Paper 1: Topic 4: Psychopathology Flashcards

1
Q

What are the 4 different definitions for abnormality

A

-statistical infrequency
-deviation from the social norms
-failure to function adequately
-deviation from the ideal mental health

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2
Q

Define statistical infrequency

A

Someone is abnormal if their mental condition is very rare in the population. objectively using statistics, comparing the individual’s behaviour to the rest of the population.

abnormal if its frequency is more than two standard deviations away from the mean incidence rates represented on a normal distribution curve so falls out of the range of the normal distribution

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3
Q

Define deviation from social norms

A

an unwritten expectation of behaviour passed through socialisation
-can vary from culture to culture and change over time.
-people who’s behaviour deviates from these societal expectations on how ‘normal’ people behave, may be seen as abnormal or social deviants

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4
Q

Define failure to function adequately and example

A

The individual is defined as abnormal if they cannot cope in their everyday lives, including their ability to interact with the world and meet their challenges

Eg: Failure to maintain basic nutrition, hygiene and relationships

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5
Q

Define deviation from the ideal mental health and who developed criteria of the ideals

A

abnormality is the absense of signs of good mental health
those who do not meet the particular criteria for psychological well-being are abnormal.
Positive definition and comes from a humanistic perspective, focusing on ways to improve and become a better person rather than dysfunction or deficit.

Jahoda developed criteria of these ideals
1) Accurate perception of reality
2) Positive attitude to themselves (good self-esteem and lack of guilt)
3) Self actualisation – reach potential
4) Resistance to stress
5) Environmental mastery
6) Be independent of other people (autonomy)

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6
Q

Give an example of statistical infrequency

A

IQ is measured in a normal distribution so people who score outside of the normal distribution can be defined as abnormal
Below 70 are abnormal and diagnosed with intellectual disability disorder

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7
Q

Give an example of deviation from social norms

A

-Someone walking around streets of London naked can be seen as abnormal but it’s normal in certain remote African tribes
-Acceptance of homosexuality
-Face and hair covering
-level of modesty in clothing choices

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8
Q

Who proposed the signs of failure to function adequately

A

Rosenhan & Seligman

Proposed the following signs:
-not conforming to interpersonal rules (eye contact)
-experience of severe personal distress
-behaviour is irrational or dangerous to themselves/others

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9
Q

What’s the strength and limitation of the definition of statistical infrequency

A

Strength
P: it is an appropriate measure in certain circumstances
Eg: IQ is measured in terms of normal distribution for those who are two or more standard deviations below the mean or less than 70 can be considered abnormal and can be diagnosed with intellectual disability disorder
Becks Depression inventory (BDI) measures depressive traits, and a score of >30 indicates severe depression
Ex: definition has real life application as it is used as a real measure for certain behaviors
L: increases validity as it’s an objective measure to define abnormality.

Limit:
P: many abnormal behaviours are desireable.
Eg: very few people have an IQ over 150, but having such an IQ is not undesirable. there are some common behaviors that are seen to be undesirable
Ex: for example, experiencing depression is relatively common but the disorder is considered abnormal and undesirable
Link: so we’re unable to distinguish between desirable and undesirable behavior.

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10
Q

What’s the strength and limitation of the definition of deviation from social norms

A

Strength:
P: it can be useful for clinical practice.
Eg: key defining characteristic of antisocial personality disorder is the failure to conform to culturally acceptable ethical standards
Ex: deviation from social norms is helpful in diagnosing schizotypal personality disorder involving ‘strange p’ beliefs and behaviour
Link: means that it’s useful in psychiatric diagnosis

Limit:
P: social norms change across time periods and therefore it is not consistent across time
Eg: homosexuality is today socially acceptable in most western cultures but I’m the past it was a classification in the DSM and even illegal In the UK before 1967 and considered a mental illness until 1973
Ex: whether someone is defined as abnormal is then dependant upon the prevailing social morals and attitudes
Link: can then produce inconsistent results across history so the measure lacks temporal validity

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11
Q

What’s the strength and limitation of the definition of failure to function adequately

A

Strength:
P: it takes into account the patient’s subjective perspective.
Eg: allows us to view the mental disorder from the point of view of the person experiencing it
Ex: relatively easy to judge objectivity because we can list behaviours eg: can dress themselves and prepare meals, and check whether a person is functioning
L: therefore if treatment and support is required it can be specific to the patients needs

Limit:
P: it requires an objective judgement of a way of life
Eg: some may not see unemployment as a failure to function adequately, but others of an alternative lifestyle may disagree. Those who enjoy extreme sports may also be seen to be behaving in a maladaptive way
Ex: if we treat these as ‘failures’ of adequate functioning, we might be limiting personal freedom and discriminating minority groups
Link: posing a challenge for this definition because it may depend on who is making the judgement rather than the behaviour itself

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12
Q

What’s the strength and limitation of the definition of deviation from ideal mental health

A

Limit:
P: it sets high standards for mental health which may be unachievable for most people
Eg: less people achieve full ‘self actualisation’. It’s hard to even be sure what this is for each person. So this definition says a large number of people have aspects of abnormality
Ex: so the criteria is difficult to measure for example how easy is it to assess whether someone has the capacity for personal growth
Link: therefore its argued that this definition is not usable when it comes to defining abnormality but may be better within the field of positive psychology at criteria to strive for.

Strength:
P: the criterion is highly comprehensive
Eg: Jahoda’s concept includes a wide range of criteria, and covers most of the reasons people seek mental health support
Ex: allows mental health to be discussed meaningfully with a range of professionals with different theoretical views, eg psychiatrist or CBT therapist
L: ideal mental health provides a checklist against which we can assess and discuss psychological issues

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13
Q

Define cultural relativism

A

idea that one cannot judge behaviour properly unless it is viewed in the cultural context from which it originated.
Lack of cultural relativism can result in the norms of the home culture being used to assess the behaviour of individuals from another culture – example of ethnocentrism.

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14
Q

Give 2 examples of cultural relativism

A

-Australia in the early 1970s homosexuals were given electric shocks to cure them of their illness
-China people fear the wind as it is believed by some to carry negative energy (yin)

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15
Q

Give the limitation of all 4 abnormality definitions relating to cultural relativism

A

P: A limitation of [deviation from ideal mental health, statistical infrequency, failure to function adequately, deviation from social norms] definition of abnormality is that it does not consider cultural relativism.

statistical infrequency:
Eg: symptoms of Schizophrenia (hearing voices) are common and not considered abnormal in some cultures. Whereas in other cultures hearing voices is seen less typically.
E - This shows that some behaviours can be more statistically frequent in some cultures compared to others.

deviation from social norms:
Eg: the DSM which is used to diagnose disorders is largely based on Western social norms.
E – This shows that what is classed as abnormal is based on Western social norms and it ignores Eastern social norms and values and it is therefore ethnocentric to use the DSM to classify people from Eastern cultures as abnormal.

failure to function adequately:
Eg: The idea of whether a patient is functioning is related to cultural ideas of how people should live their lives and this could be class dependant.
E : This may explain why lower-class and non-white patients are diagnosed with mental disorders more often – because their lifestyles are different from those who are making the definitions.

deviation from ideal mental health:
E – For DIMH, some of Jahoda’s criteria are specific to European and American cultures, they are culture-bound. For example, self- actualisation is more common in individualistic cultures. Whereas collectivist cultures may see independence as a negative thing.
E – Therefore, generalising this definition may be seen as ethnocentric as it is judging the concept of “normal” by Western and therefore individualistic standards.

Link: therefore it doesn’t consider cultural differences and therefore cannot be used as a universal explanation of abnormality due to ethnocentrism

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16
Q

What are the 2 diagnostic manuals most commonly used in psychiatry?

A

Books which are used by professionals to diagnose/categorise mental disorders:

1) DSM – diagnostic statistical manual, published by American Psychiatic Association
2) ICD – International statistical classification of diseases. Published by World Health organisation (WHO)

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17
Q

What are the 3 categories of symptoms that you need to be aware of?

A

Emotional – feelings
Behavioural – actions
Cognitive – thoughts

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18
Q

Phobias:
What is the definitions of a phobia?

A

Persistent irrational fear that is disruptive to everyday life of a specific situation, object or activity (a stimulus) so is avoided or endured with distress

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19
Q

Phobias:
What are the 3 categories of phobias recognised by DSM-5?

A

Specific phobia – phobia of an object, eg: animal or body part, or a situation eg: flying or injections
Social phobia (social anxiety) – phobia of a social situation eg: public speaking
Agoraphobia – phobia of being outside or In a public space

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20
Q

Phobias:
What are the diagnostic criteria for phobias for DSM-5?

A

> 6 months, intensity, distress
Presence of the emotional, behavioural and cognitive responses is almost always triggered in repossess to the phobic stimulus for a period of 6 months or more

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21
Q

Phobias:
Describe the emotional (feelings) symptoms associated with phobias

A

Anxiety - phobias involve the emotional response of anxiety: high arousal
Fear - immediate and unpleasant response when we encounter or think about a phobic stimulus
Unreasonable - disproportionate to any threat posed

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22
Q

Phobias:
Describe the behavioural (actions) symptoms associated with phobias

A

Panic - can cause shortness of breath, shaking, and high heart rates
Avoidance - show effort to avoid the phobic stimulus (which can affect their daily life, e.g. reducing amount of sleep)
Endurance - person chooses to remain in the presence of the phobic stimulus; eg a person with arachnophobia staying in a room with a spider to keep an eye on it, rather than leaving.

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23
Q

Phobias:
Describe the cognitive symptoms associated with phobias

A

Selective attention – person finds it hard to look away from phobic stimulus
Irrational beliefs – phobic person doesn’t respond to evidence eg: scared of flying even if flying is less dangerous than driving so phobia isn’t reduced
Cognitive distortions – thoughts about the phobic stimulus are distorted eg: someone with arachnophobia sees spiders bigger than what they really are

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24
Q

Define cognitive

A

How people process info in relation to the phobic stimulus – thoughts

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25
Q

Depression:
What is the definition of a depression?

A

Mental health disorder that’s characterised by Persistent sadness & lack of interest in pleasure in previously rewarding or enjoyable activities. It can disturb sleep and appetite; tiredness and poor concentration are common

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26
Q

Depression:
What are the 4 categories of depression recognised by DSM-5?

A

Major depressive disorder – severe but short term depression
Persistent depressive disorder – long term or recurring depression, including sustained major depression (dysthymia)
Disruptive mood dysregulation disorder – childhood temper tantrums
Premenstrual dysphoric disorder – disruption to mood prior to and/or during menstruation

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27
Q

Depression:

What are the diagnostic criteria for depression for DSM-5?

A

5 symptoms every day, 2 weeks
(Depressed mood most of the day, nearly every day, anhedonia, and at least 5 of the listed symptoms persisting for at least 2 weeks)

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28
Q

Depression:
Describe the emotional symptoms associated with depression

A

Low mood (required symptom: - feeling ‘empty’ and ‘worthless’ or ‘hopeless
Anhedonia - loss of interest or pleasure in hobbies and activities that were once enjoyed; may be accompanied by avolition (loss of motivation to perform goal-directed activities)
Anger - directed towards others or self – comes from the general feeling of being emotionally hurt
Low self-esteem - can lead to self-loathing

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29
Q

Depression:
Describe the behavioural symptoms associated with depression

A

Low activity level / reduction in energy - sufferers show a sense of tiredness, desire to sleep, and lower activity; can be the opposite: psychomotor agitation
Disrupted sleep (insomnia or increased sleep)
Disrupted eating (appetitive changes) - eat more or less
Aggression/self-harm - increased irritability; can become verbally or physically aggressive; can lead to ending a job or relationship; self harm can result in cutting or suicide attempts

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30
Q

Depression:

Describe the cognitive symptoms associated with depression

A

Poor concentration - can’t focus on a task as much as normal and find it difficult to make decisions
Attention to the negative – negitive thoughts including negative self-beliefs such as guilt and a sense of worthlessness
Absolutist thinking - See things as ‘black and white’ – can catastrophise situations, seeing something unfortunate as an absolute disaster
Memory bias - cognitive bias of remembering unhappy events more easily – negitive schema

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31
Q

OCD:
What is the definition of a OCD?

A

Obsessive compulsive disorder
Common mental health condition where someone had Obsessive thoughts (internal) & compulsive behaviours (external)

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32
Q

OCD:
What are the 4 categories of OCD recognised by DSM-5?

A

OCD - obsessive, recurring thoughts, images, and or compulsions (repetitive behaviours, such as handwashing)
Trichotillomania - compulsive hair-pulling
Hoarding disorder - compulsive gathering of possessions and the inability
to part with anything, regardless of value
Excoriation disorder - compulsive skin-picking

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33
Q

OCD:
What are the diagnostic criteria for OCD for DSM-5?

A

> 1hr/day; distress
Presence of obsessions, compulsions or both, which are time-consuming (>1hr per day), or cause significant distress of impact daily functioning

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34
Q

OCD:
Describe the emotional symptoms associated with OCD

A

Anxiety & distress - Obsessive thoughts are intrusive and frightening. The urge to compulsively repeat behaviour produces anxiety.
Depression - OCD is often accompanied by depression; compulsive behaviour can bring relief, but is short-term only
Guilt/disgust - often aware that their obsessive thoughts are irrational and that their compulsive behaviours are abnormal. Alternatively, they can suffer guilt over minor moral issues. Disgust may be direct towards the self, or externally, like dirt.

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35
Q

OCD:

Describe the behavioural symptoms associated with OCD

A

Repetitive/ritualistic compulsive behaviours - feel compelled to act on their obsessive thoughts with repetitive behaviours acts, called compulsions, such as handwashing. behaviours are repetitive, unpleasant, and interfere with daily life.
Anxiety (compulsions reduce anxiety) - caused by obsessions
Avoidance - avoid situations which trigger obsessions and compulsions, e.g. avoiding obsessive thoughts about germs by not emptying their bin

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36
Q

Describe the cognitive (thoughts) symptoms associated with OCD

A

Obsessive thoughts - obsessions are intrusive/recurring/unwanted thoughts. 90% of OCD sufferers experience them. repetitive, unpleasant, and interfere with daily life. They are present on most days, for a period of 2 weeks or more
Hypervigilance - selective attending and increased awareness of source of obsession in new situations
Cognitive coping strategies - eg a religious person tormented by guilt may respond by praying or meditating, which helps manage anxiety, but can become a distraction
Insight / Sufferer is aware these obsessive thoughts are irrational - aware that their cognitions are irrational. Despite this they maintain constant alertness and focus on potential hazards.

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37
Q

What is the behavioural approach?

A
  • learning theory which states all behaviors are learned through interaction with the environment through conditioning.
  • Behaviour is a response to environmental stimuli.
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38
Q

Behavioural approach:
What is classical conditioning?

A

Learning through association
Two stimuli are repeatedly paired together and the neutral stimulus eventually produces the same response as the unconditioned stimulus alone

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39
Q

Behavioural approach:
Explain the famous research associated with classical conditioning?

A

Pavlovs salivating dogs:
1) UCS (food) -> UCR (salivating)
2) UCS + NS (bell) -> UCR (salivating)
3) CS (bell) -> CR (salivating)

Watsons Little Albert
researchers initiated a phobia of a white rat when he learned to associate the rat (NS) with a loud noise (UCS). The phobia was then generalised to other white, furry items including Santa Claus’ beard

Conditioned - learnt through pairing
Unconditioned - automatic and not learnt
Neutral stimulus - paired with a response (UCR) to become a conditioned stimulus paired with a response (CR)

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40
Q

Behavioural approach:
What is operant conditioning?

A

Learning through consequences

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41
Q

Behavioural approach:
Explain the famous research associated with operant conditioning?

A

Skinners box:
- Positive reinforcement: behaviour that is rewarded is reinforced (repeated)
- Negative reinforcement: behaviour that avoids an unpleasant stimulus (eg shock) is reinforced (repeated)
- Punishment: behaviour that is results in an unpleasant outcome (shock) will not be repeated

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42
Q

Behavioural approach:
What is Mowrer’s (1960) two process model?

A

used learning theory to propose the behavioural explanation of phobias
It explains avoidance behavior but not phobic cognitions.

2 process model:
-Phobias are acquired or initiated through classical conditioning
-Phobias are maintained or continued through operant conditioning

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43
Q

Behavioural approach:
How are phobias initiated?

A

a phobia is acquired through learning an association
(classical conditioning)

Eg: can explain why someone develops a fear of dogs after being bitten:

Eg:fear of dogs
Being bitten (UCS) -> automatic fear (UCR).
dog (NS) is associated with being bitten (UCS) then the dog (now CS) then produces a fear response (now CR) on its own

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44
Q

Behavioural approach:

How are phobias maintained?

A

through operant conditioning which takes place when behaviour is reinforced
Eg: the likelihood of a behaviour being repeated is increased if the outcome is rewarding – positive reinforcement

  • person avoids a feared object to reduce anxiety -> negative reinforcement because a person avoids the situation to escape from an unpleasant situation
  • Such behaviour results in a desirable consequence which means the behaviour will be repeated
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45
Q

Behavioural approach:
Strengths of the behaviour approach as an explanation of phobias and two process model

A

Strength:
P: there’s supportive empirical case study evidence
Eg: Watson and Rayner used classical conditioning to create a phobia in an infant called Little Albert. Researchers iniated a phobia of a white when he learnt to assossiated the rat (NS) with a loud noise (UCS). Phobia was generalised to other white fury items like Santas beard.
Ex: supports CC as little Albert had no phobias before experiment. He developed the fear when pairing the loud noise with the whiter rat
L: increases validity of theory that phobias are learnt not innate as proposed by evolutionary explaination, as theory predicted the research findings

Strength of 2 process model
P: evidence for a link between bad experiences and phobias
Eg: De Jongh (2006) found that 73% of dental phobics had experienced a trauma, mostly involving dentistry
Ex: Further support came from the control group of people with low dental anxiety, where only 21% had experienced a traumatic event
Link: This supports the proposal that the association between stimulus (dentistry) and an unconditioned response (pain) can lead to a phobia

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46
Q

Behavioural approach:
Limitations of the behaviour approach as an explanation of phobias

A

Limit:
P: it does not offer a complete explanation of phobias
Eg: Bounton highlights that evolutionary factors could play a role in phobias, especially if the effects of a particular stimulus (e.g. snakes) could have caused pain or even death to our ancestors. Consequently, evolutionary psychologists suggest that some phobias (e.g. snakes and heights) are not learnt but are in fact innate, as such phobias acted as a survival mechanism for our ancestors
Ex: This innate predisposition to certain phobias is called biological preparedness (by Seligman) and casts doubt on the two‐process model since it suggests that there is more to phobias than learning as it doesn’t explain phobic cognitions
L: Whilst the behavioural explanation of phobias may explain the development of some phobias it does not explain ones that appear to be innate and have not been learnt through experience.

P: ignores the role of cognition (thinking)
Eg: Cognitivists argue that phobias develop as a result of irrational thinking, not just learning. For example, sufferers of claustrophobia may think ‘I am going to be trapped in this lift and suffocate’, which is an irrational thought that is not taken into consideration in the behaviourist explanation
Ex: Cognitive behavioural therapy (CBT) which is a treatment for phobias is suggested to be a more successful treatment than the behaviourist treatments which could indicate that the cognitive component of developing phobias is more important than the stimulus-response link.
L: challenges the validity of the behavioural explanation and suggests that the cognitive explanation of phobias may be a more appropriate one

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47
Q

Behavioural approach to treating phobias:
What are the 2 behavioural treatments / therapies

A

Systematic desensitisation
Flooding

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48
Q

Behavioural approach to treating phobias:
What treatment is systematic desensitisation and flooding behavioural treatments based on?

A

Counterconditioning:
A new response to the phobic stimulus is learned by pairing with relaxation instead of anxiety

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49
Q

Behavioural approach to treating phobias:
Define systematic desensitisation

A

Form of therapy for phobias that involves establishing a fear/anxiety hierarchy and teaching patients relaxation techniques. Use of relaxation at every level of the hierarchy gradually causes extinction of the fear.

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50
Q

Behavioural approach to treating phobias:
What is meant by reciprocal inhibition?

A

Patients learn to respond to a feared stimuli with relaxation instead of anxiety because fear and relaxation cannot co-exist.
This is what counterconditioning is based on

51
Q

Behavioural approach to treating phobias:
Explain the 3 steps of Anxiety hierarchy Of systematic desensitisation

A
  • 1) Anxiety heriachy -> SD involves the client and therapist designing a list or hierarchy of frightening / stressful events or objects.
  • 2) Relaxation -> client is taught deep muscle relaxation. As it’s impossible to experience fear and relaxation at the same time (reciprocal inhibition), can also 3) involve drugs eg: Valium, or hypothesis
  • Gradual exposure -> therapist helps client to work their way up the heirachry while maintaining this deep relaxation.
52
Q

Behavioural approach to treating phobias:
5 stages of systematic desensitisation

A

Stage 1) SD is based on couterconditioning procedure. Fear is replace with relaxation
Stage 2) SD gradually increases exposure to feared stimulus so it becomes more familiar
Stage3) Exposure is through an anxiety heirachy -least to most fearful – eg: phobia of dogs: see pictures of dogs -> hear a dogs bark -> go in a room with a dog -> touch the dog
Stage 4) client learns relaxation techniques to practise at each stage of heirachy. Must be achieved before they move onto the next stage
Stage 5) fear and relaxation can’t coexist – reciprocal inhibition. Client achieves relaxation at last stage of the heirachy then phobia is extinguished / extinct

53
Q

Behavioural approach to treating phobias:

How does flooding differ from SD in terms of exposure? With example

A

involves exposing phobic patients to their fear but without a gradual build-up in an anxiety hierarchy.
Eg: patient with arachnophobia may have a large spider crawl on their face

54
Q

Behavioural approach to treating phobias:
What does flooding stop a patient from doing?

A

flooding involves immediate exposure to a very frightening situation to prevent avoidance

55
Q

Behavioural approach to treating phobias:
How many sessions are needed for flooding to work?

A

Flooding sessions are longer than systematic desensitisation, with one session usually lasting 2-3 hours.
Sometimes only one long session is needed to cure a phobia

56
Q

Behavioural approach to treating phobias:
How does flooding work?

A
  • Flooding stops phobic responses very quickly as it prevents avoidance behaviour, so patient quickly learns that the phobic stimulus is harmless. - In classical conditioning terms this process is called extinction
  • learned response is extinguished when the conditioned stimulus (e.g. a dog) is encountered without the learnt response of fear (CR) as the association with the UCS has been broken
  • result is that the conditioned stimulus no longer produces the conditioned response (fear)
  • some cases the patient may achieve relaxation simply because they become exhausted by their fear response due to the immediate exposure
57
Q

Behavioural approach to treating phobias:
Strengths and limitation of systematic desensitisation as a treatment of phobias

A

Strength:
P: supportive empirical evidence to demonstrate its effectiveness
Eg: McGrath et al (1990) reported that 75% of patients with phobias responded to SD. It’s effective due to the in vivo techniques i.e. actual contact with the fear stimulus being more effective than in imagery- based techniques
Ex: Gilroy et al (1990) examined 42 patients with arachnophobia using 3x45 minute sessions, and found reduced fear 33 months later, compared to a control group (relaxation techniques only)
L: empirical evidence increases the validity of the treatment as a way to overcome phobias

Strength:
P: compared to flooding is that it is often preferred as a treatment for phobias by patients
Eg: Eg: it does not cause the same levels of distress that can occur when presented with the fear‐inducing stimulus immediately and as a result there are low attrition rates.
Ex: therefore considered a more appropriate treatment for individuals who may suffer from severe anxiety disorders since learning the relaxation techniques can be a positive and pleasant experience
L: SD may be seen as a more ethical treatment for these patients

Limit:
P: not effective in treating all phobias.
Eg: Patients with phobias which have not developed through a personal experience (classical conditioning), such as a fear of snakes, are not effectively treated using systematic desensitisation as it cannot be that their phobia has been learnt and therefore cannot be unlearnt.
Ex: Some psychologists believe that certain phobias have an evolutionary survival benefit and are not the result of learning
L: highlights a limitation of systematic desensitisation, which is ineffective in treating evolutionary phobias which have an innate basis.

58
Q

8/16 marker hasn’t come up before:

Behavioural approach to treating phobias:

Strength and limitations of flooding as a treatment of phobias

A

Strength:
P: it is at least as effective as other treatments for specific phobias but more cost effective
Eg: Ougrin (2011) compared flooding to cognitive therapies and found that flooding is highly effective and quicker than alternatives. This quick effect is a strength because it means that patients are free of their symptoms as soon as possible and that makes the treatment more-cost effective.
Ex: This evidence has implications for the economy as it could reduce the financial burden on the NHS by offering a quicker and cheaper treatment for those suffering from phobias
L: Therefore flooding can be seen as a useful treatment and perhaps should be the first type of treatment for NHS patients to overcome their phobias.

Limit:
P: it is not appropriate for all patients due to how traumatic it can be.

Eg: Schumacher (2015) found that patients and therapists rated flooding as significantly more stressful than SD. The problem is not that flooding is unethical because patients give informed consent, but that patients are often unwilling to see it through to the end as it can be extremely distressing.
Ex: The intensity of the experience can lead to high attrition rates (people that drop out) and it can actually make the phobia even worse it the treatment is not completed.
L: This shows that individual differences can be a limitation of how effective flooding is as treatment for phobias.

Limit:
P: it is not appropriate for phobias that involve high level of cognition, such as social phobias.
Eg: a sufferer of a social phobias does not simply experience an anxiety response but thinks unpleasant thoughts about the social situation
Ex: therefore may be more beneficial for the more complex phobias to be treated with cognitive therapies because such therapies tackle the irrational thinking
L: Therefore whilst flooding may be appropriate in some situations it may not be suitable for all phobias and therefore this reduces its usefulness as a treatment

59
Q

Behavioural approach to treating phobias:
Define flooding

A

A form of therapy for phobias where a patient is exposed to a huge amount of fear stimuli in order to help a patient associated the stimulus with safety

60
Q

Behaviours approach:
Define relaxation techniques of SD

A

Technquies taught to patients to erase uncomfortable emotions of fear arousal, which can help eliminate a fear response in a phobia, as per reciprocal inhibition

61
Q
  1. Cognitive approach to explaining depression

Cognitive theories of depressions state what is the cause of depression?

A

Cognitive approach links psychological disorders like depression to cognitive distortions
This is dysfunctional or irrational thinking

The 2 cognitive theories:
-becks cognitive triad
-ellis’ irrational thinking (ABC model)

62
Q
  1. Cognitive approach to explaining depression

Beck (1967) Negative triad:
What 3 biases does faulty information processing lead to?

A

This is automatic and can produce cognitive biases

-over-generalising: holding extreme beliefs on the basis of a single incident and applying it to different and inappropriate situation
-absolutist thinking: ‘all or nothing’ ‘good or bad’ approach to viewing the world
-catastrophizing: where a minor setback becomes exaggerated and viewed as disastrous

63
Q
  1. Cognitive approach to explaining depression

Beck (1967) Negative triad

What is a negative schema?

A

A negitive cognitive framework for interpreting future events pessimistically so adults with depression have negative thoughts/biases towards themselves and interpret the world more negatively

Develop during childhood, based on negative experiences

64
Q
  1. Cognitive approach to explaining depression

Beck (1967) Negative triad

Give 3 examples of negative schema

A

-ineptness schema, which makes sufferers expect to fail
-self-blame schema that makes them fell responsible for any misfortunes
-a negative self-evaluation schema that constantly reminds them of their worthlessness

65
Q
  1. Cognitive approach to explaining depression

Beck (1967) Negative triad

What is the cognitive triad?

A

These thoughts occur automatically and are symptomatic of depressed people

Negative views about the world: creates impression where’s no hope anywhere
Negative views about the future: reduces any hopefulness and enhances depression
Negative views about oneself: enhances existing depressive feelings because they confirm the existing emotions of low self-esteem

66
Q
  1. Cognitive approach to explaining depression

Ellis (1962) ABC Model

States that depression is caused by…

A

This model was developed to explore the response to negative events – how people react differently to stress and anxiety. Ellis suggested it’s through irrational thinking

67
Q
  1. Cognitive approach to explaining depression

Ellis (1962) ABC Model

Describe the ABC sequence of events?

A

A - activating event to which there’s a reaction
B - role of beliefs about why the situation occurred
C - consequences, feelings and behaviour the belief now causes

68
Q
  1. Cognitive approach to explaining depression

Ellis (1962) ABC Model

What does ellis believe about good mental health and depression

A

Ellis’ believes good mental health is the result of rational thinking allowing people to be happy and pain free, but depression is result of irrational thinking preventing us from being happy and pain free

69
Q
  1. Cognitive approach to explaining depression

Ellis (1962) ABC Model

What is mustabatory thinking?

A

Ellis believes the source of irrational beliefs lies is in mustabatory thinking

Ellis’ identified the 3 most important irrational beliefs:
-I must be approved of or accepted by people I find important
-I must do well or very well, or I am worthless
- the world must give me happiness or I will die

Individual with these expectations is bond to be disappointed and at risk of becoming depressed. In order to treat depression which arises out of negative thinking, such irrational thoughts need to be challenged and turned into more positive beliefs

70
Q
  1. Cognitive approach to explaining depression

Strengths of becks negative triad

A

strength:
P: Beck’s explanation that faulty information processing is linked to depression has supportive evidence that this predisposes people to become depressed
Eg: Clark & Beck’s literature review concluded that these were not only more common in depressed people, but preceded symptoms
Ex: supported in a prospective study by Cohen et al. which tracked 473 adolescents, and confirmed that cognitive vulnerability predicted later depression
L: This temporal evidence supports the association that cognitive vulnerability can lead to symptoms of depression.

strength
P: Beck’s cognitive model of depression has application in screening and treatment for depression
Eg: Cohen et al found that the ability to identify cognitive vulnerability in high-risk individuals prior to onset of depressive symptoms, enabled them to be monitored, and offered treatment in the acute phase of the expression of symptoms
Ex: This application of an understanding of cognitive vulnerablity also supports the application of cognitive behavioural therapy (CBT), which Gautum states that research has consistently found CBT to be one of the most effective treatments for depression by challenging irrational beliefs and thoughts
L: supports the application of Becks model not only to screening and early treatment intervention strategies

71
Q
  1. Cognitive approach to explaining depression

Limitatioms of Ellis ABC model

A

A limitation of Ellis’ ABC model is that it only explains reactive depression, but not endogenous depression.

Eg: Our response to what Ellis conceives of as ‘activating events’which consist of life events that can trigger depression, are likely to be partly effected by our beliefs. However, many cases of depression are not traceable to specific life events, and the cause is not readily identifiable
Ex: This is termed ‘endogenous depression’and Ellis ABC is less effective in explaining this
L: means that Ellis model can only explain some cases of depression, so is a partial explanation

72
Q
  1. Cognitive approach to explaining depression

General strength and limitation of the cognitive explaination of depression

A

A strength of the cognitive explanation of depression is that negative manipulation of cognition can exacerbate symptoms.
Eg: Boury et al found patients with depression were more likely to misinterpret information negatively (cognitive bias) and feel hopeless about their future (cognitive triad).
Ex: This demonstrates the presence of altered cognitive processing in depression, which is also supported by Bates et al. who gave depressed patients negative automatic thought statements to read and found that their symptoms became worse
L: findings support Becks theory and the idea that negitivr thinking is involved in depression, by demonstrating that by manipulating cognition positively and negatively,the expected change in symptoms occurs

A limitation of the cognitive explanation of depression can be criticised for being reductionist, as it only considers the role if thinking as the cause of depression.
Eg: argues that depression is caused by thinking in a negative or irrational way i.e. mustabatory thinking, but does not account for other symptoms as well, such as extreme anger
Ex: This assumption ignores that biological research has indicated that depression can be as a result of low levels of the neurotransmitter serotonin, and that SSRIs can be effective treatments
L: so cognitive approach can be seen to be too simplistic in that it does not account for all depressive phenomena, and that other approaches need to also be considered offering a more holistic view of depression

73
Q
  1. Cognitive approach to treating depression

What is the cognitive and behavioural element of CBT?

A

Cognitive: aims to identify irrational and negative thoughts and replace these negative thoughts with more positive ones

Behavioural: encourages patients to test their beliefs through behavioural experiments and homework

74
Q
  1. Cognitive approach to treating depression

What is cognitive behavioural therapy (CBT)?
And it’s 2 forms

A

2 forms:
- becks Cognitive therapy
-ellis rational emotive behaviour therapy (REBT)

-most commonly used treatment in the NHS for depression
-based on Becks Negative Triad (negative thoughts about the self, the world, the future)

75
Q
  1. Cognitive approach to treating depression

What is the central premise of CBT?

A

-thoughts, feelings and behaviour impact each other, so if an irrational thought can be identified it can also change people’s emotions and behaviour
Thoughts: what we think affects how we act and feel
Behaviours: what we do affects how we think and feel
Feelings: what we feel affects how we think and what we do

76
Q
  1. Cognitive approach to treating depression

Explain how CBT is administered

A

The therapist and patient challenge negative thoughts against reality and/or puts new rational beliefs into practice by:
• discussing evidence for/against
• homework outside of the sessions eg: thought diaries

77
Q
  1. Cognitive approach to treating depression

What are the 3 key features of CBT?
(For both Becks and Ellis’ model)

A

Initial treatment: CBT therapist works with the patient to identify the patients problems

Goal setting: patient and therapist agree on a set of goals and a plan of action to achieve them

Identify automatic negative and irrational thoughts: in relation to themselves, their world and their future (Beck’s negative triad) or activating events and beliefs (Ellis’ ABC model)

78
Q
  1. Cognitive approach to treating depression

What does Beck mean in by patient as scientist, cognitive reconstructing and thought catching and bheavioural action in his cognitive therapy?

A

Patient as scientist: generalising and testing hypotheses about the validity of their irrational thoughts; when they realise their thoughts don’t match reality, this will change their schemas

Cognitive reconstructing: the irrational thoughts can be discarded so perspectives are reframed, leading to a change in feelings and behaviours

Thought catching: identifying irrational thoughts coming from the negative triad of schemas

Behavioural action:
In CBT homework, where patients engage in more active and enjoyable activities (eg: travelling, sports), important to combat depressive symptoms of isolation and loss of interest

79
Q
  1. Cognitive approach to treating depression

What is REBT therapy?

A

REBT extends Ellis’s ABC model to ABCDE model
D for dispute: therapist asks patient to challenge their irrational thoughts and beliefs as Utopianism
E for effect: new responses - therapist asks client to think of more rational responses

main technique for REBT is to identify and challenge irrational thoughts

80
Q
  1. Cognitive approach to treating depression

What are the types of disputing in Ellis’s ABCDE model in REBT therapy?

A

Empirical disputing – assessing whether there’s evidence for the thought
Logical disputing - assessing whether the thoughts follow from the facts
Pragmatic disputing - assessing whether the thoughts is helpful

81
Q
  1. Cognitive approach to treating depression

What’s a strength of CBT as a treatment of depression

A

P: evidence to support its effectiveness, especially in combination with antidepressant treatment
Eg: March examined 327 adolescents diagnoses with depression and looked at the effectiveness of CBT, antidepressants and a combonation of CBT and antidepressants.
After 36 weeks, 81% of the antidepressant group and 81% of the CBT group had significantly improved. Showing the effectiveness of CBT in treating depression.
However, 86% of the CBT and antidepressant group had significant improved
Ex: shows that CBT is an effective treatment as 81% of patients symptoms improved demonstrating its efficacy, but the research also suggests that a combination of both treatments may be the most effective
L: suggesting that cognitive treatment of depression is effective, but not comprehensive, and physiology also needs to be taken into account which can be addressed in drug therapy

82
Q
  1. Cognitive approach to treating depression

2 limitations of CBT as a treatment for depression

A

1) may not be suitable for patients with learning difficulties
2) high relapse rates

P: it may not be suitable for all patients, such as those with learning disabilities.
Eg: Sturney (2005) proposed that patients with learning disabilities may not be able to access the complex rational thinking of any form of ‘talking therapy’. Similarly, patients whose depression is so severe, may not be able to motivate themselves to engage with the cognitive work of CBT, suggests that CBT may not be appropriate for all patients with depression.
Ex: However, recent evidence conflicts with this: Lewis & Lewis found that efficacy of CBT for severe depression was as equal to antidepressants, and Taylor et al. (2008) found that CBT, with appropriate adjustments, could be used with patients with learning difficulties
L: This supports the idea that the use of CBT may be more broadly applicable than
has been previously considered, but that its application may need to be modified in certain populations

P: has high relapse rates
Eg: Ali et al. assessed depression in 439 clients every month for 123 months following a course of CBT. 42% of patients relapsed into depression within 6 months and 53% within a year
Ex: This suggests that relatively few earlier studies had looked at the long-term effectiveness, which may not be as high as was assumed. One reason for this is that CBT requires motivation, so patients with severe depression may not engage with CBT or even attend the sessions. Drug therapy does not require the same level of motivation, and so may be more effective in these cases.
L: evidence supports the concern that a limitation of CBT is that it lacks prolonged efficacy, which may limit its application to patients of moderate severity, whereby motivation can be maintained for longer duration

83
Q
  1. Biological explanation of OCD

What are the 2 biological explainatioms for OCD

A

-genetic explanations
-neural explanations (neurotransmitters and brain structures)

84
Q
  1. Biological explanation of OCD
    Genetics: How do alleles relate to disease vulnerability?
A

variations in the sequence of nucleotides within a gene.
The diversity in alleles eg: mutations, contributes to variation in humans affecting how genes function.
Depending on the role of the gene, these effects may have no effect, or can be beneficial. But sometimes they cause harmful biological changes, which can lead to various diseases
This is the genetic basis of psychopathological disorders

85
Q
  1. Biological explaination of OCD
    Genetics: In what way do monozygotic and dizygotic twins differ?
A

• Fraternal (dizygotic, DZ)
eggs released during menstruation and both eggs are fertilised zygotes (fertilised eggs), they share 50% of their DNA
• Identical (monozygotic)
1 egg released during menstruation. Fertilised then splits into two eggs.
Now 2 zygotes, but came from 1 zygote, they share 100% of their DNA

86
Q
  1. Biological explaination of OCD
    Neurotransmitters: how do neurons communicate
A

1) Electrical: electrical signal/ nerve impulse passes down the body of the neuron to reach the axon terminal to the synaptic gap / synapse
2) Chemical: as the electrical signal arrives at the end of the axon terminal of the pre-synaptic neuron, it causes a neurotransmitter to be released across the synapse
Receptors on the post-synaptic neuron on the other side of the synapse The neurotransmitter eg; dopamine binds to the complementry neurotransmitter.
This activation of thr receptors determines whether the post-synaptic neuron will generate a electrical signal

87
Q
  1. Biological explaination of OCD
    Neurotransmitters:
    How might changes in neurotransmitters causes brain disorders?
A

Changes in communication between neurons can disrupt brain function and lead to psychopathological disorders

88
Q
  1. Biological explanation of OCD
    Genetic explaination:
    What evidence is there from family studies that OCD has a genetic component?
A

Nestadt eg al. Found first-degree relatives (parents, siblings and children) of OCD sufferers had a higher chance of developing the disorder.
12% chance for those with first degree relatives diagnosed with OCD
3% risk for control group ppts
Marini & Stebnick found people with a family member with OCD is approx 4 times as likely to develop it as someone without
Family members are more closely genetically related so supports genetic vulnerability

89
Q
  1. Biological explaination of OCD
    Genetic explanation:
    Which 3 candidate genes that create vulnerability to OCD?
A

1) COMT gene
2) SERT gene
3) 5-HT1D
These genes produce changes in neurotransmitters in the brain

90
Q
  1. Biological explaination of OCD
    Genetic explanation: how does the COMT gene cause changes relevant to OCD?
    And who’s research supported this?
A

Mutation of COMT gene causes low levels of COMT enzyme
This enzyme metabolises neurotransmitters
Low levels of COMT enzyme means less dopamine is metabolised so there’s high levels of dopamine
Supported by: Turkel et al. (2013) found that the low-activity version of the COMT gene was more common in patients with OCD compared to controls.

91
Q
  1. Biological explanation of OCD
    Genetic explaination: how does the SERT gene cause changes relevant to OCD?
    And who’s research supported this?
A

SERT gene creates/codes for the serotonin transporter protein
Transporters detect the amount of neurotransmitter in the synapse, and remove from the synapse after it’s released.
Mutations of SERT gene can create too much seratonin transporter so serotonin levels go down as the transporter is removing serotonin from the synapse
Supported by: Ozaki et al. found two families with the high- activity version of the gene (which made too much of the protein): 6/7 people in these two families had
OCD.

92
Q
  1. Biological explanation of OCD
    Genetic explaination: how does the SERT gene cause changes relevant to OCD?
A

Chemical name for serotonin is 5HT
Receptor sub types respond differntly to neurotransmitters (1D in 5-HT1D)
5-HT1D gene codes for a pre-synaptic receptor, 5-HT1D
This is a pre-synaptic receptor involved in monitoring the level of serotonin released in the synapse.
Pre-synaptic receptors uptake serotonin back into the presynaptic neuron

93
Q
  1. Biological explaination of OCD
    Genetic explaination: What evidence is there that OCD may be polygenic?
    And who supported this?
A

means OCD is caused by more than one genetic variation that together cause significantly increased vulnerability
Supported by: Taylor found evidence of up to 230 candidate genes - OCD is likely to be polygenic
These are often associated with the functioning of neurotransmitters, such as dopamine and serotonin, both associated with regulating mood.

94
Q
  1. Biological explaination of OCD
    Genetic explanation:
    What does it mean to say that OCD is aetiologically heterogenous?
A

meaning different combinations of genes cause different types of OCD in different people.

95
Q
  1. Biological explanation of OCD
    Genetic explanation:
    1.4 What is the diathesis-stress model in relation to OCD?
A

certain genes leave some people more likely to suffer a mental disorder but it is not certain as some environmental stress is necessary to trigger the condition.

Diathesis = genetic vulnerability Stress = environment

suggests that some have a genetic vulnerability towards developing depression. For example, Lewis et al. found that of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD.

Genetic predisposition and childhood trauma can lead to vulnerability to mental disorders. This can either lead to:
1) minimal stressful circumstances resulting in lower probability of mental disorder
Or
2) inability to cope with excessive stressful circumstances resulting in a higher probability of mental disorder

96
Q
  1. Biological explanation of OCD
    Genetic explaination:
    A strength of the genetic explaination
A

P: the increased concordance between monozygotic compared to dizygotic twins.
Eg: Nestadt (2010) shows that there is a higher concordance rate for OCD in MZ twins (68%) compared to DZ twins (31 %)
Ex: supports the role of genetics in OCD, since MZ and DZ twins grow up sharing similar environments like food, upbringing and education, and life events like bereavement or parental divorce, so non-genetic factors can be controlled for when comparing MZ and DZ twins.
Cou: However, increased concordance rates does not necessarily indicate a role of genetics: monozygotic twins may be treated more similarly because they look alike, compared to dizygotic, non-identical twins. Also, since the concordance rate was 68% and not 100%, there must also be an environmental component to OCD
L: suggests that the additional shared DNA in MZ twins may be responsible for the increased concordance rate, but that this evidence should be treated cautiously, and may be best understood as a diathesis stress model, whereby a genetic vulnerability is inherited and triggered by an environmental stressor

97
Q
  1. Biological explanation of OCD
    Genetic explanation:
    2 limitations of the genetic explanation
A

1) environmental factors
2) alternative explainatioms
P: there are also environmental factors.
Eg: Cromer et al. ) found that over half of the OCD patients in their sample had experienced a traumatic life event, and that OCD was more severe in those, suggesting a diathesis-stress model, suggesting a diathesis-stress model one or more traumas.
Ex: supports the idea that OCD is not entirely genetic in origin, and that environmental factors can also trigger, or increase the risk, of developing OCD.
L: This means that genetic vulnerability only provides a partial explanation for OCD, and may therefore be too reductionist, which limits the validity of this explanation.

P: there are credible alternative explanations for the development of OCD, such as the two-process model proposed by behaviourists, that suggest that learning plays a crucial role.
Eg: Eg: Albucher eg al. found in the success of behavioural treatments for OCD where symptoms of patients are improved for 60-90% of adults
Eg: Initial learning of the feared stimulus could occur through classical conditioning’s associative process where, for example, dirt is paired with anxiety. This behaviour pattern would be maintained through operant conditioning and negative reinforcement whereby the stimulus is avoided so the anxiety is removed. This could result in an obsession forming which is linked to the develooment of a combulsion. e.g. washing of hands, which serves to reduce the anxiety felt.
L: This suggests that the genetic model may only provide a partial explanation for
OCD

98
Q
  1. Biological explanation of OCD
    Neural explanations: how are neurotransmitters important?
A

COMT AND SERT and 5-HT1D genes produced changes in neurotransmitters
Neurotransmitters are important for communication within the brain. They can either excite or inhibit neurons - either increase or decrease brain activity.

99
Q
  1. Biological explanation of OCD
    Neural explanations: how is serotonin improved in OCD? And who supports this
A

important for the regulation of mood. It has an overall calming effect on the brain.
Low levels of it means the brain doesn’t communicate information about mood
effectively
The reduction of it functioning is linked to OCD
Low levels of serotonin have been associated with the symptoms of OCD e.g. anxiety
The reduction of serotonin can explain some cases of OCD
SUPPORTED BY: Piggot et al. reported that SSRIs, which reduce the uptake of serotonin, and so prolong its action at the synapse, are effective in treating OCD

100
Q
  1. Biological explaination of OCD
    Neural explanations: how is dopamine involved in OCD?
A

Dopamine: neurotransmitter which is important for maintaining interest and
motivation and salience
High levels of dopamine help to maintain a compulsive thought or behaviour, leading to some of the symptom of OCD, in particular, compulsive behaviours
Dopamine levels are thought to be abnormally high in people who suffer from OCD

101
Q
  1. Biological explaination of OCD
    Neural explanations:
    What 2 brain regions are implicated in OCD?
A

basal ganglia (made up of the putamen and caudate head) and orbitofrontal cortex.

102
Q
  1. Biological explaination of OCD
    Neural explanations: how is the region basil ganglia assossiated with OCD and research to support
A

It’s involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD-like symptoms, following their recovery.

made up of the putamen and the cluster of neurons, including the caudate nucleus

Max et al. (1994) found that when the basal ganglia is disconnected from the frontal cortex during surgery, OCD-like symptoms are reduced, providing further support for the role of the basal ganglia in OCD.

103
Q
  1. Biological explaination of OCD
    Neural explanations: how is the region orbitofrontal cortex is assossiated with OCD
A

Region which converts sensory information into thoughts and actions. PET scans have found higher activity in the orbitofrontal cortex in patients with OCD. it may increasethe conversion of sensory information to actions (behaviours) which results in compulsions. The increased activity also prevents patients from stopping their behaviours.

104
Q
  1. Biological explaination of OCD
    Neural explanations: explain the parahippocampal gyrus region linked to OCD
A

an area of cortex close to the hippocampus on the brain’s underside, is also linked to OCD. It is responsible for regulating and processing unpleasant emotions and has been seen to function abnormally in cases of OCD.

105
Q
  1. Biological explaination of OCD
    Neural explanations: what’s gyri
A

a ridge on the cerebral cortex. It is generally surrounded by one or more sulci (depressions or furrows; sg. : sulcus). Gyri and sulci create the folded appearance of the brain in humans and other mammals. Gyrus.

folds in the brain due to compacting the brain to increase surface area

106
Q
  1. Biological explaination of OCD
    Neural explanations: explain the ‘worry circuit’ linked to OCD
A

1) OFC involved in converting sensory info into thoughts and actions. It sends ‘worry’ signal to basil ganglia to report on things which should cause worry, e.g. a potential germ hazard or a door which might not be locked.
2) In normal functioning, the basal ganglia filter out minor worries coming from the OFC, but if this area is hyperactive, even small worries get to the thalamus, which is then passed back to the OFC, forming a loop (recurring obsessive thoughts)
3) Repetitive motor functions (compulsions) are an attempt to break this loop. While carrying out the compulsion may give temporary relief, the hyperactive basal ganglia will soon resume the worry circuit.

107
Q
  1. Biological explaination of OCD
    Neural explanations: explain the cortio-striatio-thalamic-circuit in OCD
A

OCD is a frontal striatal disorder

The 2 out of the 5 parallel circuits assossiated with OCD is the
-‘sensorimotor’ CSTC circuit: the stimulus-response-based habitual behaviour
-‘ventral motivatiomal’ CSTC circuit: stimulus outcome based motivational behaviour

108
Q
  1. Biological explaination of OCD
    Neural explanations: 2 strengths of the neural explaination of OCD
A
  • OFC has empirical supportive evidence from structal and functional imaging studies
  • empirical evidence from the effects of SSRI’s that neurotransmitters do play a role

P: OFC has empirical supportive evidence from structal and functional imaging studies

Eg: Menzies et al. found that OCD sufferers and their family members had reduced grey matter in the key regions of the brain including the OFC. In addition, several neuroimaging studies using PET scanners have shown hyperactivity in the OFC and the caudate nucleus in people with OCD both while scanning the brain at rest and when symptoms are stimulated
Ex: This supports the involvement of the ventral motivation cortico-striato-thalamic circuit in OCD, also known as the ‘worry circuit’
Cou: However, one problem with this evidence is that it is correlational: researchers cannot be sure if the hyperactivity in these areas is the cause of OCD or a consequence of having OCD. Maia et al. (2008) reviewed evidence from other lines which permitted stronger causal inferences, including the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD.
L: findings therefore suggest that there are multiple lines of evidence which support the
involvement of the OFC and caudate in OCD, which strengthens the
validity of the biological explanation

P: empirical evidence from the effects of SSRI’s that neurotransmitters do play a role
Eg: A meta-analysis by Soomro et al. (2008) demonstrated SSRIs are more effective than placebos, suggesting there is serotonergic involvement in OCD
Ex: These drugs are effective at reducing OCD symptoms, and SSRIs work by increasing the levels of this neurotransmitter by blocking the serotonin reuptake process, the data therefore suggests that serotonin does play a role
in OCD.
Cou: However despite altering levels of serotonin in the synapse within hours, these drugs take weeks to reduce symptoms, and 40% to 60% of patients show no or just partial symptom improvement
L: findings suggest low levels of serotonin have a role to play in OCD but are not the sole cause of OCD

109
Q
  1. Biological treatment of OCD
    What does SSRI stand for?

Give 1 example of an SSRI

A

Selective serotonin reuptake inhibitors

Common Brand names include: prozac and sertraline

110
Q
  1. Biological treatment of OCD

What levels of serotonin are associated with OCD and how does this link to SSRI’s

A

Low levels of serotonin neurotransmitters
SSRI increase levels of serotonin in the brain to regulate mood and anxiety
Remember: high levels of serotonin transporter = low levels of serotonin bc the transporter is removing serotonin from the synapse

111
Q
  1. Biological treatment of OCD
    How do SSRI’s work
A

Neurontramsitters are stored in pre-synaptic vesicles
-when an action potential stimulates it, the vesicle is pushed to the end of the axon terminal and fuses with the presynaptic neurons membrane to relapse the neurotransmitters stored inside it across the synapse from the pre-synaptic neuron to the post-synaptic neuron
-the neurotransmitter bind to the post-synaptic receptors which increase or decrease the likelihood of the post-synaptic neuron firing (excites it over the threshold charge so more likely and inhibits lower than the threshold charge so less likely)
-the neurotransmitter is cleared from the synapse by reuptake mechanisms
-serotonin is a neurotransmitter
-OCD is thought to involve a lack of serotonin at the synapse
-SSRI’s block the reuptake of serotonin, so increase its presence at the synapse
-this reduces symptoms of OCD as the serotonin transporter is removing less serotonin from the synapse so there’s an increase in serotonin levels

SSRI’s interfere with step between 3 and 4:
-when serotonin is released into the synapse (step 3), it either binds to the postsynatic receptors (step 4) or it’s removed from the synapse by reuptake mechanisms
- SSRI’S block this reuptake, so more serotonin is present in the synapse so it can bind to post-synaptic receptors

Summary:
acts to inhibit the re-uptake or re-absorption of serotonin in the brain
enabling the serotonin to remain active at the synapse
where it continues to stimulate the post-synaptic neuron

112
Q
  1. Biological treatment of OCD
    What are the 3 alternatives to SSRI’s
A

Tricyclic antidepressants
-SNRI’s (serotonin and noradrenaline reuptake inhibitors)
-benzodiazepines

113
Q
  1. Biological treatment of OCD
    What does SNRI’s stand for and give 2 examples
A

serotonin and noradrenaline reuptake inhibitors

Venlafaxime and duloxetine

114
Q
  1. Biological treatment of OCD
    How do SNRI’s work (mechanism)?
A

SNRI’s (more selective than tricyclics) block the transporter mechanism that re-absorbs serotonin and noradrenaline
-there’s a lot of evidence supporting the idea that noradrenaline is involved in OCD.
In low levels: person is unable to focus their attention which can result in anxiety and compulsions
-although low noradrenaline may not cause OCD, preventing reuptake of this neurotransmitter (increasing it) has been assossiated to relief symptoms and anxiety

115
Q
  1. Biological treatment of OCD
    How are SNRI’s used clinically
A

-2nd line of treatment for those non-responsive to SSRI’s
-they habe an advantage of targeting more than one neurotransmitter.
-BUT they have greater side effects so only used as a 2nd line treatment if SSRI’s aren’t effective

116
Q
  1. Biological treatment of OCD
    Give an example of tricyclic antidepressants
A

Clomipramine – 1st medication approved for OCD

117
Q
  1. Biological treatment of OCD
    How do tricyclic antidepressants work
A

increase serotonin and noradrenaline by blocking their reuptake, causing increase I’m levels of these transmitters at the synapse.
-they act at various other receptors (makes them less selective) so can contribute to clinical efficiency and also side effect

118
Q
  1. Biological treatment of OCD
    How are tricyclic antidepressants used clinically
A

Has more servere side effects that SSRI’s, so used only for those who don’t respond to SSRI’s and SNRI’s

119
Q
  1. Biological treatment of OCD
    Give an example of benzodiazepines
A

Valium and diazepam

120
Q
  1. Biological treatment of OCD
    How do benzodiazepines work
A

increase activity of neurotransmitter GABA (gamma-aminobutyric) which is an inhibitory neurotransmitter, which calms and reduces activity of neurons
-when GABA docks at the receptor site of a neuron, it makes it less likely to fire an action potential

121
Q
  1. Biological treatment of OCD
    How are benzodiazepines used clinically
A

commonly used to reduce anxiety

122
Q
  1. Biological treatment of OCD
    Give 2 strengths of drug therapy/treatment of treating OCD
A

P: drug therapy is more cost effective and less disruptive on patients loved compared to talking therapies
Eg: As SSRIs are cheaper than talking therapies it has economic implications for the UK. It is better for the NHS as it could reduce the financial pressure on an already struggling public service
Ex: Drug therapies are also less disruptive on a patients life. The patient just needs to take one tablet a day compared to attending weekly sessions and completing homework for CBT
Cou: However, a systematic review by Skapinakis et al. (2016) found that cognitive and behavioural (exposure) therapies were more effective than SSRIs for OCD
L: For these reasons drug therapies can be the preferred treatment for many patients, however, increased efficacy of SSRIs may be a better long term solution

P: drug treatment has considerable supporting evidence
Eg: Eg: Soomro et al (2009) reviewed studies comparing SSRIs to placebos in the treatment of OCD and concluded that all 17 studies (meta-analysis) showed significantly better results for the SSRI groups in the short term
Ex: This supports the argument that biological treatments are effective as on average 70% of OCD patients had improved symptoms with drug therapy, also suggesting serotonin has a role in the development of the disorder.
Cou: However, a limitation of the studies is that they were typically 3-4 months long and therefore there is little data on the long-term effects of drug therapy.
L: suggests that randomized, double-blind clinical trials of SSRIs of 12 months or longer to establish whether efficacy observed in shorter trials is maintained, and whether additional side effects emerge

123
Q

8/16 marker hasn’t come up before:

  1. Biological treatment of OCD
    Give 2 limitations of the biological approach to treating OCD
A

P: drug therapy often has unpleasant side effects
Eg: Even first line treatments such as SSRIs can cause indigestion, blurred vision and a loss of sex drive. Clomipramine can also cause more serious problems: more than 1 in 10 experience erectile dysfunction and weight gain; 1 in 100 become aggressive and experience heart-related problems.
Ex: Ashton (1997) recommends that drugs for OCD are used for no longer than 4 weeks due to the side effects.
L: It could therefore be argued that drug therapies are therefore not an effective long- term treatment for OCD.

P: drug treatments are critisized for treating the symptoms of the disorder and not the cause
Eg: Koran et al. (2007) suggest that psychological treatments such as CBT may be a more effective long‐term solution to provide a lasting treatment and a potential cure
Ex: because although SSRIs work by increasing the levels of serotonin in the brain, which reduces anxiety and alleviates the symptoms of OCD, but it does not treat the underlying cause of OCD. Furthermore, once a patient stops taking the drug, they are prone to relapse
L: suggests that the biological issues that drug treatments are intended to target may not be fundamental to the disease, so only have symptomatic effects. This means that the use of drug therapy is only a temporary treatment for OCD, and that the biological causes of the disease may be unknown.

124
Q
  1. Biological treatment of OCD

Outline the use of one or more drugs in the treatment of obsessive-compulsive disorder

A

attempt to increase or decrease levels of neurotransmitters or the activity of neurotransmitters in the brain
general purpose is to decrease anxiety, lower arousal, lower blood pressure or heart rate
antidepressants - SSRIs - prevent the reuptake of serotonin and prolong its activity in the synapse in order to reduce anxiety / normalise the ‘worry circuit’ tricyclics - block the transporter mechanism that re-absorbs both serotonin and noradrenaline, again prolonging their activity
anti-anxiety drugs - such as benzodiazepines - enhance the activity of GABA and therefore slow down the CNS causing relaxation
SNRIs - more recent drugs which also increase levels of serotonin and nor-adrenaline and are tolerated by those for whom SSRIs are not effective.