challenging behaviours workshop professor alasdair vance ...€¦ · challenging behaviours...

Challenging Behaviours Workshop

Professor Alasdair VanceConsultant Child and Adolescent PsychiatristDepartment of PaediatricsUniversity of MelbourneRoyal Children’s HospitalEmail: [email protected]

mailto:[email protected]

Definition of challenging behaviours

Outline:

1. -common paediatric behavioural problems-their detection and brief assessment

2. -diagnosis of disruptive behaviour disorders

3. -diagnosis of depressive disorders

Common paediatric behavioural problems

Key Principles:

1. Common: -5-10% prevalence in our community-anxiety symptoms/disorders and disruptive behaviour/disordersmost common; similar prevalence estimatesin other cultures-anxiety symptoms include generalised anxiety disorder, specific phobia,separation anxiety disorder, social anxiety disorder;obsessive compulsive disorder; panic disorder +/-agoraphobia rare in childhood; bed wetting after alternative other physical causes excluded; somatisation-primarily headaches, stomachaches,nausea, dizziness, limb pain/reduced movement


Key Principles:

1. Common: -rarely conversion symptoms occur, although these symptoms are more common in [1] childhoodrather than adulthood and [2] in hospital ratherthan community settings; PTSD rare, althoughtraumatic events unfortunately common-disruptive behaviour includes Attention DeficitHyperactivity Disorder (ADHD),oppositional defiant disorder, conduct disorder-depressive disorders: dysthymic disorder, majordepressive disorder

2. Externalising and internalising symptoms are commonly linked:-disinhibition, oppositional defiant behaviour,

motor restlessness can be markers of anxiety


Key Principles:

3. Multi-informant assessment:-parent perspective, child perspective, teacher perspective, clinician/other perspective-concordance between perspectives can be low-parental attitudes towards, understanding of a givenchild’s symptoms and behaviour are crucial to the priorities of the treatment plan at any given time

4. Family context:-family system’s flexibility and adaptiveness tochange within the life cycle


Key Principles:

5. Developmental context:-the social and cultural forces that shapethe nature and strength of the interpersonallinks between a given child and their family members and school peer group/teachers need to be considered in the longitudinal assessment

6. Developmental context:-age, gender, IQ


Key Principles:

7. Comorbid developmental vulnerabilities:-speech/language, fine/gross motorcoordination, specific learning difficulties

Oppositional defiant disorder

-a recurrent pattern of negativistic, defiant, and hostile behaviour

-onset usually before 7 years of age

-usually first emerges in the home setting

-always a precursor for Conduct disorder (approximately 3% ofchildren with ODD develop CD)

-prevalence (2%-16%) have been reported (Loeber et al. 2000)

-comorbid conditions: ADHD, combined type, language learning difficulties

Conduct disorder

-repetitive and persistent pattern of behaviour in whichthe basic rights of others and/or major age-appropriate normsor rules are violated, evidenced by three or more of the following criteria within the previous 12 months, with at leastone criterion present in the past 6 months:

Aggression/Cruelty towards people and/or animalsDestruction of propertyTheftSerious violations of social rules/norms

-behaviours are clinically impairing in the domains of social, academic or occupational functioning

->/= 18 years of age, criteria for antisocial personality disorder not met

ADHD

-six or more symptoms, at least six months duration, maladaptive/inconsistent with developmental level-inattention dimension and/or hyperactivity-impulsivity dimension

-evident in at least two settings-onset before seven years of age-impairment in social, academic, occupational functioning-symptoms not due to a PDD, Psychotic, Mood, or Anxiety Disorder

subtypes: combined type, inattentive type, hyperactive-impulsive type

Major depressive disorder

– one or more major depressive episode(s)characterized by the following: period of two weeks or more -depressed and/or irritable mood predominant and/or-loss of interest or pleasure-3 or 4 or more of the following; feelings of worthlessness or excessive or inappropriate guilt,>5% weight change in a given month, in/hyper somnia, psychomotoragitation/retardation, anergia (fatigue),decreased concentration or ability to think or decisiveness, recurrentthoughts of death, suicidal ideation, suicide plan or suicide attemptsymptoms cause impairment in interpersonal, social, academic,occupational functioningnot due to a substance, medical condition or bereavement

Dysthymic disorder

is characterized by the following: 1 year or more (most of the day, for more days than not), <2 months absence in a given year

-depressed and/or irritable mood predominant-2 or more of the following: feelings of hopelessness, low self-esteemappetite change, in/hyper somnia, anergia (fatigue), decreased concentration or decisivenessno major depressive episode evident in first year of the symptomssymptoms cause impairment in interpersonal, social, academic,occupational functioningnot due to a substance, medical condition or bereavement

Summary

-Careful and systematic assessment

-Multi-informant reports used

-Age, gender, IQ effects considered

-Comorbid conditions considered

-Longitudinal assessment performed

Medication treatment

Outline:

-key principles of medication use

-key types of medication in clinical use


Key Principles:

1. Medication:-‘do no harm; least number and the lowest dosepossible’

-clear goals that include the following: 1. arousal regulation2. mood regulation3. executive functioning-planning, organising

prioritising abilities4. motor acitivity, for example, restlessness-diagnosis driven medication use is debatable-systematic clinical research is imperative


Key Principles:

2. Synergism between medication and psychological interventions:-particular goals for both medication and psychological treatments that are interdependentand additive

3. Developmental Context:- the prioritisation of particular interventionsgiven a child’s developmental stage

4. Monitoring of psychological and medication interventions:

5. Coordination of other specialised treatment programmes:- speech therapy- occupational therapy- psychology/educational psychology


Key Principles:

6. Referral to specialist mental health services should be considered if any of the factors below fail to be achieved:

- Engagement- Negotiate a management plan- Gain multi-informant information- Assess and monitor treatment goals- Goals of treatment not being met- Enmity between key informants prevents any of the above

A model for intervention

-assessment and treatment focuses on delineation of risk factors andresilience factors-biologically (eg, executive function deficits; good arousal regulation) psychologically (eg, externalise blame; balanced critical self-reflection) and socially (eg, hostile critical interpersonal environment; confiding, nurturing consistent interpersonal environment)

-monitoring of these risk and resilience factors and their response totreatment through developmental phases

A model for intervention-a practical approach

[A] psychological and social treatment approach implementedfor 4-6 weeks (may take 6 months of new habit formation beforesustained behavioural change)

key elements are the interpersonal and the intra-individual milieuinterpersonal: positive reinforcement, response cost, token economy, contingency planning (turn taking, active listening, active ignoring, empathy skills, etc), making and keeping friendsintra-individual: controlled breathing, muscle biofeedback,guided visual imagery


- a practical approach

[B] key other vulnerabilities addressed – vision, hearing, specific verbal and/or visuospatial learning difficulties, developmental coordination difficulties, speech and language difficulties


a practical approach

[C] medication use to facilitate availability of the young person to learn from the psychological and social interventions through

better executive functioningbetter mood regulationbetter arousal regulation


Summary- medication can aid a child’s ability to invest ina psychosocial treatment program and learn from this program

- can take 6 months of practice before new habits are formed

- biological and psychosocial treatments maximize resilienceand minimize risk factors through shared effects on the brainand the mind

A useful clinical model for understanding these problems

Executive functioning

Response inhibition: motor and cognitionoptimise response speed and accuracy

Working memory: verbal and visuospatialoptimise span and strategy

A useful clinical model for understanding these problems

Mood dysregulation: decrease irritabilityincrease emotional salience

Arousal dysregulation: optimise physiological arousaloptimise habituation

Useful medication approaches

Response inhibition:

motor and cognition stimulant medication-linear dose response

speed and accuracy clonidine higher dose

Working memory:

span stimulant medication-inverted parabolic response

strategy stimulant medication-linear dose responseclonidine higher dose

Useful medication approaches

Mood dysregulation:

irritability stimulant medicationSSRITCAantipsychotic medication

emotional salience stimulant medicationSSRI?TCA?

Arousal regulation:

physiological arousal clonidinebenzodiazepinesTCAantipsychotic medication

habituation response clonidinebenzodiazepinesTCA?antipsychotic medication?


- stimulant medication is the first line treatment

short-acting forms: methylphenidate, dexamphetamine long-acting forms: OROS-methylphenidate, LA-methylphenidate

clear and substantial evidence for methylphenidate efficacy up toa dose of 60mg daily for treatments periods of approximately 12 months

methylphenidate and dexamphetamine similar efficacy and adverse effects profile although individual preferences manifest


- Stimulant medication benefits

decrease core symptoms of ADHDdecrease aggressionincrease quality of social interactionsincrease compliance

- Stimulant medication indications

ADHD diagnosis and psychosocial interventions insufficient


- Stimulant medication adverse effects

initial insomnia,appetite suppression

nervousness, restlessness, dysphoria,easy crying, agitation, depressive symptoms, stomach acheheadache, dizziness, rash, motor tics, mannerisms

in overdose: delirium, sweating, tremor, twitching, vomiting


- Stimulant medication adverse effects

growth retardation (MTA 3y f/u: 2cm /2.7kg )weight loss

epileptic seizures not adverse effects but careful psychotic episodes monitoring neededabuse potential in vulnerable patients


- Atomoxetine is the second line treatment

specific potent noradrenaline re-uptake inhibitor indicated when stimulant medication ineffective,associated with significant adverse effects

common adverse effects: nausea, drowsiness, initialinsomnia, appetite suppression


- Imipramine is a third line treatmenttricyclic compound similar to atomoxetine(a phenylpropanolamine derivative) but with lessspecific noradrenaline effect and significant cardiac adverse effects

- Clonidine is a third line treatmentcentral α-2 noradrenergric agonistsignificant effect; primarily hyperactivity/impulsivenesssignificant drowsiness, hypotensive and cardiac adverse effectsgradual withdrawal because of rebound hypertension and tics


- Neuroleptic medication is a third line treatmentatypical neuroleptic medication: eg risperidone / aripiprazolelow doses (up to risperidone 1.5mg daily equivalent)severe aggression, affective lability, PDD, ID

typical neuroleptic medication: eg pericyazine - thioridazineequivalent (now withdrawn)

third line treatments only used with careful monitoring and involvement in a treatment-resistant unit

Executive functioningConclusion

- start low, go slow, finish slow, although ensure optimal dosesare used

- medication facilitates each child’s ability to learn in the classroom, playground and home environment: new habitscan take 6 months to evolve

- Comprehensively assess and treat with approved medicationand/or psychosocial treatments all comorbid conditions

Mood regulation

- SSRI fluoxetine first line treatment

clear and substantial efficacy in the short and longer-terms4-6 weeks for clinical effect; can be earlier

primary adverse effects: nausea, drowsiness, initial insomniairritability, increased inner tension, suicidal ideation (rare)\

monitor first 5-7 days daily, then weekly

1-2 terms (3-6 months) duration of use before trial of weaning

We need an adequate evidence base for medication treatment,psychosocial treatment and their combination….

In the context of

careful

systematic

comprehensive

training…

TRANSLATIONAL CLINICAL SCIENTISTS

From laboratory bench, social/cultural factors toclinical practice

Tools for Translation: 2008

Genes Cells Systems Individual SocialWGASSequencingTransgenicsEpigeneticsDatabases

Stem CellsTranscriptprofilesProteomicsOpticalimagingDatabases

Electrode ArraysZebrafishPETfMRIDTIDatabases

SensorsEye gazeCognitivetools

Web 2.0Knowledgemanagement

Repositories – Data Sharing - Integration

Future research directions

Outline:

-individual tests of treatment responsivenesssymptoms, cognition, neurophysiological measures

-individual pharmacogenomics

ADHD: developmental stages

Common possible developmental pathways: all associated witheducational, social, occupational under-achievement, alcohol/substance abuse/dependence disorders, altered adult personality

childhood adolescence adulthood

ADHD-CT ADHD-IA ADHD-IA

ADHD-CT Depressive d Depressive d

ADHD-CT Conduct d ASPD

r2= .52

-1-0.5

00.5

11.5

22.5

-4 -2 0 2 4 6Cognitive z-composite score

Beh

avio

ural

z-c

ompo

site

scor

e

r2 = .73

-2

0

2

4

6

-4 -2 0 2 4 6Cognitive z-composite score

Beh

avio

ural

z-c

ompo

site

scor

e

Composite z-scoresADHD children in thelow dose and high dose Condition (dex. 2.5mg/7.5mg) (Mollica et al.,Human Psychopharmacology 2004)

Spatial working memory task - CANTAB

0

5

10

15

20

25

30

35

40

BSE2 BSE3 BSE4 BSE6 BSE8

Level of Difficulty

Bet

wee

n Se

arch

Err

ors

(mea

n)

ADHD-CT(um)ADHD-CT(m)Controls

Total cerebral growth curves

900

1000

1100

5 7 9 11 13 15 17 19 21Age (y)

mL

NV Males

ADHD Males

NV Females

ADHD Females

Castellanos et al., JAMA 2002

Controls > ADHD

p<.003

Silk, Vance et al, B J Psych 2005 N=14, CBCL inattention subscale T score: 72.23 (10.72)

Region of activation BA C (mm) ZControl Group greater than ADHD-CT GroupParieto-Occipital

R Precuneus 19 24 -70 32 3.53R Cuneus 19 32 -90 28 2.82

Posterior ParietalR Inf. Parietal 40 36 -40 50 2.82

Frontal/SubcorticalR Caudate Nucleus, Body 18 -12 22 2.82

Vance et al, Mol Psych 2007 N=24, CBCL inattention subscale T score: 72.14 (9.43)

N=14, CBCL inattention subscale T score: 70.88 (9.75)

Cognitive deficits in ADHD are associated with thesekey candidate genes:

Healthy children:

DAT1 3’ VNTR 10-repeat alleleDAT1 intron 8 VNTR 3-repeat allele R spatial inattentionDAT1 3’ UTR VNTR 10-repeat allele (η2 = .07/.08/.08)

- this 10/3DAT1 haplotype – ADHD (OR 2.58)

challenging behaviours workshop professor alasdair vance ...€¦ · challenging behaviours...

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