CAMS - Midterm Review

Sessions 1-8

Importance of Study of Child/Adolescent Psychopathology

• ½ of all lifetime cases of mental illness begin by 14 (3/4 by 24)

• Rapid cognitive and emotional dev

  • Brain still developing (prefrontal cortex)

  • Melatonin peaks later at night, drops later in morning

• Psychosocial transitions (education, employment, relationships/sexuality, sense of self, beliefs)

• Traumatic childhood experiences affect > 50% children

• Suicide among top 10 causes of death in adolescents; depression, self-harm, anxiety disorders among top 10 causes of illness/disability

Sigmund Freud

• Psychoanalysis

• Gave meaning to adult psychopathology by linking it to childhood experiences

• → Course of mental disorders finally not seen as inevitable

Drive Theory (Freud)

Aggressive and sexual “drives” primary motivating forces in our quest for pleasure. end goal of development: sexual maturity

1. Oral Phase (birth-18mo): infant interaction through the mouth

2. Anal Phase (18-36mo): primary focus on controlling bladder + bowel movements

3. Phallic-Odeipal Phase (3-6yr): children discover differences b/w males and females

4. Latency Phase (6-11yr): development of social skills, values, and relationships

5. Genital Stage (11+; ends at adulthood): puberty → strong interest in opposite sex

Psychosocial Theory (Erikson)

1. Basic Trust vs. Mistrust (Birth-1yr) - trust/mistrust that basic needs will be met

2. Autonomy vs. Shame and Doubt (1-3yr) - develop sense of independence

3. Initiative vs. Guilt (3-5yr) - take initiative on some activities; may develop guilt if unsuccessful

4. Industry vs. Inferiority (6-11yr) - develop self-confidence in activities when competent; inferiority when not

5. Identity vs. Role Diffusion (11 yr-end of adolescence) - develop identity & roles

6. Intimacy vs. Isolation (21-40yr) - establish relationships w/ others

7. Generativity vs. Stagnation (40-65yr) - contribute to society + be part of family

8. Integrity vs. Despair (65+) - make sense of life & meaning of contributions

Stages of Cognitive Development (Piaget)

1. Sensorimotor Stage (birth-2yr): learn senses and body movement

2. Preoperational Stage (2-7yr): learn language, symbols, and pretend play

3. Concrete Operational Stage (7-adolescence): start thinking logically

4. Formal Operational Stage (adolescence): can think about abstract ideas

Object Relations (Mahler)

• More modern adaptation of psychoanalytic theory that places less emphasis on drives of aggression and sexuality as motivational forces

• More emphasis on human relationships as primary motivational force in life

Separation-Individuation (Mahler)

Six stages of development lead to normal object relations, predicated upon a recognition of “separateness”

1. Normal Autism (birth-2mo): unaware of outside world

2. Symbiosis (2-5mo): baby is a single unit w/ primary caregiver

3. Differentiation (5-10mo): show interest in world beyond caregiver

4. Practicing Sub-Phase (10-18mo): crawling and active exploration

5. Rapprochement (2-5yr): separate identities from caregiver

Risk Factor

A variable that precedes a negative outcome and increases the chance of that outcome occurring

• Situational risk factors: poverty, death of a loved one, homelessness, community disasters

• Inconsistent/deficient caregiving in early childhood

• Family history of mental illness

• Neonatal complications

Resilience/Protective Factor

A variable that increases one’s ability to avoid or cope w/ negative outcomes despite a risk for psychopathology

• Self-confidence

• Flexibility in problem solving

• Intelligence

• Coping skills

• Social and emotional support

Gender and Psychology

• Girls have more internalising sx → increased anxiety, depression, somatisation, eating disorders, emotional withdrawal

• Boys have more externalising sx → more difficulties w/ aggression, hyperactivity, delinquency

• Gender diverse/trans youth have higher rates of mental health struggles than cis peers

Race + Ethnicity and Psychology

• Minorities overrepresented in encountering poverty, limited access to care, and poorer quality of care → more difficulties in many mental disorders

• Racism, not race itself, is contributor to mental ill-health

Intersectional Therapeutic Framework

How overlapping social identities (e.g., gender, race, class, sexuality, etc.) create a unique system influencing a client’s mental health and wellbeing

Window of Tolerance

• An optimal zone of emotional and physiological arousal

• Stress, trauma, or overstimulation can push person outside of their zone into hyper-arousal (fight or flight) or hypo-arousal (withdrawal/dissociation)

• Person needs to return to optimal zone through regulation/co-regulation

• When person goes into hyper-/hypo- arousal, activity increases in brainstem and decreases in prefrontal cortex

• During acute and chronic stress, brain flooded w/ adrenaline and cortisol

Key Stages of Neurodevelopment

1. Prenatal period

2. Postnatal - adolescence

3. Adolescence - adulthood

Early Brain Development

• Child’s brain develops due to genes and env.

• Genes provide initial map for brain dev

• Significant wiring occurs during first years of a child’s life

  • Age 3: ~1000 trillion brain connections → Adolescence": ~500 trillion

• Synaptic pruning heavily influenced by experience and env.

Synaptic Pruning

• Infants born with ~2,500 synapses per neuron

• By 3, ~15,000 synapses per neuron

• Early adolescent brain loses as many as 30,000 synapses per sec

• Frontal lobes are “closed for construction”

Adolescent Brain Development

• Amygdala: fear, anxiety, aggression; less volume in youth = risk assessment not as developed; hypoactivity

• Nucleus Accumbens: dopamine sensitivity, reward system; hyperactivity

• Prefrontal Cortex: high-level executive function, inhibition, assessment of situations; “closed for construction” during youth; not interacting w/ other parts of brain

Adolescence - The Risky Brain

• Darwinian Argument: need to become more of a risk taker and sensation seeker when you strike out on your own and leave safe home env. to survive

• Neurological Argument: high activity in reward system and motivation; less refined activity in PFC

• Peer Pressure: greater social sensitvity

Neuroplasticity

The brain’'s ability to change/adapt by forming new connections, strengthening old ones, and reorganising pathways in response to learning, env, or injury

• Firing together: active nerve cells build stronger links

• Pruning: unused connections fade away over time

• Brain keeps changing and growing at any age, not just in childhood

Diathesis-stress Model

• Mental disorders develop from a combination of pre-existing vulnerability (diathesis) + environmental stress

  • an individual w/ a high predisposition to mental illness requires less stress to trigger the disorder

  • resilience factors reduce likelihood of disorder developing

Health Paradox of Adolescence

• Adolescence physically healthiest time of life

• Yet…

  • Depression increases from 4% prevalence in childhood to 17% in adolescence

  • Substance abuse, eating disorders, psychotic disorder, etc. all increase greatly during teen years → major increases in morbidity

  • Adolescence has high rates of risk-taking behaviour, sensation-seeking, emotionally-influenced behaviour

Mental Disorder

• A clinically significant disturbance in cognition, emotion regulation, or behaviour reflecting dysfunction in psychological, biological, or developmental processes

• Characteristic must include:

  • Distress or impairment in functioning

  • Not merely a normal response to stress/loss

  • Not simply social deviance

  • Risk of further suffering/harm

• Nosology: classification of disorders

Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association (DSM)

• “Statistical” in sense that historically, its progenitor was an attempt to gather epidemiological info (“stats”) on the number of various types of mental illness in nation

• Symptom-driven document that describes mental illness w/o etiological explanation

DSM (1952) and DSM-II (1968)

Provided brief descriptions of characteristic sign and sx of the disorders but no criteria

DSM-III (1980) and DSM-III-R (1987)

• Diagnostic criteria for various disorders provided

• Better inter-rater reliability and evidence of predictive reliability

• Specified group of disorders as “usually first evident in infancy, childhood, or adolescence”: Reactive attachment disorder, separation anxiety disorder, overanxious disorder, and avoidant disorder

• Anxiety diagnoses applicable to adults were available for diagnosing children

DSM-IV (1994) and DSM-IV-TR (2000)

• Further clarified diagnoses and refined diagnostic criteria

• Some new diagnoses added (Asperger, ADD became ADHD, etc.)

• Intro of multi-axial system

• TR was a Text Revision w/ increased background info regarding risk factors, epidemiology, and course, and development of disorders

Multiaxial System in DSM-IV

• Axis I: Clinical mental disorders

• Axis II: Personality disorder & mental retardation

• Axis III: Major medical diagnoses

• Axis IV: Psychosocial and environmental stressors

• Axis V: Global Assessment of Functioning (GAF), a numeric scale (0-100) used to rate social, occupational, and psychological functioning

DSM-V (2013) and DSM-V-TR (2022)

• Removal of multiaxial system and introduction of single axis diagnostic approach (single diagnostic list w/ each disorder using standardised codes and noting psychological, environmental stressors, and disability)

• Reorganisation of diagnostic chapters based on shared underlying mechanisms and developmental patterns

• Introduction of dimensional assessments (spectrum disorders)

DSM Changes - Removal of Multiaxial System

• Multiaxial system complex and unreliable

• Changed to a single diagnostic list → each disorder has standardised codes and notes psychosocial, env stressors, disability

DSM Changes - Removal of Some Disorders

• DSM-I and II (1952)

  • Homosexuality: "s*xual deviation disorder”

• DSM-II (1973)

  • Homosexuality removed → changed to “s*xual orientation disturbance”

• DSM-III (1980)

  • Ego-dystonic homosexuality

• DSM-III-R (1987)

  • All mention of homosexuality removed

DSM Changes - Dimensional Disorders

• Categorical System: traditional system; DSM classifies disorders into distinct categories; artificial yes/no boundaries; comorbidity

• Dimensional System: measures sx on continuums of severity; captures variations in sx

• DSM 5 combines categorical diagnoses and dimensional severity measures

Pros of Mental Health Diagnosis

• Provides clarity

• Validates experiences

• Provides opportunity for evidence-based treatment

Cons of Mental Health Diagnosis

• Stigmatising psychiatric disorders → self-limiting beliefs or discrimination

• Misdiagnosis

• Overreliance of labels

Limitations of DSM

• Artificial boundaries: disorders diagnosed as absent or present

• High comorbidity

• Heterogeneity: individuals w/ same disorder may have different sx

• Sx overlap

• Limited context: environmental and cultural factors may be underemphasised

Pros and Cons of DSM

• + standardisation, research, clinical guidance

• - oversimplifies human behaviour, risk of misdiagnosis, over diagnosis, stigmatising labels

Future Diagnostic Models

• Will continue to be framed partly by categorical mental disorder concepts

• Will include a dimensional scale (disorders on spectrum of severity)

• Cross-cutting dimensional model: measures how certain sx are across multiple areas of mental health, regardless of specific disorder being considered (anxiety cross-cutting sx for GAD and panic disorder)

Diagnosis vs. Differential Diagnosis

• Diagnosis: identification of a disorder based on a person’s sx and other clinical features (do this person’s sx satisfy the recognized criteria for a particular disorder?)

• Differential diagnosis: distinguishing a condition from others with similar sx and other clinical features (based on current sx, what other disorder could this be?)

Clinical Evaluation

• What are the diagnostic features

• Hypothesis (initial hunches)

• Testing

  • what specific sx do these hypotheses include?

  • what would discount them?

  • are there any sx that differentiate one condition from another?

• Consult DSM

Clinical Evaluation Conducted with Child & Family

1) Identify problem and formulate theory

2) Identify history of child and family

3) Test theory with assessments and interviews

4) Conduct Mental Status Examination

5) Provide diagnosis (if necessary)

Formulation

• A summary of main clinical problems and the factors that may have contributed to development of those problems

• Biopsychosocial formulation (biological factors, psychological factors, social factors)

Strengths Based vs. Problem-focused Formulation

• Strength based formulation: identifying and utilising an individual’s existing strengths to facilitate change, rather than concentrating solely on deficits

• Problem-focused/diagnosis-focused formulation: identify and address a client’s specific, current difficulties. focuses on identifying triggers and underlying mechanisms of problem

Clinical History

1) History of presenting problem

2) Child history

3) Family history

History of Presenting Problem

• Evaluating present problem (sx, duration, frequency, severity)

• Past psychiatric history

• Environmental and cultural context

Child History

• Developmental history

• Education history

• Medical history

• Relationships

• Physical history

• Strengths

Family History

• Family history: enquire about each parent’s family of origin, mental health history, and relationships

• Family conflict, parenting styles

• How do the parents manage difficulties in child?

• Are there any cultural/religious considerations? Divorce/separation?

Mental Status Examination (MSE)

1) Appearance (grooming, hygiene, clothing, physical signs of neglect)

2) Behaviour and psychomotor activity (eye contact, cooperation, activity lvl)

3) Speech (rate, volume, fluency, vocab)

4) Mood and affect (mood = internal emotional experience; affect = observable expressions of emotion)

5) Thoughts (thought process = how thoughts organised - ex: coherent; thought content = what they’re thinking about - ex: excessive worries)

6) Perception (hallucinations, illusions, distorted perceptions?)

7) Cognition (orientation, attention/concentration, memory, intellectual functioning)

8) Insight and Judgement (insight = awareness of difficulties; judgement: make appropriate decisions and understand consequences)

Engaging with Adolescents

• Establish rapport

• Define confidentiality

• Non-judgmental w/o condoning risky behaviour

• Address parents’ concerns and involve them; decide with adolescent which issues to discuss w/ parents

• Beware of splitting/countertransference (over-identifying w/ adolescent or parents)

Autism Spectrum Disorder (ASD) in DSM

A) Persistent deficits in social communication and social interaction across multiple contexts:

1. deficits in social-emotional reciprocity

2. deficits in nonverbal communicative behaviours used for social interaction

3. deficits in developing, maintaining, and understanding relationships

B) Restricted, repetitive patterns of behaviour, interests, or activities, at least 2:

1. stereotyped/repetitive motor movements, use of objects, or speech

2. insistence on sameness, inflexible adherence to routines, or ritualized patterns or verbal speech

3. Highly restricted, fixated interests that are abnormal in intensity or focus

4. Hyper or hypoactivity to sensory input or unusual interests in sensory aspects of the env.

C) Sx must be present in early developmental period

D) Sx cause clinically significant impairment in social, occupational, or other important areas of current functioning

E) These disturbances are not better explained by intellectual disability or global developmental delay

ASD - DSM Specifiers

Specify Severity Level

• Requiring support

• Requiring substantial support

• Requiring very substantial support

Specify if:

• With or w/o accompanying intellectual impairment

• With or w/o accompanying language impairment

Specify if:

• Associated with a known genetic or other medical condition or environmental factor

• Associated with a neurodevelopmental, mental, or behavioural problem

Specify if

• With catatonia

Communication Impairment Examples (ASD)

• Using communication for social purposes

• Difficulty changing communication to match context or needs of listener

• Difficulty following rules for conversation or storytelling

• Difficulties understanding what is not explicitly stated and non-literal meanings

Language Impairment Examples (ASD)

• Developmental language delay

• Echolalia (repetition of words/phrases/sounds)—immediate or delayed

• Pronoun reversal (e.g., mixing “you” and “i”)

• Idiosyncratic word use and jargon (talking like “little professors”)

Course of ASD

• 12-24 mos: first sx recognised

• 2-4 yrs: developmental plateaus or regression

• 4+ yrs: restricted/repetitive behaviours clear

• Adolescence: sx may be less obvious

*ASD can be reliably diagnosed by age 2

Prevalence of ASD

• ASD occurs all over world, affecting 1-2% of pop.

• Boys : Girls → 3 : 1

  • Girls who are diagnosed are more likely to have an ID

Masking Impairments

• Conscious or unconscious effort to hide, compensate for, or minimise behaviours associated w/ autism

  • suppressing self-soothing behaviours, forcing eye contact, rehearsing convos beforehand, learning scripts

Interoceptive Awareness

Ability to listen to our body and understand its messages

Genetic Factors of ASD (Aetiology)

• High heritability - associated with more than 100 genomic variants

  • Fragile X gene, FXR1, Chromosome 15 variant

  • 10-30% of children w/ fragile X syndrome have autistic sx

• Much higher concordance in monozygotic twins than dizygotic twins

*Having ASD gene variant alone often not enough to result in ASD manifestation

Environmental Factors of ASD

• Advanced maternal (> 40 yrs) and paternal (> 50 yrs) age

• Short interpregnancy intervals (< 2 yrs)

• Maternal stressors (maternal stress, maternal hypertension, maternal metabolic difficulties)

• Premature birth (< 32 weeks)

• Low birth weight (< 1500 grams)

• Diet

Neurobiological Factors of ASD

• ASD also has neurobiological factors

Visual Tracking

• Individuals with ASD do not follow the most salient features when viewing faces or watching other people

• A person w/o ASD would typically watch eyes to gather social info

• Person with ASD more likely to look at mouth (helps them process what’s being said)

Assessment of ASD

• Autism Diagnostic Interview-Revised (ADI-R)/Autism Diagnostic Observation Schedule (ADOS)

• Checklist for Autism in Toddlers Screening Tool (CHAT)

• The Childhood Autism Rating Scale (CARS)

• The Profile-Revised (PEP-R)

• Social Responsiveness Scale

ADOS

• 4 modules for different developmental ability

• Semi-structured assessment that presents various activites that elicit behaviours directly related to an ASD diagnosis

ADI-R

• Structured interview used for diagnosing autism

• Clinical interview for parents or guardian

Treatment for ASD

• Psychoeducation for parents

• Applied Behavioral Analysis (ABA)

• Social skills training

• Neuro-affirming care

Psychoeducation for Parents

Therapeutic approach that teaches individuals and their families about mental health conditions, sx, and treatment options

Applied Behavioural Analysis (ABA)

• ABA Therapy: focuses on improving specific behaviours, communication, and learning, through positive reinforcement techniques

• Principles:

  • Correct response = reward + reinforcement

  • Incorrect response = no reward

  • Reward every time → reward once every X times

• Helps develop skills they may not acquire naturally + reduce dangerous behaviours (EX: self harm)

• Focus: skill development and redirection of problem behaviours, not trying to take away neurodiversity

Social Skills Training

• Improve social interaction, including conversational skills, non-verbal cues, relationship building

• Often group-based

Neuro-affirming Care

• Views autism as natural variation of human brain, not something to be “fixed”

• Learning neuro-affirming regulation strategies

• Focus on sensory processing, body awareness, and finding regulatory needs

• Functional communication and self-advocacy, not just speech reproduction

Specific Learning Disorder in DSM

A) Difficulties learning and using academic skills, at least 1 sx for min 6 months (despite interventions that target those difficulties)

B) Affected academic skills substantially below expected for age + interference w/ academic/occupational/daily living as shown by standardized assessment. (if 17+, documented history of learning difficulties sub assessment)

C) Learning difficulties begin during school-age but may not fully manifest until demands for affected academic skills exceed person’s limited capacities

D) Learning difficulties not better accounted for by intellectual disabilities, uncorrected visual/auditory acuity, other mental/neurological disorders, psychosocial adversity, lack of proficiency in lang of academics, or inadequate educational instruction

Specific Learning Disorder Specifiers (DSM)

Specify if

• With Impairment in Reading (Dyslexia - word reading accuracy, reading rate/fluency, reading comprehension)

• With Impairment in Written Expression (Dysgraphia - spelling accuracy, grammar & punctuation, organisation of written expression)

• With Impairment in Mathematics (Dyscalculia - number sense, memorisation of arithmetic facts, accurate calculation, accurate math reasoning)

Specify current severity

• Mild, moderate, severe

Course of Specific Learning Disorder

• Preschool yrs: sx manifest as subtle lang and motor delays

• Early elementary school: gap b/w child’s intellectual potential and academic performance becomes visible

• Adolescence: decoding can be mastered, but reading/maths/written word remains effortful and challenging

*Recognition and diagnosis usually occurs during elementary school

SLD - Dyslexia

• Phonological decoding impaired, but meaning retained

• Distortions, substitutions, or omissions in reading (“aminals” for “animal”)

• Automaticity doesn’t develop: 50ms (control group) vs. 400 ms (dyslexia) to identify words

→ increased school refusal

→ difficulties w/ esteem, anxiety sx, depressed mood

→ children w/ learning disorders 2x more likely to drop out of school

Aetiology of SLD

1) Genetic Factors: strong heritability of SLDs

2) Perinatal and Prenatal Factors: premature birth, low birth weight, maternal stressors

3) Environmental Factors: low SES or limited access to early education can exacerbate severity

4) Neurobiological Factors

Assessment of SLD

• Wechsler Preschool and Primary Scale of Intelligence (WPPSI): 2.5 - 7.5 yrs

• Wechsler Intelligence Scale for Children (WISC): 6 - 16 yrs

• Wechsler Adult Intelligence Scale (WAIS): 16+

• Wechsler Individual Achievement Test (WIAT)

WISC

• Assesses a full-scale Intelligence Quotient (IQ) and provides rankings for

  • verbal comprehension

  • visual spatial

  • fluid reasoning

  • working memory

  • processing speed

• WISC for SLD

  • In SLD, IQ within avg range

  • WISC helps differentiate SLD from an ID

WIAT

• Consists of 20 activities

• WIAT identifies impairment and severity in reading, written expression, and mathematics

Diagnosing SLD

• SLD typically diagnosed if their scoring in a WIAT domain (reading, written expression, mathematics) is 2 SDs lower than predicted lvl from WISC

• General IQ for most people: mean IQ: 100 and SD: 15

• With no SLD, IQ of 100 means predicted reading ability of 100 (WIAT score)

→ Nelly scores 100 on IQ test so her expected reading ability score ~100. She scores 65 on the WIAT reading index = diagnosis of a reading disorder

Treatment Plans for SLD

• Phonological Awareness Training

  • Phonemic awareness: critical phonological skill for reading and spelling

  • Auditory-based, crucial early literacy intervention focusing on identifying and manipulating sound structure of spoken lang

• School-based Supports and Accommodations

  • Individual Education Plan (IEP): legal protection for students w/ SLDs to receive free and appropriate education

  • Customised educational env that has specific goals, adjustments, and support strats

• Psychological Support

  • Help address additional mental health sx (low self-esteem, anxiety, school avoidance)

Intellectual Developmental Disorder (Intellectual Disability) in DSM

A) Deficits in intellectual functions confirmed by clinical assessment and individualized, standardized IQ testing (IQ below 70)

B) Deficits in adaptive functioning that result in failure to meet developmental and sociocultural standards for personal independence and social responsibility

C) Onset of intellectual and adaptive deficits during developmental period

• Severity (determined by adaptive functioning)

  • Mild (85%)

  • Moderate (10%)

  • Severe (5%)

  • Profound (1%)

Course of ID

• 12-24 mos: delayed motor, lang, and social milestones

• Preschool: mild impairments

• Adolescence: skill gap b/w peers widens

• Adulthood: focus on building autonomy, vocational readiness, and community inclusion

ID - Associated Difficulties

• Increased rates of accidental injury

• Lack of communication skills → predispose aggressive behaviours

• Exploitation

• Common comorbidities w/ epilepsy, cerebral palsy, medical complications, other psychiatric conditions

Aetiology of ID

• No clear aetiology can be found in 30-40% of cases

• Specific aetiologies often found in those w/ severe/profound ID

• Most common causes:

  • Down Syndrome

  • Fragile X Syndrome

  • Foetal Alcohol Syndrome Disorder

Down Syndrome

• Extra copy of chromosome 21

• Caused by an error in division of sperm or egg cells, risk increases in prenatal age at conception

• Most have mild to moderate ID

Fragile X Syndrome

• Most common inherited cause of ID

• Occurs in 1/4000 males and 1/8000 females

• Full mutation of FMR-1 gene on the X chromosome

• This gene produces the FMR-1 protein which is essential for normal brain function

Foetal Alcohol Spectrum Disorder (FASD)

• Caused by consuming alc during pregnancy

• Characteristic physical features

• Behavioural Sx: impulsivity, poor memory, short attention span

• ID: ADHD, learning disabilities, anxiety, depression, lang disorders

Assessment of ID

• Often known since birth

• Instruments same as SLD

  • WISC - assesses IQ

  • WIAT - assesses cognitive ability

→ if ID is typically classified by an IQ < 70, then expect WISC and WIAT scores to be < 70

Treatment Plan for ID

Focus on building life skills, autonomy, and managing co-occurring sx

• Psychoeducation

• ABA

• School-based Supports and Accommodations

• Therapy for Psychological Challenges Related to ID

Attention-deficit/Hyperactivity Disorder in DSM

A) Persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development

B) Several of these sx present before age 12

C) Several of these sx present in 2 or more settings (at home, school, work; with friends or relatives; in other activities)

D) Clear evidence that sx interfere w/ or reduce quality of social, academic, or occupational functioning

E) sx do not occur exclusively during course of schizophrenia or another psychotic disorder and are not better explained by another mental disorder

Inattention and Hyperactivity Sx

1) Inattention (> 6)

• poor attention to detail

• difficulty sustaining attention in tasks/play

• doesn’t seem to listen when spoken to

• difficulty following instructions

• difficulty organizing tasks

• Avoids tasks requiring sustained mental effort

• loses items necessary for tasks

• easily distracted

• forgetful in daily activities

2) Hyperactivity (> 6)

• fidgets

• leaves seat

• runs/climbs excessively

• difficulty engaging in leisure activities quietly

• “on the go”

• talks excessively

• blurts out answers early

• difficulty waiting turn

• interrupts others

ADHD Specifiers

• Type

  • Predominantly inattentive

  • Predominantly hyperactive

  • Combined

• Severity

  • Mild

  • Moderate

  • Severe

*Sx persist into adulthood but can decrease over time

ADHD - Associated Problems

• Early maladaptive schema/core beliefs

• School dropout rate 2x

• More likely to repeat grades and face disciplinary action

• May have neuro-cognitive deficits (working memory, reaction time variability, response inhibition)

Course of ADHD

Sx difficult to distinguish from normal behaviors < 4 yrs old

• Preschool: signs of hyperactivity and excessive movement

• Elementary school: often when ADHD identified, inattention becomes more prominent and hyperactivity confined or internalised

• Later school years: increased risk-taking, challenges w/ planning and org, emotional dysregulation, high comorbidity

• Adulthood: hyperactive sx less common, inattention and comorbidities can persist

Prevalence of ADHD

• Most commonly diagnosed behavioural disorder of childhood

• Combined presentation most common subtype

• High comorbidity w/ oppositional defiant disorder, ASD, personality & substance use disorders

ADHD Sex Paradox

• Male : Female → 2 : 1 (girls typically less hyperactive, fewer conduct problems, less externalising behaviours)

  • girls w/ condition experience higher sx severity, greater functional impairment, and greater distress

ADHD - Genetic Factors

• Heritability of ADHD ~75%

• Among individuals w/ ADHD, heritability closer to 90%

• Polygenic risk: multiple genes associated (EX: genetic variants involved in dopamine regulation)

ADHD - Environmental Factors

• Early development: premature birth, low birth weight, perinatal stress

• Social factors: low SES, high family dysfunction, social isolation, education difficulties

• Trauma: childhood trauma (abuse, neglect, household dysfunction) impacts brain development and stress response

ADHD - Neurobiological Factors

• Lower levels of neurotransmitters: dopamine and noradrenaline

• Dopamine (DA): dopamine impacts reward and motivation pathways (DA deficiency in ADHD increases impulsivity and reward seeking)

• Norepinephrine/noradrenaline (NE): norepinephrine (derivative of dopamine) affects arousal and cognitive control (NE deficiencies in ADHD decreases alertness and focus)

ADHD Hypothesis: Weak Dopamine & Norepinephrine (NE) Signals

• Reduced DA released in brain signaling = hypo-dopaminergic

  • Affects PFC (exec function), nucleus accumbens (reward), and motor control brain regions (striatum)

  • Hypodopaminergic state = difficulties in: impulsivity, reward-seeking, physical activity

• NE levels lower in ADHD

  • NE affects widespread brain regions to regulate arousal, attention, and stress

  • Deficiencies contribute to difficulties in alertness and focus

*DOPAMINE LEVELS IMPACT NA LEVELS; NA LEVELS DON’T IMPACT DOPAMINE; THIS IS WHY COMBINED TYPE MOST COMMON THEN INATTENTIVE TYPE SECOND MOST COMMON

The ADHD Brain

• PFC responsible for executive functioning → ADHD = executive dysfunction

• Strengths of ADHD brain

  • hyperfocus

  • creativity

  • high energy and drive

  • resilience and adaptability

  • sensory sensitivity

  • quick thinking and intuition

Assessment of ADHD

• Common validated instruments:

  • Conners’ Rating Scales

  • Child Behaviour Checklist (CBCL)

  • Vanderbilt ADHD Diagnostic Rating Scale (VADRS)

• Functional assessments (stroop task, trail making test)

VADRS

• 55 items, for 5-12 yr olds

• Rates sx by severity across inattention, hyperactivity and impulsivity, co-occurring conditions, and performance (academic and social)

• Parent and teacher report versions

• Clinical cut off requires score of at least 6/9 items for each subscale to be rated as “often” or “very often”