspirin relieves headaches but does not mean headaches are caused by a lack of aspirin.
Genetic studies indicate a hereditary component to OCD. Carey and Gottesman (1981) found an 87% concordance rate for obsessive symptoms in identical twins, and Nestadt et al. (2010) reported higher OCD rates in identical twins (68%) than non-identical twins (31%), supporting a genetic link. However, no study has shown a 100% concordance rate, meaning environmental factors also play a role.
A key weakness of the brain structure explanation is its reductionism—it overlooks cognitive and behavioral factors. Learning theories propose that OCD can develop through classical conditioning and be maintained through operant conditioning. For example, compulsions like handwashing reduce anxiety, reinforcing the behavior. This suggests OCD may stem from learned behaviors rather than purely structural brain abnormalities.
describe a non-bio exp./theory for ocd - cog
Cognitive Explanation of OCD
OCD is characterized by intrusive thoughts (obsessions) and repetitive behaviors (compulsions). The cognitive model suggests that while intrusive thoughts are common, individuals with OCD attach excessive meaning to them, leading to distress and compulsive behaviors aimed at reducing anxiety.
Key cognitive traits linked to OCD include self-doubt, perfectionism, and an inflated sense of responsibility (Salkovskis, 1999). People with OCD believe they must prevent harm, leading to compulsions that reinforce obsessive thinking.
Libby et al. (2004) studied cognitive biases in OCD and found that individuals with OCD scored higher on responsibility, thought-action fusion, and perfectionism. Their study supports the idea that cognitive processes contribute to OCD symptoms.
Pace et al. (2011) identified six key cognitive variables in OCD, emphasizing how external criticism may contribute to OCD development. People with OCD often interpret criticism negatively, reinforcing dysfunctional thinking patterns.
Rachman (1998) highlighted two cognitive biases that contribute to thought-action fusion, where individuals mistakenly believe that thinking about an action is equivalent to carrying it out. This leads to compulsions to “neutralize” distressing thoughts.
Studies by Tolin et al. (2006) and Stekett et al. (1998) show that obsessive thoughts and compulsive behaviors are correlated, with neurophysiological evidence linking OCD to executive function deficits (Greisberg & McKay, 2003) and increased left frontal cortex activity (Martinot et al., 1990).
Limitations: Abramowitz et al. (2005) found that exposure and response prevention (ERP), based on behavioral learning theory, is as effective as cognitive therapy. This suggests that OCD may not be solely explained by cognitive factors, as behavioral therapies are also effective.
evalutions of the cognitive explanation for ocd
Strengths
CBT is successful as a therapy for OCD (see section on CBT) and works on the idea that thoughts guide feelings that lead to behaviour, which reinforces the thoughts; as Libby et al. (2004) found in their research between responsibility, perfectionism and though-action fusion.
The cognitive explanation has supporting evidence from neurophysiological studies of the brain, such as Martinot et al. (1990), these studies have high reliability as they are an objective measure of brain processes using scientifically credible scanning techniques.
The cognitive approach has resulted in CBT which is a therapy based on changing thought processes rather than using medication and drug treatment such as SSRI’s, this can be considered less invasive for the individual and there are no physical side effects of CBT, unlike drug treatments.
It could be argued that the cognitive model for OCD gives power to the patient when working to overcome their OCD. The individual can work to change their intrusive thoughts, for example, by changing their behaviour and this is in their power – therefore it is less deterministic that a biological explanation.
Weaknesses
If symptoms of OCD are cognitive in nature, such as anxious and self-doubting thoughts and ideas about perfection, then using a cognitive model to explain OCD is just repeating these symptoms. In this sense, it explains the symptoms but does not necessarily explain the cause of the symptoms, so it is descriptive. A biological explanation seems a better explanation as it looks at the function of the brain to explain how or why these begin in the first place.
ERP, which is a therapy largely based on learning principles, is found to be just as effective as cognitive therapy (CBT) according to Abramowitz et al. (2005) which goes against cognitive explanations for OCD. McLean et al. (2001) also found that ERP seemed to be more effective than CBT. Therefore, the explanation for OCD may lie in learning theories and the processes of classical and operant conditioning, not cognitive thinking.
Evidence from studies such Libby et al. (2004) as use patient rating scales and questionnaires, these methods could be considered subjective as the respondents may show social desirability when completing their responses and the data gathered may lack reliability.
Evidence from neurophysiological studies of the brain, such as Martinot et al. (1990) lack ecological validity as the scanning is in an unnatural environment and the tests used, such as the Stroop test, have limited task validity as they do not reflect the day to day experiences of living with OCD. Therefore, the supporting evidence may not be valid.
A biological explanation for OCD and a cognitive explanation for OCD may not be separate, although they have a different focus, with one looking at how the brain functions and the other explanation looking at thinking patterns related to how a person functions. Perhaps it is the brain functioning that underpins cognitive functioning, so the cognitive model of OCD can be supported by biological evidence. For example; the cognitive model involves executive functioning and cognitive control, which occurs in the prefrontal lobe.
describe and evaluate drug treatments for ocd
Biological Treatment for OCD: Drug Therapy
Two main drug classes are used to treat OCD: SSRIs/SRIs (Selective Serotonin Reuptake Inhibitors/Serotonin Reuptake Inhibitors) and Benzodiazepines (BZs). SSRIs, such as Prozac, Zoloft, and Clomipramine, increase serotonin availability in the brain, which may help regulate obsessive-compulsive symptoms. While the exact mechanism is unclear, SSRIs are widely used due to their effectiveness in reducing anxiety and compulsions.
Effectiveness of SSRIs/SRIs:
Randomized controlled trials and placebo studies show SSRIs are effective.
Soomro et al. (2009) and Dougherty et al. (2002) provide evidence supporting their use.
However, the treatment aetiology fallacy suggests that just because drugs treat symptoms does not mean low serotonin causes OCD.
Benzodiazepines (BZs):
These anti-anxiety drugs enhance GABA, slowing brain activity to reduce anxiety.
However, major psychiatric organizations (e.g., APA) do not recommend BZs for OCD due to limited evidence of effectiveness.
Evaluation of Drug Treatments
Strengths:
Drugs are convenient and non-disruptive, making them more accessible for those unable to engage in psychological therapy.
Drug therapy can help prepare patients for CBT, allowing them to manage anxiety better.
Studies (e.g., POTS team) show that combining CBT with medication is more effective than either alone.
Placebo-controlled trials ensure scientific credibility in drug effectiveness research.
Weaknesses:
High relapse rates – Simpson et al. (2004) found that 45% of SSRI-treated patients relapsed within 12 weeks, compared to 12% in behavioral therapy.
Does not address root causes – SSRIs manage symptoms rather than curing OCD.
Side effects – SSRIs can cause nausea, insomnia, or severe effects like hallucinations. BZs are addictive and linked to memory issues.
Short-term effectiveness – Without psychological intervention, symptoms may return after stopping medication.
describe and evaluate cbt for ocd
Cognitive Behavioural Therapy (CBT) for OCD
CBT focuses on how thoughts influence emotions and behaviors. It helps patients recognize and challenge intrusive thoughts rather than engaging in compulsions.
A key component of CBT for OCD is Exposure and Response Prevention (ERP), where individuals face their fears without performing compulsions. Over time, this reduces anxiety and weakens the OCD cycle.
CBT also helps patients identify cognitive distortions, such as inflated responsibility and thought-action fusion, and challenges these beliefs to break obsessive-compulsive patterns.
Evaluation of CBT for OCD
Strengths:
Addresses core cognitive distortions rather than just symptoms, potentially leading to long-term improvement.
Strong evidence base – Studies (e.g., van Oppen et al., 1995; Greist et al., 2003; Abramowitz, 2006) show CBT is effective for many patients.
Effective for around 70% of OCD patients (Cordioli, 2008), improving quality of life.
ERP is an effective component of CBT, and both cognitive therapy and ERP have shown comparable results in treating OCD.
Weaknesses:
Not effective for all patients – Around 30% do not respond to CBT.
ERP may be more effective long-term – Cottraux et al. (2001) found ERP showed greater improvement one year after treatment than cognitive therapy alone.
Therapist dependency – Success can depend on the therapist’s skill level, making results inconsistent.
Ethical concerns – Patients may struggle to give fully informed consent due to anxiety or lack of understanding of the treatment process.
Does not address root causes – CBT challenges faulty beliefs but does not explore their origins, meaning symptoms may persist if underlying causes remain unaddressed.
describe dev. diff in ocd
Development of OCD: Nature vs. Nurture
Nature (Biological Factors)
Prenatal & Early Development: Damage during pregnancy affects development more globally than postnatal damage, with boys being more vulnerable due to biological differences.
Genetics: OCD may have a genetic basis, as it tends to run in families, though identical twins do not always both develop OCD, indicating other contributing factors.
Brain Development: Accelerated growth of the prefrontal cortex (PFC) between ages 8-14 (when OCD symptoms often appear) suggests a link to abnormal brain development. Differences in the caudate nucleus and orbitofrontal cortex (OFC) development between boys and girls may explain why early-onset OCD is more common in boys.
PANDAS & Infections: Some children develop OCD symptoms after severe infections like strep throat, possibly due to the immune system mistakenly attacking parts of the brain. However, the infection is believed to trigger rather than cause OCD in genetically predisposed individuals.
Nurture (Environmental & Psychological Factors)
Negative Life Events: Studies (Khanna et al., 1988) suggest major stressors (e.g., bereavement, divorce, job loss) increase the risk of developing OCD.
Childhood Trauma: Individuals who experienced childhood sexual abuse (Saunders et al., 1992) are five times more likely to develop OCD.
Psychodynamic Theories (Freud & Others):
Ego Defense Mechanisms: OCD symptoms arise from inner conflicts, leading to:
Isolation: Viewing intrusive thoughts as alien.
Undoing: Performing acts (e.g., excessive cleaning) to counteract unwanted impulses.
Reaction Formation: Adopting opposite behaviors (e.g., celibacy to suppress sexual urges).
Anal Personality Theory: OCD may develop due to harsh toilet training in early childhood, leading to excessive cleanliness, orderliness, and control issues.
describe individual differences for ocd
Cultural & Gender Differences in OCD
Gender Differences in OCD
Neurobiological & Psychosocial Factors: Gender influences OCD through biological differences and social expectations (Mathis et al., 2011).
Prevalence & Symptom Differences:
Men: Earlier onset, greater severity of obsessions, more social impairment, and higher rates of sexual, religious, and aggressive symptoms, as well as substance use disorders (Bogetto et al., 1999).
Women: More contamination/cleaning symptoms, anorexia, and impulse-control disorders (Bogetto et al., 1999).
Social & Life Impact:
Men: More likely to remain single, live with family or in assisted homes (Sobin et al., 1999).
Women: More likely to involve family members in rituals (Matsunaga et al., 2000).
Pregnancy & OCD: 69% of female patients reported symptom onset or worsening during pregnancy/childbirth (Buttolph & Holland, 1990), suggesting OCD may be linked to perceived responsibility rather than gender itself.
Nature vs. Nurture in OCD Development
Nature (Biological Factors)
Genetic predisposition, brain structure differences, and hormonal influences may contribute to OCD.
Nurture (Learning Theory Explanation)
Classical Conditioning: Neutral stimuli (e.g., shaking hands) become associated with anxiety.
Operant Conditioning: Compulsions (e.g., handwashing) reduce anxiety, reinforcing the behavior (Mowrer, 1947).
Empirical Support: Exposure to obsessions triggers anxiety, and compulsions reduce it (Rachman & Hodgson, 1980).
Treatment Implications
Exposure Therapy (ERP): Prevents compulsions, helping patients learn their fears are unfounded.
Weaknesses of Learning Theory:
Ignores biological factors, cognition, and genetic influences.
Deterministic: Suggests behavior is solely shaped by the environment, ignoring individual control.
describle masellis contemp. study for ocd
George Phipps:
Xx
Mum:
On way home xxx
Summary of Masellis et al. (2003) Study on OCD and Quality of Life
Background & Aims:
The study aimed to assess the impact of obsessions, compulsions, and depression on the quality of life of individuals with OCD. It investigated whether the severity of symptoms influenced quality of life ratings.
Methodology:
*Participants: 43 OCD patients (18-65 years old) from an Anxiety Disorders Clinic in Canada.
*Measures Used:
◦Yale-Brown Obsessive Compulsive Scale (Y-BOCS) – Measures severity of obsessions and compulsions.
◦Illness Intrusiveness Rating Scale (IIRS) – Assesses the extent to which OCD interferes with different life domains.
◦Beck Depression Inventory (BDI) – Evaluates depression severity.
*Analysis: Statistical tests were conducted to determine relationships between symptoms and quality of life intrusiveness.
Results:
*Demographic factors (age, gender, marital status, education, etc.) did not predict OCD intrusion.
*Obsessions (r = 0.62, p < 0.01) and compulsions (r = 0.53, p < 0.01) correlated with intrusion, but compulsions were less significant.
*Depression was the strongest predictor of intrusiveness (54% of the variance), followed by obsessions (39%).
*Compulsions had no significant association with intrusiveness (p = 0.91), suggesting that treating compulsions alone may not improve quality of life.
Conclusions:
*Obsessions and depression significantly impact quality of life in OCD, while compulsions play a smaller role.
*Current OCD treatments focusing on compulsions may not be effective; cognitive therapy targeting obsessions and addressing depression may be more beneficial.
*Supporting research suggests that 17-44% of OCD patients do not exhibit compulsions, further emphasizing the need for obsession-focused treatment.
Evaluation:
✅ Strengths:
*Reliable and valid measures (Y-BOCS, IIRS, BDI).
*Comprehensive statistical analysis strengthens findings.
*Independent diagnosis using DSM-IV criteria enhances credibility.
*Findings have practical applications in improving therapy for OCD.
❌ Weaknesses:
*Limited generalizability – Sample from a single clinic may not represent all OCD patients.
*Small sample size – 43 participants is not reflective of the wider OCD population (~2.5%).
*Self-report bias – Social desirability and stigma may affect responses.
*Cross-sectional design – A single moment in time may not accurately reflect long-term symptoms; a longitudinal study would be more informative.
