3/5 will appear
Diagnostic and Classification
Both groups would need to be able to evaluate strengths and limitations to classification
systems (DSM and ICD), although essay can mainly focus on DSM (as lectures tended to
focus on this)- should be able to make a few comparisons/examples where different with ICD
criteria
Conduct Disorder
Be able to evaluate the risk and protective factors in the development of a conduct disorder in
relation to two onset types (Child vs adolescent)
Be able to evaluate the general risk and protective factors in the development of a conduct
disorder
Psychosis and Schizophrenia
Psychosis: Concept and Aetiology
Q1. Describe the various aetiologies for schizophrenia and evaluate whether schizophrenia
results from an accumulation of multiple risk factors or individual aetiologies which have the
same endpoint.
Q2. Evidence indicates a number of different possible causes of schizophrenia suggesting
multiple different aetiologies. Describe the evidence and discuss whether psychosis has
multiple different, or just a few similar, causes.
Q3 .Is schizophrenia a neurodevelopmental disorder? Critically review the epidemiological
evidence in order to answer this question.
Cognitive Therapies
Describe Beck’s theory of depression and evaluate how it is implemented in the practice of
CBT.
Outline and compare the theory and practice of any two cognitive therapies (e.g. CBT and
RET or cognitive behaviour therapy and cognitive analytic therapy) with or without reference
to a specific mental health problem such as depression.
Describe cognitive behavioural theory with reference to depression, or one other disorder,
and evaluate its application to the process of cognitive behavioural therapy.
Describe Beck's theory of depression and evaluate how this is implemented in Cognitive
Behaviour Therapy (CBT
You Tube videos of ‘cognitive therapy ‘frequently confuse principles from Beck’s Cognitive
Behaviour Therapy (CBT) and Ellis’ Rational Emotive Therapy (RET). Describe the key
theoretical principles of both CBT and RET and evaluate the similarities and differences
between these two approaches both in terms of theory and therapy practice
,Critically compare the Behavioural and Cognitive Theories for depression.
Describe and critically compare at least 2 psychologically based theories of depression and in
so doing reveal the main psychological mechanisms behind each theory.
Behavioural Model of Depression: Learned Helplessness.2.Early Cognitive : Hopelessness
Theory.3.Current Cognitive : Ellis ABC Theory; Becks Cognitive Theory.
25Behavioural Model Of Depression
26Helplessness Theory Based on principles of Operant Conditioning•A response to an
environmental stimulus becomes automatic If repeatedly REINFORCED.oPositive
Reinforcement = pleasant experience.Learn
to APPROACH for rewardoNegative
Reinforcement = unpleasant experience.Learn
to AVOID •Helpful response to repeated
Negatively Reinforced Stimuli (e.g. interview failures )o Learn how to AVOID negative
affect.•Helplessness response to Negatively Reinforced StimulioAVOIDANCE response not
learnt.o‘Do nothing’ becomes the Automatic Response•Reinforced learning is the mechanism
behind AI .
27Behavioural Model Of DepressionSeligman ( 1971)
28Helplessness Theory Relevance to Human Experience ?•Life Events : •Pakel prevalence of
depression increases with Negative Life Events.•Prevalence of depression increases in
proportion to exposure to Negative Life Events.•Depression seen as a learnt
behaviour.Problems with Helplessness Theory•‘Helplessness’ in dogs only when electricity
turned on e.g. CS + no electricity then dogs cease to be helpless.•ie dissipates quickly ( e.g.
48 hours), whereas depression is long lasting •Helplessness is a cognitive construct – one has
a concept of being helpless even if the environment can be managed OK.•Extension of Learnt
Helplessness to cognitive models •Hopelessness
Describe and evaluate the main cognitive theories of depression
•What do we know about the aetiology of depression?
Aetiology : Genetics and Unipolar Depression( from McGuffin and Katz 1989; See ‘General
Reading’)Authors%Concordance RatesMZDZSlater and Shield 38%25%(1969)Shapiro
55%14%(1971)Torgerson53%45%(1985)
13Aetiology - C21 Summary of Research :Genetics and Major Depression•Twin Studies
indicate a genetic component.–See McGuffin and Katz 1989•3X increased risk if a 1st degree
relative is depressed.•Genetic relationship increases with-frequency of recurrence in family-
early age of onset of family members-severity of depression in affected members.•Molecular
genetics studies .–Search for Candidate genes for monamine neurotransmitters ( serotonin) .–
, Linkage studies .–little discovered from various molecular genetic studies .•complex
interactions between genes and known environment risk factors.
14Tip- DepressionAetiology : Adverse Social/Environmental Experience(see Gottlib
&Hammen 2014 CH 15)Adverse event = any personally stressful event that causes
humiliation, social defeat, actual or virtual loss . Examples :•Pakel prevalence of depression
increases with Negative Life Events (self report-retrospective !) • Roy (1987) :
unemployment , poor marriage,separation from parent before 17, first degree relative with
D.•Early Adverse Environments (See Gotlib and Hammen 2014 Ch 11) : neglectful/harsh
parenting; early abuse ; parental loss )Child
sexual abuse Hill et al (2001)- a good model of a
developmental psychopathology account of adult depression.Comment: Best understood with
reference to psychological theories of depression
Critically evaluate the evidence that Reactive Attachment Disorder and Disinhibited Social
Engagement Disorder should be considered as two distinct attachment conditions.
The Theory of Attachment was founded by John Bowlby and later expanded on by Mary
Ainsworth “Strange Situation Classification” which observed the behaviours of an infant
when separated and reunited with a caregiver/mother, the study concluded in identifying 4
attachment styles. Since then, the psychological studies of attachment have become important
in child research, particularly in those who were institutionalised as previous research shows
increased risk of developing unhealthy attachment styles and overall behaviours.
Spitz (1952) documentary “Psychogenic Disease in Infancy” pinpointed the emotional
damage that institutionalization and a lack of maternal care can have on an infant during early
years. He concluded that infants deprived of their mother during the first year of life
consecutively for over 5 months become progressively worse (lethargic, slow/limited
mobility, weight and growth stunt, empty expressions) and a total of 37.3% of cases showed
progressive deterioration which eventually led to nutrient deficiency and death by the end the
end of the second year of life (Invisible silent storm, 2015).
Tizard and Rees (1975) set out to investigate the effect of early institutional upbringing on
affectional relations and behavioural problems. They collected the data from a total of 26
children who were neglected and raised in institutional settings in London, caregivers were
advised against forming attachments to these children to increase the validity of the study. By
4 years of age, it was reported that over half of the participants (18/26) displayed abnormal
attachment styles. The results described 10 children as socially outward and aimless whilst 8
children were viewed as emotionally distant and unresponsive. The remaining 8 were able to
develop stable bonds to their caregivers.
RAD was classified as a non-attachment condition in the DSM in 1980 (Potteretal.,2009).
Two types of RAD were described in the DSM-IV: inhibited (IRAD) and disinhibited
(DRAD). Despite the fact that there are two different subtypes, evidence did suggest that they
can coexist (Smyke, Dumitrescu, &Zeanah,2002). In recent years, RAD has been split into
two distinct disorders (APA, 2013); the inhibited RAD and the inhibited RAD. The inhibited
type is now classified as RAD, whereas the disinhibited form is now known as Disinhibited
Social Engagement Disorder (DSED). According to Lehmann, Breivik, Heiervang, Havik,
and Havik (2016), the DSM-5 conceptualization of the diseases as distinct aspects of infant
Diagnostic and Classification
Both groups would need to be able to evaluate strengths and limitations to classification
systems (DSM and ICD), although essay can mainly focus on DSM (as lectures tended to
focus on this)- should be able to make a few comparisons/examples where different with ICD
criteria
Conduct Disorder
Be able to evaluate the risk and protective factors in the development of a conduct disorder in
relation to two onset types (Child vs adolescent)
Be able to evaluate the general risk and protective factors in the development of a conduct
disorder
Psychosis and Schizophrenia
Psychosis: Concept and Aetiology
Q1. Describe the various aetiologies for schizophrenia and evaluate whether schizophrenia
results from an accumulation of multiple risk factors or individual aetiologies which have the
same endpoint.
Q2. Evidence indicates a number of different possible causes of schizophrenia suggesting
multiple different aetiologies. Describe the evidence and discuss whether psychosis has
multiple different, or just a few similar, causes.
Q3 .Is schizophrenia a neurodevelopmental disorder? Critically review the epidemiological
evidence in order to answer this question.
Cognitive Therapies
Describe Beck’s theory of depression and evaluate how it is implemented in the practice of
CBT.
Outline and compare the theory and practice of any two cognitive therapies (e.g. CBT and
RET or cognitive behaviour therapy and cognitive analytic therapy) with or without reference
to a specific mental health problem such as depression.
Describe cognitive behavioural theory with reference to depression, or one other disorder,
and evaluate its application to the process of cognitive behavioural therapy.
Describe Beck's theory of depression and evaluate how this is implemented in Cognitive
Behaviour Therapy (CBT
You Tube videos of ‘cognitive therapy ‘frequently confuse principles from Beck’s Cognitive
Behaviour Therapy (CBT) and Ellis’ Rational Emotive Therapy (RET). Describe the key
theoretical principles of both CBT and RET and evaluate the similarities and differences
between these two approaches both in terms of theory and therapy practice
,Critically compare the Behavioural and Cognitive Theories for depression.
Describe and critically compare at least 2 psychologically based theories of depression and in
so doing reveal the main psychological mechanisms behind each theory.
Behavioural Model of Depression: Learned Helplessness.2.Early Cognitive : Hopelessness
Theory.3.Current Cognitive : Ellis ABC Theory; Becks Cognitive Theory.
25Behavioural Model Of Depression
26Helplessness Theory Based on principles of Operant Conditioning•A response to an
environmental stimulus becomes automatic If repeatedly REINFORCED.oPositive
Reinforcement = pleasant experience.Learn
to APPROACH for rewardoNegative
Reinforcement = unpleasant experience.Learn
to AVOID •Helpful response to repeated
Negatively Reinforced Stimuli (e.g. interview failures )o Learn how to AVOID negative
affect.•Helplessness response to Negatively Reinforced StimulioAVOIDANCE response not
learnt.o‘Do nothing’ becomes the Automatic Response•Reinforced learning is the mechanism
behind AI .
27Behavioural Model Of DepressionSeligman ( 1971)
28Helplessness Theory Relevance to Human Experience ?•Life Events : •Pakel prevalence of
depression increases with Negative Life Events.•Prevalence of depression increases in
proportion to exposure to Negative Life Events.•Depression seen as a learnt
behaviour.Problems with Helplessness Theory•‘Helplessness’ in dogs only when electricity
turned on e.g. CS + no electricity then dogs cease to be helpless.•ie dissipates quickly ( e.g.
48 hours), whereas depression is long lasting •Helplessness is a cognitive construct – one has
a concept of being helpless even if the environment can be managed OK.•Extension of Learnt
Helplessness to cognitive models •Hopelessness
Describe and evaluate the main cognitive theories of depression
•What do we know about the aetiology of depression?
Aetiology : Genetics and Unipolar Depression( from McGuffin and Katz 1989; See ‘General
Reading’)Authors%Concordance RatesMZDZSlater and Shield 38%25%(1969)Shapiro
55%14%(1971)Torgerson53%45%(1985)
13Aetiology - C21 Summary of Research :Genetics and Major Depression•Twin Studies
indicate a genetic component.–See McGuffin and Katz 1989•3X increased risk if a 1st degree
relative is depressed.•Genetic relationship increases with-frequency of recurrence in family-
early age of onset of family members-severity of depression in affected members.•Molecular
genetics studies .–Search for Candidate genes for monamine neurotransmitters ( serotonin) .–
, Linkage studies .–little discovered from various molecular genetic studies .•complex
interactions between genes and known environment risk factors.
14Tip- DepressionAetiology : Adverse Social/Environmental Experience(see Gottlib
&Hammen 2014 CH 15)Adverse event = any personally stressful event that causes
humiliation, social defeat, actual or virtual loss . Examples :•Pakel prevalence of depression
increases with Negative Life Events (self report-retrospective !) • Roy (1987) :
unemployment , poor marriage,separation from parent before 17, first degree relative with
D.•Early Adverse Environments (See Gotlib and Hammen 2014 Ch 11) : neglectful/harsh
parenting; early abuse ; parental loss )Child
sexual abuse Hill et al (2001)- a good model of a
developmental psychopathology account of adult depression.Comment: Best understood with
reference to psychological theories of depression
Critically evaluate the evidence that Reactive Attachment Disorder and Disinhibited Social
Engagement Disorder should be considered as two distinct attachment conditions.
The Theory of Attachment was founded by John Bowlby and later expanded on by Mary
Ainsworth “Strange Situation Classification” which observed the behaviours of an infant
when separated and reunited with a caregiver/mother, the study concluded in identifying 4
attachment styles. Since then, the psychological studies of attachment have become important
in child research, particularly in those who were institutionalised as previous research shows
increased risk of developing unhealthy attachment styles and overall behaviours.
Spitz (1952) documentary “Psychogenic Disease in Infancy” pinpointed the emotional
damage that institutionalization and a lack of maternal care can have on an infant during early
years. He concluded that infants deprived of their mother during the first year of life
consecutively for over 5 months become progressively worse (lethargic, slow/limited
mobility, weight and growth stunt, empty expressions) and a total of 37.3% of cases showed
progressive deterioration which eventually led to nutrient deficiency and death by the end the
end of the second year of life (Invisible silent storm, 2015).
Tizard and Rees (1975) set out to investigate the effect of early institutional upbringing on
affectional relations and behavioural problems. They collected the data from a total of 26
children who were neglected and raised in institutional settings in London, caregivers were
advised against forming attachments to these children to increase the validity of the study. By
4 years of age, it was reported that over half of the participants (18/26) displayed abnormal
attachment styles. The results described 10 children as socially outward and aimless whilst 8
children were viewed as emotionally distant and unresponsive. The remaining 8 were able to
develop stable bonds to their caregivers.
RAD was classified as a non-attachment condition in the DSM in 1980 (Potteretal.,2009).
Two types of RAD were described in the DSM-IV: inhibited (IRAD) and disinhibited
(DRAD). Despite the fact that there are two different subtypes, evidence did suggest that they
can coexist (Smyke, Dumitrescu, &Zeanah,2002). In recent years, RAD has been split into
two distinct disorders (APA, 2013); the inhibited RAD and the inhibited RAD. The inhibited
type is now classified as RAD, whereas the disinhibited form is now known as Disinhibited
Social Engagement Disorder (DSED). According to Lehmann, Breivik, Heiervang, Havik,
and Havik (2016), the DSM-5 conceptualization of the diseases as distinct aspects of infant
