Advances in the assessment and treatment of ADHD … Adult ADHD.pdf · 2014-04-10 · Advances in...

Advances in the assessment and treatment of ADHD in adults with ID

Dr Dimitrios Paschos MRCPSych Consultant Psychiatrist & Hon. Research Fellow •Islington Learning Disabilities Partnership •Adult ADHD Service, Camden & Islington NHS FT •Institute of Psychiatry, King’s College London

These slides are the intellectual property of Dr Paschos and must not be reproduced

Aims

• Increase confidence in recognising ADHD across the range of ID

• Increase confidence in prescribing & monitoring stimulant medication



http://endthelie.com/2011/08/24/drugs-prescribed-to-children-for-adhd-are-molecularly-identical-to-street-drugs-and-are-really-powerful-psychotropic-mind-altering-chemicals/attachment/7731/

• Does ADHD exist?


• Does ADHD co-exist with ID?


Still controversial?

From medical colleagues:

• ‘ADHD does not exist’ or ‘Everyone has ADHD’

• ‘No one had ADHD when I was growing up’

• ‘He doesn’t have ADHD – he was able to concentrate well during the consultation (7 mins)’


WHY DIAGNOSE ADHD?

• Common (3-4% of children & 1% of adults)

• Disabling (academic, occupational & social impairment)

• High risk of psychiatric co-morbidity

• Treatable

• USA: over 90% of adults with ADHD never diagnosed


DSM-IV Diagnostic Criteria

A: 1) 6 out of 9 inattention items

2) 6 out of 9 hyperactivity / impulsivity items

B: symptoms were present before age 7 years

C: impairment present in two or more settings (e.g. at school [or work] and at home)


DSM-IV Diagnostic Criteria

D: clear evidence of clinically significant impairment in social, academic, or occupational functioning

E: symptoms do not occur exclusively during the course of:

• Autism

• Schizophrenia or other Psychotic Disorder

• Symptoms not better accounted for by Mood, Anxiety or Personality Disorder


Inattention symptoms

Often.. 1. fails to give close attention to details or makes careless mistakes in schoolwork,

work, or other activities 2. has difficulty sustaining attention in tasks or play activities 3. does not seem to listen when spoken to directly 4. does not follow through on instructions and fails to finish schoolwork, chores, or

duties in the workplace (not due to oppositional behavior or failure to understand instructions)

5. has difficulty organizing tasks and activities 6. avoids, dislikes, or is reluctant to engage in tasks that require sustained mental

effort (such as schoolwork or homework) 7. loses things necessary for tasks or activities (e.g., toys, school assignments, pencils,

books, or tools) 8. easily distracted by extraneous stimuli 9. forgetful in daily activities


Hyperactivity symptoms

Often… 1. fidgets with hands or feet or squirms in seat 2. leaves seat in classroom or in other situations in which

remaining seated is expected 3. runs about or climbs excessively in situations in which it is

inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness)

4. has difficulty playing or engaging in leisure activities quietly 5. is “on the go” or acts as if “driven by a motor” 6. talks excessively


Impulsivity symptoms

Often…

1. blurts out answers before questions have been completed

2. has difficulty awaiting turn

3. interrupts or intrudes on others (e.g., butts into conversations or games)


DSM-5 changes

• 5 instead of 6 symptoms in adults

• Age of onset changed to 11 years old ( from 7)


Validity of diagnostic construct

• Reliability for operationally defined ADHD well established

• Validity questioned because of : - Symptom overlap with other common mental

disorders -Symptoms lie in a continuum in the general

population -No natural boundary between affected and

unaffected individuals


Validating criteria I

• Symptom clustering

-consistent research finding for both subtypes

• Distinguishing symptoms

-ADHD often precedes the development of conduct disorder- the reverse does not occur


Validating criteria I – COMT gene

• Catechol-O-Methy Transferance gene

(causing increased breakdown of dopamine)

• associated with antisocial behaviour in adolescents with ADHD (finding reported in 4 separate samples)


catechol-O-methyltransferase (COMT) polymorphism

(Eisenberg, 1999)

• n=164

• DSM IV criteria, Conners Teaching Rating Hyperactivity scale, Continuous Performance Test False Alarm scale

• impulsive-hyperactive type of ADHD associated with the high enzyme activity COMT val allele.


Validating criteria II

• Distinguishing ADHD from normal range of inattention, hyperactivity, impulsivity

-Severity in comparison to norms

-Non-fluctuating course

-Risk for co-occuring disorders

-Association with functional impairment


Cognitive models of ADHD

• Problems with state regulation (related to arousal and activation levels)

• Delay aversion

• Inhibitory deficits: poor executive functioning

• Mood / motivation dysregulation


Impairment in motivation functions (Barkley et al, 2008)

Item ADHD % Clinical % Community %

Can’t get things

done unless

there is an

imminent

deadline

89 82 6

Has trouble

motivating self

to start work

80 72 6

Has difficulty

doing work by its

priority

84 63 4


Cognitive models of ADHD II

• Multivariate family and twin analyses found 2 cognitive factors accounting for most ADHD:

-Reaction time and reaction time variability

-Omission and commission errors in continued performance tasks


Intra-individual variability of ADHD impairments

• Transient but frequent lapses of attention

• Moment to moment variability in performance

Most studies focused on differences in performance between individuals with ADHD and those without


Aetiology: genetic, environmental and neurobiological factors

• Association with wide range of measures

• Both environmental and genetic factors likely to play important role


Structural and functional neuroanatomy of ADHD

• reductions in volume in cerebrum and cerebellum

• activation of more diffuse areas than controls during the performance of cognitive tasks

• hypoactivation of the dorsal anterior cingulate cortex, the frontal cortex and the basal ganglia


Dorsal anterior midcingulate cortex

Critical role in attention, novelty detection, response inhibition and motivation

Most evidence of dysfunction in ADHD across all studies

Embedded in both reward processing and attention network


Role of dopamine

• Role in attention, cognition and reward / learning

• SSRIs did not show the same symptom relief


Role of dopamine II

• Blocking of DAT by MPH correlates with symptom improvement


Environmental risks

• Diet

• Toxins: Lead, Mercury

• Pregnancy and delivery complications

• Fetal alcohol exposure

• Psychosocial adversity


EPIDEMIOLOGY

Prevalence of ADHD in Adults

• 2.5 to 4.3% (Kessler et al, 2006)

• Male to female ratio 2:1 - 3:1

• Prescription data (UK): discontinuation rates in young adults far in excess of what would be expected by remission rates (McCarty et al, 2009)


EPIDEMIOLOGY

• Kooij et al (2005) validity of adult ADHD in a population based sample (n=1815) of adults18-75 yrs

• Prevalence in adults: 1% (cut-off 6 Sx; and 2.5% cut-off 4 Sx)


Intelligence and ADHD

• IQ tests not comprehensive assessment of higher executive functions (Delis et al, 2007)

• Sample of 49 high IQ (>120) children with ADHD showed pattern of cognitive, psychiatric and behavioural features typical of children with average IQ and ADHD

• High IQ young adults with ADHD & impairments in working memory


Differences in the development of cortical thickness of children with ADHD and below median IQ ADHD versus

matched controls

• De Zeewu et all, 2013 n=200

• no differences from controls in cerebral gray matter volume in ADHD with below-median IQ, but a delay of cortical development in a number of regions, including prefrontal areas


ADHD in adults with Mild / Borderline ID

Maltezos, 2008 • N= 48 LD-ADHD (IQ< 80) vs 221 ADHD non -LD

(IQ>=80) • LD group higher number of the current

inattentive symptoms' ratings and higher scores for all items during childhood

• Non-LD group: most symptoms improved from childhood to adulthood

• LD Group: five components accounted 73.98% of the variance for informants' ratings


Genetic Syndrome /

Behavioural Phenotype

ADHD or hyperactivity /

impulsivity traits

Ref

Fragile X syndrome Yes

Full FMR1 mutation increases

risk

Hatton et al, 2006; Hagerman et

al, 2009

Prader-Willi Syndrome Yes

Early onset

Comorbidity more common in

maternal uniparental disomy

Whittington & Holland, 2010;

Cassidy & Driscoll, 2009;

O'Brien & Bevan, 2011

Tuberous Sclerosis

Complex

mutation

Yes

Up to 50%

Possibly higher frequency in

mutation in TSC2

Holmes et al, 2007; O'Brien &

Bevan, 2011; Jones et al, 1999;

Northrup et al., 1999 & 2011

Williams syndrome Yes O'Brien & Bevan, 2011; Lo-

Castro et al, 2011

16p11.2 microdeletion Yes

highly penetrant cause of ID

may account for 1% of cases of

ASD

Weiss et al, 2008;

Ousley et al, 2007

22q11 deletion Yes

Also strong association with

schizophrenia

Baker & Skuse, 2005; Horowitz

et al, 2005; Harrison & Owen,

2003

Neurofibromatosis 1 Yes Lo-Castro et al, 2011

Klinefelter Syndrome Yes Lo-Castro et al, 2011


Psychopathology and cognition in children with 22q11.2 deletion (Niarchou et al, 2014)


Psychopathology and cognition in children with 22q11.2 deletion (Niarchou et al, 2014)


ADHD in boys with the fragile X permutation (Farzin et al, 2006)

• full mutation >200 CGG repeats in the FMR1 gene • premutation (55-200 CGG repeats) considered unaffected by FXS • Conners' Global Index-Parent Version, IQ scores similar in all groups

Group ADHD ASD

Probands 93% 79%

nonproband premutation 38% 8%

sibling controls 13% 0%


ASSESSMENT: Principles

• History of childhood ADHD is essential

• Collateral history always necessary

• Continuous rather than episodic features (developmental disorder)


ASSESSMENT

1. Structured full psychiatric interview with focus on – Family history – Personal, developmental, educational, occupational, and social

history – Current ADHD symptoms – Co morbid conditions / substance misuse

2. Neuropsychological evaluation


MSE during assessment for ADHD

• Restlessness and distractibility may not be seen

• Sensitivity of symptoms to stimulating or novel situations

• Patients can normalise behaviour for short periods of time


ASSESSMENT – rating scales

• Variety of validated questionnaires (Connors, Barkley) to assess current symptoms, monitor response to treatment

• Scales for retrospective childhood diagnosis, side effects

• Semi-structured interview schedules


Adult ADHD Self-Report Scale (ASRS-v1.1) Symptom Checklist (WHO, available free on the web)


Barkley Adult ADHD Rating Scale–IV (BAARS-IV)© Results Summary

Section Raw

score Symptom

count Percentile Significance

Inattention 31 8 99+ Markedly/severely

symptomatic Hyperactivity 14 4 96th Moderately

symptomatic Impulsivity 15 4 99+ Markedly/severely

symptomatic Total ADHD 60 16 99+ Markedly/severely

symptomatic

Total ADHD: 99+ centile


DIVA (Kooji, 2010 -available free on the web)


Children with ID and ADHD – use of rating scales

(Deb et al, 2008) • Aim to find cut-off scores for the Conners’ Parent Rating

Scales-Revised (CPRS-R) and the • Conners’ Teacher Rating Scale-Revised (CTRS-R) • CPRS-R total score of 42: sensitivity of 0.9 and specificity of

0.67 • CTRS-R total score of 40: sensitivity of 0.69 and specificity

of 0.67 • CPRS-R scores may distinguish between children with ID

with and without ADHD but not the CTRS-R scores • Need to develop an ADHD screening instrument specifically

for ID


Neuropsychology Assessment

1. General Intellectual Functioning

– WAIS

2. Attention

a. Selective

b. Divided

c. Switching

d. Sustained

3. Impulsivity

4. Executive Function


Neuropsychological characteristics of adults with comorbid ADHD and borderline/mild ID (Rose et al, 2009)

• ADHD and mild-borderline ID (N = 59), ADHD and normal intellectual functioning (N = 95)

• co morbid group had significantly lower scores

• Differences remained significant after co-varying for level of intellectual functioning

• ADHD and ID group vulnerable to ‘double deficit’


Neuropsychological characteristics of adults with comorbid ADHD and borderline/mild ID (Rose et al, 2009)


What is QbTest? Simultaneously measures attention, impulsivity and motor activity Performance compared to an age and gender matched normative control group Data Management System


How is the test performed?

…

… 6-12 years

12-60 years

… with a Continuous Performance Test

specifically designed for age groups

QbTest combines a motion capturing

camera…





Psychometric testing



CO-MORBIDITIES: Adults

• Anxiety disorders 50%

• Mood disorders, antisocial disorders, and alcohol/drug: substantial prevalence rates

ADHD and Epilepsy (children)

• Kaufmann et al, 2009 • 20% of children with epilepsy have ADHD vs 3% to 7% • Possible causes: common genetic propensity,

noradrenergic system dysregulation, subclinical epileptiform discharges, seizures, antiepileptic drug effects

• Children with ADHD: higher than normal rate of electroencephalography abnormalities (5.6-30.1% vs. 3.5%)

• MPT equally efficient in children with isolated ADHD and in children with ADHD and epilepsy (70%-77%)

• Caution: reports of seizure aggravation in MPT-treated children with uncontrolled epilepsy have raised concern.

ADHD and criminality

• N= 25,656

• Significant reduction of 32% in the criminality rate for men and 41% for women as compared with non-medication periods

Lichtenstein et al, 2012

ADHD, BAD, BPD: similarities and differences (Handbook for ADHD in adults, UKAAN 2013)

Borderline Bipolar

Similarities with

ADHD

Childhood or adolescent onset Chronic trait like course Impulsivity – anger Impaired social relationships Mood instability Pervasive across situations

Overactivity Pressured speech Impulsivity Depressive episodes Sleep problems Mood instability Short attention span

Differences from

ADHD

Identity disturbance Recurrent suicidal behaviour Chronic feelings of emptiness Frantic efforts to avoid

abandonment

Episodic course Elated mood Psychosis Often lacks insight

TREATMENT

• Psychosocial interventions

• Pharmacotherapy


PSYCHOSOCIAL INTERVENTIONS

• CBT

• Family /couple interventions

• ADHD coaching

• Self-help groups

• Anger management, skills development


Amphetamines promote release of dopamine

and noradrenaline

Methylphenidate inhibits reuptake of dopamine

Atomoxetine inhibits reuptake of

noradrenaline

ADHD medication


Drug treatment of ADHD

• Part of a holistic treatment programme

• Before starting and every 6 months: pulse, blood pressure, weight

• Bloods and ECG

• Review need to continue treatment annually


Stimulants Non-stimulants

Methylphenidate

Short acting: Medikinet,

Ritalin

Long Acting: Concerta XL,

Equasym XL, Medikinet XL

Atomoxetine

Strattera

Dexamphetamine

Dexedrine

Elvanse

Licensed medication for treatment of ADHD in children in the UK


Stimulants for adults with ADHD and ID

Jou et al, 2004

• Small open label study

• Aberrant Behaviour Checklist-Community Version (ABC-C)

• Clinical Global Impression scale

• Significant improvements in the hyperactivity and irritability subscales of the ABC-C

• Adverse events minimal


Methylphenidate in Children with ADHD With or Without LD

(Williamson et al, 2014)

• 6-week, double-blind,randomized, placebo-controlled, crossover studies evaluating individually determined doses of OROS methylphenidate versus placebo (n=135)

• In children with ADHD with or without comorbid LD, behaviour and performance improved during treatment


Case A- treatment

• Bloods, ECG, BP, Pulse normal

• No other psychiatric problems

• No substance misuse

• Started on Methylphenidate 5mg bd, titrated up to 10mg tds

• Highly significant improvements in all core ADHD deficits, academic performance and self management






Stimulants: Efficacy

Children response rates 25-73%

Reduced efficacy in adults

1) Lack of consistent diagnostic criteria

2) Inadequate dosage

3) Presence of comorbidity

4) Poorly developed outcome measures


Stimulants side effects

• Well tolerated in adults • Common side effects: insomnia, edginess, diminished

appetite, dysphoria, headache • Usually remit spontaneously over time • Effect on BP/HR usually minimal • US 1999 to 2003: 25 deaths, 26 serious adverse events such

as heart attack or stroke


ELVANSE® (lisdexamfetamine dimesylate)

• Inactive pro-drug

• Slow release, long lasting effect

• Less potential for abuse


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Non - stimulants

• Atomoxetine (Strattera)

• noradrenaline reuptake inhibitor (NRI) or adrenergic reuptake inhibitor (ARI)


Other pharmacological treatments

• MAOIs

• Alpha 2 agonists e.g. clonidine

• Beta blockers

• Venlafaxine

• Modafinil

• Zyban

Not many controlled trials in adults


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Advances in the assessment and treatment of ADHD … Adult ADHD.pdf · 2014-04-10 · Advances in...

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