Adult ADHD in Forensic Populations
Russell J. Wilson
Consultant Clinical Psychologist
Friday 28th February, 2003
Product of a sufferer of ADHD
Short chapters
Fun drawings
Breezy writing
style
So if you’ve got
ADHD yourself,
it’s worth a read
Why Is It A Problem for Us?
Incidence of ADHD in the Prison Population
Combined prevalence (all subtypes) in adults generally of 4-5%, BUT:
20 - 80 % (most undiagnosed), with some symptoms (imp. of FAS)
First line treatment: stimulants -- but huge potential for abuse in prison
Comorbidity with Psychiatric Disorders (Equal in child and adults)
Oppositional Defiant Disorder (60%) Personality Disorders (APD 12-27 %)
Conduct Disorder (20 - 50 %) Depression (9 - 32 %)
Learning Disabilities Bipolar Disorder (6 - 20 % + CD)
Tourette’s Disorder dopamine and serotonin Obsessive-Compulsive Disorder
Anxiety (30 - 50 %) Substance Abuse (27-46%)
Somatoform disorders (24 - 35 %) Impulse Control (Sex, Gambling)
Intermittent Explosive Disorder Asperger’s Syndrome
75 % of adults with ADHD have 1 or more comorbid psychiatric conditions
ADHD: An Evolving Concept -- 1950s - 1980
Historically -- “minimal brain dysfunction” -- until 1950’s
Concept rejected: no evidence of brain damage per se;
unitary concept of brain damage not plausible;
MBD: “vague, inconclusive, of little or no prescriptive value, without
much neurological evidence” but valuable as it placed emphasis on
neurological as opposed to parental and family factors. Moving on to:
Hyperactive child syndrome: placing emphasis on activity,
cross-situational and not just with parents or teachers, non-blaming,
behavioral syndrome rather than either/or organic/situational
Up to 1969: focus on brain “mechanisms”, not damage, homogeneous
set of symptoms = treatments: stimulants, psychotherapy
1970s: emphasis on “attention deficits” , impulsivity, poor frustration,
aggression, focus on psychophysiology
The 1980s -- Part 1:Diagnostic Criteria
(Overheads: DSM Criteria)
DSM-III: Change from Hyperkinetic Reaction of Childhood to ADD (+/- H)
Much more specific symptom lists, numerical cutoff scores, guidelines
for age of onset and duration of symptoms, exclusion of other disorders,
controversial creation of theoretical subtypes (no research available)
DSM-IIIR: Only diagnostic criteria for ADD+H were stipulated. ADD-H no
longer officially recognised as subtype of ADD but “undifferentiated” ADD
Notable in the construction of DSM-IIIR was its emphasis on the empirical
validation of its criteria through a field trial guiding the selection of items for
the symptom list and the cutoff score on that list
Early 1980s saw studies differentiating ADD+H from aggression and conduct
problems. Distinguish purely hyperactive/cognitive impaired children from
purely aggressive children without cognitive problems:
family psychopathology greater in those with aggression/conduct disorders
The 1980s -- Part 2: Sub-typing and
Rise and Fall of Attention Deficits as the Focus
Beginning in 1980s: subtyping +/- hyperactivity, +/- aggression
Later: reading/learning disabilities as basis of cognitive disorders
Pervasive Vs Situational: Degree of severity and related problems
+/- anxiety/depression: poor prognostic indicator for use of stimulants:
Use of antidepressants
1987: ADD becomes ADHD: DSM-IIIR: Single list, not three; single cut off
score, empirically-derived, specific age of onset, comorbidity with other
disorders recognised
ADHD now classified with ODD, CD as Disruptive Behaviour Disorders
No evidence found for “core” attentional deficits in perception, filtering,
processing of information, but realisation that instructional and
motivational factors play strong role in presence and degree of ADHD
symptoms
The Modern Era: DSM-IV
(Overhead: DSM-IV)
Minimal duration of symptoms: 6 months
Symptoms to a degree that is developmentally deviant
Symptoms must develop by age 7 (but!… may not be diagnosed)
Subtypes: Inattention, Hyperactivity-impulsivity, Combined
Items used to make the diagnosis based on factor analysis of scales
Cutoff points arrived at in a rigorous field trial and thus have
empirical basis for their selection and clustering into categories
Crucial importance of requirement for degree of impairment, in one
or more major domains of life activities for that age, for a diagnosis
Comorbid Disorders and Antisocial Behaviours
Psychiatric Disorders -- Disruptive Behaviour Disorders:
15-20 % of mothers, 20-30% of fathers of ADHD children have ADHD
themselves
17 - 30 % of siblings of ADHD children also have ADHD
Parents of ADHD children also have variety of other psychiatric
disorders: conduct problems/antisocial -- 25 %, alcoholism 20 %,
affective disorders 15 %,
46 % 1st degree relatives of children with ADHD and co-morbid
ODD/CD also had ODD, CD or APD, as compared to 10 % of ADHD
without co-morbid ODD/CD
Oppositional Defiant Disorder -- 20 - 67 % (average 35 %)
Conduct Disorder -- 20 - 56 %
Social Relations and Subtyping
Social Impairments:
Poor peer relationships, low social acceptance / status, increased
aggression to peers, misattribution of intentions of others
Less compliance to parental requests, poor sustained compliance,
and greater requests for assistance; receive more commands,
reprimands, and punishment
Etiology of ADHD
“A variety of genetic and neurological etiologies (e.g., pregnancy and birth
complications, acquired brain damage, toxins (e.g., maternal alcohol
ingestion), infections, and genetic defects) can give rise to the disorder
through some disturbance in a final common pathway in the nervous
system. That final common pathway appears to be the integrity of the
prefrontal cortical-striatal network. It now appears that heredity factors
play the largest role in the occurrence of ADHD symptoms in children. It
may be that what is inherited is a tendency toward a smaller and less
active prefrontal-striatal network…. Social factors alone cannot be
supported as causal of this disorder, but such factors may exacerbate
the condition, contribute to its persistence, and more likely, contribute to
the forms of comorbid disorders associated with ADHD. “
From: Barkley, 1998, pp. 176-177.
Pathophysiology of ADHD
Most likely a mix of causes but:
Genetic component -- 80 - 90% monozygotic, 30% dizygotic
dysfunction of cerebral catecholamines -- stimulants
dysfunction of dopaminergic -- defective info processing
dysfunction of norepinephrine system -- impulsivity/aggression
hypofunction of prefrontal, caudate nucleus areas, frontostriatal:
difficulties in planning, judgement, and time perception
(Overhead: Diagram of Barkley’s model, 1998)
Implications: Diffferential
No one drug/treatment for all -- mixed results diagnosis often
difficult -- False+
No one pattern of universal traits, or neuropsych results
May be more than one type of “ADHD” 2, 3, or 6?
Need for individualised assessment/treatment
(?schiz)
Guidelines for Diagnosis -- NADDA
American National Attention Disorder Association Guidelines:
Evaluate and treat the whole person
ADHD should be suspected but not presumed
ADHD may present across the lifespan
A comprehensive assessment is necessary for an accurate diagnosis
The evaluation and treatment of ADHD should be conducted by a
qualified professional
Response to medication should not be used as the basis to diagnose
ADHD
Diagnosis should be based primarily on the DSM-IV criteria
Diagnosis and treatment should involve others familiar with the
person undergoing the evaluation
Diagnosis and Treatment of ADHD
Firstly, make sure what person has IS ADHD
Provide psychoeducational material about ADHD,
particularly important to guide insight & self-management
Structure, support and coaching: organised, on task,
hopeful, minimise discouragement: manage
performance, manage mood
Psychotherapy
Medication -- often, not always, essential, especially for
lower functioning ADHDers, such as prisoners.
Social support and understanding are vital
Evaluating For ADHD
The evaluation for ADHD should be designed to answer four
fundamental questions:
Is there credible evidence that the patient experienced ADHD-type
symptoms in early childhood that, at least by the middle school
years, led to substantial and chronic impairment across settings?
Is there credible evidence that ADHD-type symptoms currently
cause the patient substantial and consistent impairment across
settings?
Are there explanations other than ADHD that better account for
the clinical picture?
For patients who meet criteria for ADHD, is there evidence for the
existence of comorbid conditions?
GENERAL GUIDANCE: Murphy & Gordon, 1998
(copy in Waikato Forensic Psychology Resource Area)
Before ADHD is Diagnosed, Ask About
Developmental History Work History
Learning Disabilities Frequent changes of job
Coordination Disorders Work Performance
Childhood Behaviour Family History
Defiant Behaviour Presence of ADHD in child, sibling, or
Self-centred or hostile parent
behaviour around peers Poor relationships with family
School Problems Psychiatric History
Inattention Depression, anxiety, OCD,
Hyperactivity substance abuse
Poor academic performance Treatment for psychiatric disorders
Discipline problems
Why ADHD is Often Missed In Females
In childhood, girls with ADHD typically present with attention problems
and over-talkativeness, rather than hyperactivity. Talking too much
does not disrupt the classroom as much as the larger-scale
misbehaviour of boys with ADHD, so the diagnosis is often missed
in these girls. Overtalkativeness was added to the DSM-III-R criteria
for ADHD in 1987, after it was recognised as a symptom of
overactivity.
Now in midlife, many women with undiagnosed ADHD have children
with ADHD. As they bring their children to treatment, these women
are recognising similar attention deficit symptoms from their own
childhoods and are getting the help they need. As adults, many
have low self-esteem, low energy, and weight problems. Amongst
adults with ADHD, these women may be the most underdiagnosed.
Decline in Number of DSM-III-R ADHD
Symptoms From Adolescence to Adulthood as
Reported by Parents
10
8
6
4 ADHD
2 Normal
0
Age Age
15y 21y
Data from Barkley, Fischer,
Fletcher, et al, (2002)
Psychometric Assessment in Evaluating ADHD
WAIS-III
CVLT-II (Barker-Collo, for NZ version) (Executive Function)
Woodcock Johnson Psychoeducational Battery - Revised
Continuous Performance Test of Attention
Wisconsin Card Sorting Test (Executive Function)
Wide Range Achievement Test-3
Rey Figure (Executive Function, some visuospatial function)
Brown ADD Scales and Forms (Behaviour Rating, plus …)
Wender Utah Rating Scale
MCMI-III (Personality)
Go-No Go Tasks (Executive Function) Careful Hx -- Informant
PICTS
Core Systems Dysfunctions in ADHD
Barkley’s (1997) unifying theory of ADHD hypothesised deficits in
four executive neuropsychological functions that include
impairments in:
behavioral inhibition
working memory
regulation of motivation
motor control
(Implicitly, an imbalance in approach/avoidance systems).
“I suspect that in 20 years we’ll look back and wonder how we
could have thought ADHD was primarily an “attention deficit” as
opposed to an impairment in response inhibition and self-
regulation.” (Comment in book review on Amazon.com)
Variety of Possible Outcomes of ADHD
Triad of Possible Outcomes
Drug addict or alcoholic, legal entanglements
Problems: marital discord, divorce, spouse abuse, psychological
scars, depression, socially isolated
“lack of core identity”
Floundering
Entrepreneur (coping, using organisers)
“brilliant” -- “a real crackup”
“creative” -- “real idea person” -- “achiever”
highly adaptive defence mechanisms -- humour, obsessive style
Characteristic Problems of Adults with ADHD
(see Handout from Barkley, 1998).
Significant negative outcomes across a broad range of domains and
situations is the hallmark of ADHD. For adults these domains include:
School/work performance
Interpersonal skills
Emotional problems
Antisocial behaviour
Adaptive behaviour problems
Parenting difficulties
Sometimes it is not until raising a child whose problems remind them of
their own youth that adults recognise they themselves suffer from
ADHD and need to be on medication like their children.
Treatment History of Hyperactive and Normal
Groups at Outcome
Substantially greater number of hyperactive individuals suffer a
broad range of poorer treatment outcomes.
(see overhead, Barkley, 1998).
Why is ADHD Associated with Addiction
As many as 50 % of adults with ADHD have substance abuse problems
(including alcohol, cocaine, marijuana, and nicotine) and as many as 30
% have antisocial personality disorder (with increased potential for drug-
seeking behaviours). Compared with the general population, persons
with ADHD have an earlier onset of substance abuse that is less
responsive to treatment and more likely to progress from alcohol to
other drugs.
The elevated risk of substance abuse in ADHD may be related to a subtle
lack of response to normal positive and negative reinforcements. Hunt
has outlined four neurobehavioral deficits that define ADHD. Besides
inattention, hyperarousal, and impulsiveness, he proposes that persons
with ADHD may have a reward system deficit. They may gravitate
toward substance abuse because drugs, alcohol, and nicotine provide
stronger rewards than life’s more subtle social interactions. Concurrent
treatment of ADHD and substance craving symptoms using Relapse
Prevention techniques has been recommended by Aviram.
Incidence of School Problems in Young Adults
With ADHD (Milwaukee Outcome Study)
75
60
45
ADHD
30 Normal
15
0
Held Back Suspended Expelled
Rates of High School and College
Entry/Completion for Individuals with ADHD
High school drop out rate:
32 % to 38 % (versus 5 % for the US national average)
College entry rate: 22 %
College graduation rate: 5 %
Employment Outcomes
Individuals with ADHD are 3 times more likely to be fired from a
job than those without ADHD
Those with ADHD change jobs at a rate of 2 to 3 times within a
10-year period
Compared with employees without ADHD, those with ADHD
receive lower work performance ratings
35 % of individuals with ADHD are self-employed by the time they
reach their early thirties
DATA: Manuzza, Klein, Bessler, et al, 1997
Driving Outcomes
40 % of drivers with ADHD have had at least 2 accidents by
young adulthood compared with only 6 % of drivers without
ADHD
The dollar damage amount for accidents involving drivers
with ADHD is almost 3 times that of other drivers
60 % of drivers with ADHD have had an accident with
injuries
drivers with ADHD are 3 times as likely as other drivers to
lose their licences
DATA: Barkley, Murphy, DuPaul, et al, 2002.
Sexual and Reproductive Outcomes
Milwaukee Outcome Study
Ration of the number of births for the ADHD group (N=158) vs.
the control group (N=76) was 42:1 by age 20 years
Less than half of those individuals with children had custody
Prevalence of sexually transmitted diseases was 4 times higher
among the ADHD group than the normal group
These poor sexual and reproductive outcomes for people with
ADHD were related to their having more sexual partners and
using contraception less often than other individuals.
Estimated Mortality Rates for Individuals with ADHD
Unknown for adults
5 times higher for children 12 or younger with ADHD than for
those without ADHD
DATA: Hinshaw, Peele, Danielson, 2002
TREATMENT OF ADHD -- General Guidelines
As there is no way to cure ADHD, the goal of treatment
is to improve the individual’s ability to cope with it
Multidisciplinary, with staff coordinating their efforts
Physician -- medication
Mental health professional / coach -- supportive
counselling for individual and family, teaches
compensatory strategies for home, school, work;
training in behaviour management
Educator -- helps remediate school-based problems:
different learning strategies than for “normal” children
Existing Treatments -- Drug Treatments
Drug Treatments
Stimulants
Stimulants -- Ritalin
Mixed Amphetamines
Antidepressants (Venlafaxine, and substance abuse)
Specific norepinephrine reuptake inhibitors
Antihypertensives
Amino acids
Cholinergic agents
Antinarcoleptics
Efficacy of Medications in Adults with ADHD
Drug or Class Number Total Type of Trials Response
of Trials N Double-blind Open-Label Rate
Stimulants
Methylphenidate >5 150-200 +
Mixed
Amphetamines 2 50-75 +
Pemoline 3-5 50-75 +/-
Specific norepinephrine
reuptake inhibitors
Atomoxetine 3-5 550-600 … +
Antidepressants
Buproprion 2 50-75 +
Desipramine 2 75-100 +
Nortriptyline 2 25-50 … +
Venlafaxine 3-5 25-50 … +
Efficacy of Medications in Adults with ADHD
Drug or Class Number Total Type of Trials Response
of Trials N Double-blind Open-Label Rate
Antihypertensives
Guanfacine 2 ‹ 25 … +/-
Propanolol 2 ‹ 25 … +/-
Amino Acids
L-tyrosine 2 ‹25 … +/-
Cholinergic agents
ABT-418 2 ‹25 … +/-
Antinarcoleptics
Modafinil 2 100-150 … +/-
Pharmacologic activities in preclinical models
PROVIGIL Methylphenidate Amphetamine
Wakefulness
Wakefulness
Mediated by dopamine 0
Locomotor activity 0/
Stereotypy 0/
Anxiety 0
Blood Pressure/
Heart Rate 0
NREM rebound 0
0 = no or minimal effect 0 / = minimal activity = moderate increase = marked
Existing Treatments -- Sites of Action Compared
Modafinil Methylphenidate Amphetamine
CA = caudate H = Hypothalamus
Data adapted from Lin, Hou, Jouvet, 1996, study in cat.
Modafinil acts selectively through the sleep/wake centres of the brain believed to regulate normal
wakefulness. It does not mediate wakefulness by a dopaminergic mechanism.
ADHD, Antidepressants, and Norepinephrine
Patients with prefrontal cortex deficits can have problems with
inattention and impulse control
Patients with ADHD have frontal lobe impairments, as
neuropsychological tests and imaging studies have shown
Norepinephrine neurones, with cell bodies in the locus coeruleus, have
projections that terminate in the prefrontal cortex, and similar projections
prefrontal to the l.c.
agents with norepinephrine activity, but without mood-altering properties
(e.g., clonidine) have been shown to improve ADHD symptoms
Hence, increasing prefrontal cortex activity (through use of drugs that
increase, norepinephrine action) may modulate some impulses that
ADHD patients cannot control, or have difficulty controlling, otherwise
There is no “high” with antidepressants, limiting their potential for abuse
Adults with ADHD who received desipramine, 200mg/d, in a double-blind trial
showed significantly less hyperactivity, impulsivity, and inattentiveness after 6
weeks of therapy than a control group that received a placebo.But: side effects
make it not a good first choice!
Source: Wilens, Biederman, Prince et al, 1996.
Improved ADHD Symptoms with Desipramine
30
25
20
ADHD-IV
15
RATINGS Placebo
10 Desipramine
5
0
Baseline
Week 2
Week 4
Week 6
PROBLEMS WITH “AVAILABLE”
ANTIDEPRESSANTS and Substance Abuse
DESIPRAMINE
side effects: sedation, dry mouth, constipation, lethal in overdose
BUPROPRION
increased risk of seizures (1:1000), don’t use with those with
eating disorders, or recent head trauma, or benzo withdrawal, lack
of robust effect with attention and concentration. BUT aids ending
nicotine use
VENLAFAXINE
not funded, not recommended by maker, SSRI/NRI -- NRI effects
only at moderate-high dosages where side effects greater --
reduced sexual function, increased blood pressure
(Upadhyaya et al, 2001)
ALWAYS PROVIDE PSYCHOTHERAPY AS WELL
Mean ADHD Rating Scale Scores in a Study of
Atomoxetine and Placebo in 21 Adults
30
20
ADHD
Ratings
10 Baseline
Endpoint
0
o
ine
eb
et
ac
x
Pl
mo
o
Data from Spencer, Biederman, Wilens, et al,
At
1998.
P = 0.001 for difference between baseline and
endpoint (3 weeks)
Managing Problems in Treatment
Things that can go wrong in treatment include:
(see overhead, Wilens, Spencer, & Biederman, 1998)
Worsened or unchanged ADHD
Emergence of side effects
Marked rebound phenomena
Emergence of dysphoria, anxiety, agitation, irritability
Emergence of psychosis
General Resources
For Clinicians, to begin with:
Seminar Handout and References
Reading -- Barkley’s Handbook and Workbook
Medscape Website:
http://www.medscape.com/pages/editorial/
resourcecenters/public/adhd/rc-adhd.ov
Lilly ADHD Website: http://www.strattera.com/
For Sufferers and Families
Support Groups (Rotorua)
Reading materials (lists available on sites like Amazon.com)
Websites
Central Importance of Therapist’s Conveying Hope and Genuineness
Other “interventions” for ADHD
Scheduling regular physical exercise
Maintaining a sense of humour
Eliminating negative self-statements and “shoulds”
Avoiding, reducing or eliminating alcohol or drug use
Enlisting a friend, relative or spouse to help finish tasks and
remember commitments, and to provide feedback
Short-term psychotherapy can help you identify how your ADHD
might be associated with a history of sub-par performance and
difficulties in personal relationships
Long-term psychotherapy can help address mood swings, stabilise
relationships, and alleviate guilt and discouragement
Enlist a coach -- ADD Association formal guidelines
Neurofeedback/biofeedback of brain wave information
ADHD: A Positive View
From: http://www.drcady.com
“Don’t be a victim (“organic brain disease”)
-- be a victor
A “capable hunter”, not a “meek farmer”
Capable of astounding discoveries
Imbued with boundless energy
In understanding, there is strength
In reconciling the ADHD syndrome with reality,
there is wisdom”
Capable of being more “in the moment” than most other people
Dwaine McCallon’s Prison Program Outcomes
Direct Outcomes:
Improvement in symptoms
Improved institutional behaviour
Improved job status: prison, post-parole (overhead)
Improved relationships, including reduced anger and reduced social
perceptive deficits
Indirect Outcomes:
Education of Corrections Officers
COs and their children get treatment they need for their ADHD
Subsequent improvement in the lives and careers of the COs
Pro’s and Con’s for Therapists of ADHD Clients
Problems:
-- drug abuse, disorganised lives, marital discord,
temper fits, legal entanglements, procrastination
Advantages:
-- wealthiest patients
-- most creative patients
-- best senses of humour, most outgoing
-- best teachers!
--many with lives of close to or AT “top performance”
New Treatments
“New” Drug Treatments
Buproprion, Venlafaxine, Atomoxetine Already briefly covered
New Non-drug Treatments
Cognitive Remediation Programme -- Stevenson, 2002
(i) retraining cognitive functions
(ii) teaching internal and external compensating
strategies
(iii) restructuring the physical environment to maximize
functioning
-- Eight (8) weekly therapist-led group sessions
-- Support people to act as coaches
-- Participants’ workbook with exercises
Stevenson’s Cognitive Remediation Programme
for ADHD
Designed to teach strategies in the following areas:
Motivation
Concentration
Listening
Impulsivity
Organization
Anger Management
Self-esteem
Support people were paired with each participant to act as coaches in
the belief that coaches should assist participants maintain focus on
their treatment programme by having a cueing or prompting role.
Effects of Cognitive Remediation Programme: 1
Pre/Post Scores:
120 ADHD and Controls
100
80
ADHD
60
Orgn
40
Self-Esteem
20
State Anger
0 Trait Anger
1
2
T1
T2
-T
-T
l-
l-
P
P
tro
tro
CR
CR
n
n
Co
Co
Effects of Cognitive Remediation Programme: 2
120
100
80 ADHD
Orgn
60
Self-Esteem
40 State Anger
Trait Anger
20
0
CRP - T1 CRP - T2 CRP - T3 CRP -T4 Pre/Post/2m/12m scores
Conclusions -- Acknowledging the Situation
It’s a REAL problem! We just haven’t been aware of it.
Most of us don’t know much about it
It IS the proper preserve of forensic mental health AND
NO one is going to help us. We don’t have the resources for dealing with
it so we need to market and sell a need for expanded resources.
We need better tools for dealing with differential diagnosis and
comorbidity issues.
We’re extremely limited in the range of medications we can use,
FORTUNATELY more and better PSYCHOLOGICAL treatment packages
are available now than before.
WE NEED TO BUILD AND MAINTAIN OUR OWN HOPE AND
OPTIMISM AND SHARE THAT WITH OTHERS
We need to educate the lawyers and the courts
We need to build supportive linkages with parents, caregivers, whanau.
Where To From Here?
Research
Assessment
Treatment