Advanced Child and Adolescent Psychiatry
Week 2 – Autism Spectrum Disorder (ASD)........................................................................... 1
Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins, and
variation in expression – Constantino & Charman (2016) ...................................................... 1
Social attention and autism symptoms in high functioning women with autism spectrum
disorders – Ketelaars et al. (2017) ........................................................................................... 5
The peer relationships of girls with ASD at school: Comparison to boys and girls with and
without ASD – Dean & Kasari (2014) .................................................................................... 7
Short summary ASD................................................................................................................ 9
Week 3 – Anxiety and Compulsions ...................................................................................... 11
The importance of practicing at home during and following cognitive behavioural therapy
for childhood anxiety disorders: a conceptual review and new directions to enhance
homework using mHealth technology – Klein et al., (2024) ................................................ 11
Maximizing exposure therapy: An inhibitory learning approach – Craske et al., (2014) ..... 16
Obsessive-compulsive disorder in children and adolescents – Barton & Heyman (2016) ... 21
VGCT Factsheet Exposure .................................................................................................... 23
Week 4 – Eating disorders ...................................................................................................... 25
Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for
the treatment of eating disorders – Hay et al., (2014) ........................................................... 25
Emotion-focused family therapy for eating disorders in children and adolescents – Robinson
et al., (2015) ........................................................................................................................... 29
Week 5 – Borderline Personality Disorder ............................................................................ 31
A life span perspective on borderline personality disorder – Videler et al., (2019).............. 31
The diagnosis that should speak its name: Why it is ethically right to diagnose and treat
personality disorder during adolescence – Hutsebaut et al., (2023) ...................................... 33
Adolescents with personality disorders suffer from severe psychiatric stigma – Catthoor et
al., (2015)............................................................................................................................... 34
Week 6 – Attachment Disorders ............................................................................................. 35
The use and abuse of attachment theory in clinical practice with maltreated children – Allen
(2021) .................................................................................................................................... 35
Misperceptions of reactive attachment disorder persist: poor methods and unsupported
conclusions – Allen (2018) .................................................................................................... 38
Practice parameter for the assessment and treatment of children and adolescents with
reactive attachment disorder and disinhibited social engagement disorder – Zeanah et al.,
(2016) .................................................................................................................................... 41
Week 7 – Psychotic Disorders ................................................................................................. 45
Psychosis in children and adolescents – McClellan (2018) .................................................. 45
Perceived social stress and symptom severity among help-seeking adolescents with versus
without clinical high-risk for psychosis – Millman et al., (2018) ......................................... 48
, Week 2 – Autism Spectrum Disorder (ASD)
Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins,
and variation in expression – Constantino & Charman (2016)
In recent years, diagnostics of ASD have become more informed by scientific discoveries
(related to symptom structure and biological cause) that have challenged traditional
perspectives. The diagnostic implications of these discoveries, are encompassed by four
overarching themes:
1. Limitations of the clinician as an expert in the diagnostic process.
2. The quantitative trait characteristics of ASD reflect evidence that the features are
continuously, and not categorically, distributed in the general population and often
arise from additive genetic influences that are shared with other neuropsychiatric
conditions.
3. Pronounced heterogeneity (differences) in the pathways of causation of ASD
phenocopies, even within families.
4. Pleiotropic effects, in which the same deleterious genetic variant can give rise to
various neuropsychiatric syndromes (e.g., ADHD, schizophrenia, epilepsy).
Aim: assimilate specific issues that have a bearing on the diagnosis of ASD.
Contemporary clinical diagnosis of ASD
Changes from DSM-IV to DSM-5:
• Collapsing the symptom criteria for ASD from 3 domains to 2 → A. Deficits in
social communication and social interaction, B. Restricted, repetitive patterns of
behaviour, interests, or activities. Because, social and communicative impairments are
closely interrelated and severity is highly correlated.
• Inclusion of new severity specifiers, which categorise the impact of symptoms on
adaptive functioning
• It is now appropriate to diagnose ASD simultaneously with other psychiatric or
developmental disorders (e.g., ADHD).
1
,Often overlooked: symptom burden (criteria A and B) and impairment in social,
occupational, and other areas of adaptive functioning (criterion D) are only partially
correlated. E.g., burden can be pronounced (many symptoms), but mild impairment, or the
other way around.
→ it can be argued that the benefits of interventions for autism are in the realm of adaptive
functioning, not core symptoms.
The three pillars of the diagnostic process of ASD:
1. Ascertainment of current symptomology sufficient to meet criteria A, B and D →
also ask teachers and caregivers for information on this
2. Acquisition of developmental history consistent with ASD (criterion C) provided
by caregiver or child
3. Clinician confirmation → clinician relies on a diversity of prompts to elicit a child’s
highest capacity for social communication, and introduce enough sensory arousal to
elicit stereotyped responses. If the child has the criteria, the clinician must determine
that the impairment in adaptive functioning is attributable to ASD, and not an
alternative disorder. Also, the child should have the criteria above the clinical
threshold, but there is tension where they should lie.
The initial descriptions of ASD were done over 70 years ago by Leo Kanner and Hans
Asperger (article is also 10 years ago, so now over 80 years ago). Infantile autism was first
introduced in the DSM-III → delay in language milestones, poor communication skills,
intellectual disability, social aloofness, motor stereotypes, preoccupations. The modern
classification systems have a broader concept, and new diagnostic labels.
• DSM-III-revised → autistic disorder and PDD-NOS (pervasive developmental
disorder not otherwise specified → milder).
• DSM-IV → Asperger’s disorder, subcategory with average or above average
intelligence and intact structural language skills
DSM-5 → Autism Spectrum Disorder. This change was made because:
• ASD syndromes are aetiologically and clinically heterogeneous
• Clinical subtypes (PDD-NOS, Asperger) did not have scientific validity in terms of
neurobiological or genetic aetiologies, or truly independent cognitive associates that
differed between the diagnostic subtypes. Most importantly, the subtypes lacked
clinical validity. (example: case study of Asperger → all cases met the criteria for
autistic disorder)
• The use of sub-classifications was unreliable and bore no relation to the symptoms
scores measured on standardised instruments.
Final important change in DSM-5 = clinical specifiers alongside the diagnosis of ASD, like
timing and nature of onset. Also, the presence or absence of the following features: language
impairment, intellectual impairment, known medical or genetic conditions, precipitating
environmental factors, other specific neurodevelopmental, or behavioural disorders,
catatonia.
One concern is that the DSM-5 has introduced a diagnostic constriction → up to 20% of
individuals who met the criteria for one of the disorders in DSM-IV, does not meet the DSM-
5 ASD criteria. In particular, those without intellectual disability. Also, subtypes might not
be biologically traceable.
2
, DSM-5 introduced social (pragmatic) communication disorder → persistent difficulties in
the use of verbal and non-verbal communication for social purposes, in the absence of
restrictive and repetitive interests and behaviours. Relation to ASD is unknown.
Also, the DSM-5 recognized that the core features of ASD can be better understood as a
spectrum of presentations.
So, main improvements of DSM-5 for ASD:
• Clarified the symptom criteria for ASD
• Operationalized the distinction between symptom burden and impairment
• Alluded to the continuous nature of autistic traits in the general population
Progress in the measurement of autistic traits
1. Standardised measures of symptom burden: several instruments have been widely
validated and used in research and clinical practice (e.g., ADI-R, 3di, ADOS-2).
There is overlap in the content of the scales, but they differ in the aspect of the
diagnostic process to which they apply (I.e., developmental history vs. current
symptom ascertainment), populations in which they are standardized, need for trained
raters, training time, cost and feasibility.
o Many have been validated in people with ASD and intellectual disability,
and in non-western cultures.
o Quantitative approaches to the measurement of autistic traits: through
this, we found the continuum. There is an arbitrary nature to diagnostic cut-
offs in ASD. The traits for ASD are as highly correlated in both the general
population and ASD population.
§ Research shows autistic traits exist on a spectrum in the general
population rather than forming a distinct category.
§ Many individuals have mild autistic traits without clinical impairment.
§ Some relatives of individuals with ASD show subclinical autistic traits,
supporting a genetic continuum theory.
§ Researchers suggest that diagnostic thresholds should be percentile-
based (as with IQ or height), but ASD diagnosis is still based on
subjective clinical judgment.
§ Due to failure to incorporate sex-specific norms in the diagnostic
process, there are significant differences in the rates of community
diagnoses for girls vs boys, wo manifest precisely the same level of
quantitative symptom burden.
Genetic and Biological Findings
Genetic studies reveal ASD is caused by a combination of factors:
1. Causal heterogeneity → rare mutations (de novo or inherited) – Found in up
to 40% of ASD cases.
2. Quantitative genetic risk → Polygenic risk – Most ASD risk comes from common
genetic variations with small cumulative effects.
3. Pleiotropy – Some ASD-associated genes also increase the risk for conditions
like ADHD, schizophrenia, epilepsy, and intellectual disability.
Understanding these genetic influences is shifting ASD diagnosis from a behavioral model
toward a biological framework.
3
Week 2 – Autism Spectrum Disorder (ASD)........................................................................... 1
Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins, and
variation in expression – Constantino & Charman (2016) ...................................................... 1
Social attention and autism symptoms in high functioning women with autism spectrum
disorders – Ketelaars et al. (2017) ........................................................................................... 5
The peer relationships of girls with ASD at school: Comparison to boys and girls with and
without ASD – Dean & Kasari (2014) .................................................................................... 7
Short summary ASD................................................................................................................ 9
Week 3 – Anxiety and Compulsions ...................................................................................... 11
The importance of practicing at home during and following cognitive behavioural therapy
for childhood anxiety disorders: a conceptual review and new directions to enhance
homework using mHealth technology – Klein et al., (2024) ................................................ 11
Maximizing exposure therapy: An inhibitory learning approach – Craske et al., (2014) ..... 16
Obsessive-compulsive disorder in children and adolescents – Barton & Heyman (2016) ... 21
VGCT Factsheet Exposure .................................................................................................... 23
Week 4 – Eating disorders ...................................................................................................... 25
Royal Australian and New Zealand College of Psychiatrists clinical practice guidelines for
the treatment of eating disorders – Hay et al., (2014) ........................................................... 25
Emotion-focused family therapy for eating disorders in children and adolescents – Robinson
et al., (2015) ........................................................................................................................... 29
Week 5 – Borderline Personality Disorder ............................................................................ 31
A life span perspective on borderline personality disorder – Videler et al., (2019).............. 31
The diagnosis that should speak its name: Why it is ethically right to diagnose and treat
personality disorder during adolescence – Hutsebaut et al., (2023) ...................................... 33
Adolescents with personality disorders suffer from severe psychiatric stigma – Catthoor et
al., (2015)............................................................................................................................... 34
Week 6 – Attachment Disorders ............................................................................................. 35
The use and abuse of attachment theory in clinical practice with maltreated children – Allen
(2021) .................................................................................................................................... 35
Misperceptions of reactive attachment disorder persist: poor methods and unsupported
conclusions – Allen (2018) .................................................................................................... 38
Practice parameter for the assessment and treatment of children and adolescents with
reactive attachment disorder and disinhibited social engagement disorder – Zeanah et al.,
(2016) .................................................................................................................................... 41
Week 7 – Psychotic Disorders ................................................................................................. 45
Psychosis in children and adolescents – McClellan (2018) .................................................. 45
Perceived social stress and symptom severity among help-seeking adolescents with versus
without clinical high-risk for psychosis – Millman et al., (2018) ......................................... 48
, Week 2 – Autism Spectrum Disorder (ASD)
Diagnosis of autism spectrum disorder: reconciling the syndrome, its diverse origins,
and variation in expression – Constantino & Charman (2016)
In recent years, diagnostics of ASD have become more informed by scientific discoveries
(related to symptom structure and biological cause) that have challenged traditional
perspectives. The diagnostic implications of these discoveries, are encompassed by four
overarching themes:
1. Limitations of the clinician as an expert in the diagnostic process.
2. The quantitative trait characteristics of ASD reflect evidence that the features are
continuously, and not categorically, distributed in the general population and often
arise from additive genetic influences that are shared with other neuropsychiatric
conditions.
3. Pronounced heterogeneity (differences) in the pathways of causation of ASD
phenocopies, even within families.
4. Pleiotropic effects, in which the same deleterious genetic variant can give rise to
various neuropsychiatric syndromes (e.g., ADHD, schizophrenia, epilepsy).
Aim: assimilate specific issues that have a bearing on the diagnosis of ASD.
Contemporary clinical diagnosis of ASD
Changes from DSM-IV to DSM-5:
• Collapsing the symptom criteria for ASD from 3 domains to 2 → A. Deficits in
social communication and social interaction, B. Restricted, repetitive patterns of
behaviour, interests, or activities. Because, social and communicative impairments are
closely interrelated and severity is highly correlated.
• Inclusion of new severity specifiers, which categorise the impact of symptoms on
adaptive functioning
• It is now appropriate to diagnose ASD simultaneously with other psychiatric or
developmental disorders (e.g., ADHD).
1
,Often overlooked: symptom burden (criteria A and B) and impairment in social,
occupational, and other areas of adaptive functioning (criterion D) are only partially
correlated. E.g., burden can be pronounced (many symptoms), but mild impairment, or the
other way around.
→ it can be argued that the benefits of interventions for autism are in the realm of adaptive
functioning, not core symptoms.
The three pillars of the diagnostic process of ASD:
1. Ascertainment of current symptomology sufficient to meet criteria A, B and D →
also ask teachers and caregivers for information on this
2. Acquisition of developmental history consistent with ASD (criterion C) provided
by caregiver or child
3. Clinician confirmation → clinician relies on a diversity of prompts to elicit a child’s
highest capacity for social communication, and introduce enough sensory arousal to
elicit stereotyped responses. If the child has the criteria, the clinician must determine
that the impairment in adaptive functioning is attributable to ASD, and not an
alternative disorder. Also, the child should have the criteria above the clinical
threshold, but there is tension where they should lie.
The initial descriptions of ASD were done over 70 years ago by Leo Kanner and Hans
Asperger (article is also 10 years ago, so now over 80 years ago). Infantile autism was first
introduced in the DSM-III → delay in language milestones, poor communication skills,
intellectual disability, social aloofness, motor stereotypes, preoccupations. The modern
classification systems have a broader concept, and new diagnostic labels.
• DSM-III-revised → autistic disorder and PDD-NOS (pervasive developmental
disorder not otherwise specified → milder).
• DSM-IV → Asperger’s disorder, subcategory with average or above average
intelligence and intact structural language skills
DSM-5 → Autism Spectrum Disorder. This change was made because:
• ASD syndromes are aetiologically and clinically heterogeneous
• Clinical subtypes (PDD-NOS, Asperger) did not have scientific validity in terms of
neurobiological or genetic aetiologies, or truly independent cognitive associates that
differed between the diagnostic subtypes. Most importantly, the subtypes lacked
clinical validity. (example: case study of Asperger → all cases met the criteria for
autistic disorder)
• The use of sub-classifications was unreliable and bore no relation to the symptoms
scores measured on standardised instruments.
Final important change in DSM-5 = clinical specifiers alongside the diagnosis of ASD, like
timing and nature of onset. Also, the presence or absence of the following features: language
impairment, intellectual impairment, known medical or genetic conditions, precipitating
environmental factors, other specific neurodevelopmental, or behavioural disorders,
catatonia.
One concern is that the DSM-5 has introduced a diagnostic constriction → up to 20% of
individuals who met the criteria for one of the disorders in DSM-IV, does not meet the DSM-
5 ASD criteria. In particular, those without intellectual disability. Also, subtypes might not
be biologically traceable.
2
, DSM-5 introduced social (pragmatic) communication disorder → persistent difficulties in
the use of verbal and non-verbal communication for social purposes, in the absence of
restrictive and repetitive interests and behaviours. Relation to ASD is unknown.
Also, the DSM-5 recognized that the core features of ASD can be better understood as a
spectrum of presentations.
So, main improvements of DSM-5 for ASD:
• Clarified the symptom criteria for ASD
• Operationalized the distinction between symptom burden and impairment
• Alluded to the continuous nature of autistic traits in the general population
Progress in the measurement of autistic traits
1. Standardised measures of symptom burden: several instruments have been widely
validated and used in research and clinical practice (e.g., ADI-R, 3di, ADOS-2).
There is overlap in the content of the scales, but they differ in the aspect of the
diagnostic process to which they apply (I.e., developmental history vs. current
symptom ascertainment), populations in which they are standardized, need for trained
raters, training time, cost and feasibility.
o Many have been validated in people with ASD and intellectual disability,
and in non-western cultures.
o Quantitative approaches to the measurement of autistic traits: through
this, we found the continuum. There is an arbitrary nature to diagnostic cut-
offs in ASD. The traits for ASD are as highly correlated in both the general
population and ASD population.
§ Research shows autistic traits exist on a spectrum in the general
population rather than forming a distinct category.
§ Many individuals have mild autistic traits without clinical impairment.
§ Some relatives of individuals with ASD show subclinical autistic traits,
supporting a genetic continuum theory.
§ Researchers suggest that diagnostic thresholds should be percentile-
based (as with IQ or height), but ASD diagnosis is still based on
subjective clinical judgment.
§ Due to failure to incorporate sex-specific norms in the diagnostic
process, there are significant differences in the rates of community
diagnoses for girls vs boys, wo manifest precisely the same level of
quantitative symptom burden.
Genetic and Biological Findings
Genetic studies reveal ASD is caused by a combination of factors:
1. Causal heterogeneity → rare mutations (de novo or inherited) – Found in up
to 40% of ASD cases.
2. Quantitative genetic risk → Polygenic risk – Most ASD risk comes from common
genetic variations with small cumulative effects.
3. Pleiotropy – Some ASD-associated genes also increase the risk for conditions
like ADHD, schizophrenia, epilepsy, and intellectual disability.
Understanding these genetic influences is shifting ASD diagnosis from a behavioral model
toward a biological framework.
3
