The Comorbidity of ADHD with

Autism Spectrum Disorder:

Implications for Diagnosis and
Management
Russell A. Barkley, Ph.D.
Clinical Professor of Psychiatry
Virginia Commonwealth University School of Medicine
Richmond, Virginia USA

Email: drbarkley@russellbarkley.org
Website: russellbarkley.org
 Early History of ADHD1

1902 1917 1937

1770-75 1809 & 1812 1867 British physician In Spain, Dr. U.S. physician C.
German M. A. British J. Haslam and British G. F. Still Rodriguez-
1960s-Now2
American B. Rush physician H. describes multiple Lafora reports Bradley reports Research
Weikard describes first trials of
describe a few cases Maudsley clinical cases of an on children with increases
ADHD-like stimulants to
of impulsive and reports cases ADHD-like dramatically on
syndrome in first ADHD-like manage ADHD-
inattentive children of impulsive syndrome “defects symptoms “the every aspect of
medical textbook like symptoms
children in moral control” ADHD
unstables”

1798 1844 1885-95 1899 1908

Scottish physician German
1917-1950s
French Scottish English Various journal
A. Crichton psychiatrist physician physician physician A. articles appear on
describes two Heinrich Hoffman D. M. T. Clouston Tredgold hyperkinesis as a
attention disorders publishes stories
Bourneville does confirms Still’s secondary
in his medical of “Fidgety Phil” describes likewise reports; consequence of
textbook – and “Johnny Head hyperactive stresses its various brain
probably studied in the Air” - impulsive permanence disorders (e.g.
with Weikard
children encephalitis,
epilepsy, head Google Scholar
trauma) Search Hits by
Diagnosis As of
4/1/2017

R. A. Barkley (2015) History. In R. A. Barkley (Ed.), Attention Deficit Hyperactivity Disorder: A handbook for Diagnosis and Treatment (4th ed.). New York: Guilford
1

Publications. 2From Shaw, P. et al. (2007). ADHD is characterized by a delay in cortical maturation. Proceedings of the National Academy of Sciences, 104, 19649-19654.
 DSM-5 Criteria for ADHD (vs. ASD)
• Manifests 6+ of 9 symptoms of either inattention or 6 of 9
hyperactive-impulsive behavior (5 for adults)
– For ASD, persistent deficits in social communication and interaction, and 2
of 4 restricted, repetitive behavior pattern, interestsor actions
• Symptoms are developmentally inappropriate
• Have existed for at least 6 months (not in ASD)
• Occur across settings (2 or more) (Not in ASD)
• Result in impairment in major life activities
• Developed by age 12 years (ASD = early development)
• Are not best explained by another disorder, e.g. Anxiety,
Depression, Severe ID, ASD, Psychosis
• 3 ADHD “Presentations” - Inattentive, Hyperactive, or Combined.
For ASD: with or without ID or language impairment
 Understanding the ADHD - HI
Symptoms
The two dimensions of neuropsychological deficits are:
1. Hyperactivity-Impulsivity (HI; Executive Inhibition)
• Deficient motor inhibition (restless, hyperactive)
• Impaired verbal inhibition (excessing talking, interrupting)
• Impulsive cognition (difficulty suppressing task irrelevant thoughts,
rapid decision making;
• Impulsive motivation (prefer immediate gratification, greater
discounting of delayed consequences)
• Emotion dysregulation (impulsive affect; poor “top down” emotional
self-regulation)
• Restlessness decreases with age, becoming more internal, subjective
by adulthood
 Understanding the ADHD Inattention
Symptoms
Inattention: But 6 types of attention exist – not all
are impaired in ADHD. What is?
Executive Attention (& Functioning)
• Poor persistence toward goals, tasks, and the
future (can’t sustain attention/action over time)
• Distractible (impaired resistance to responding to
goal-irrelevant external and internal events)
• Deficient task re-engagement following
disruptions (skips across uncompleted tasks)
• Impaired working memory (forgetful in daily
activities, cannot remember what is to be done)
• Diminished self-monitoring
 What is the Underlying Nature of ADHD?
• Deficiencies in the brain’s executive functions – the
suite of mental mechanisms that permit self-
regulation and the cross-temporal organization of
behavior toward the future
• They are types of self-directed behavior that modify
automatic behavior so as to alter later consequences:
– Self-awareness
– Inhibition or self-restraint
– Working memory (nonverbal and verbal)
– Emotional self-regulation
– Self-motivation
– Planning and problem-solving
SCT vs ADHD
 Best SCT Symptoms
Becker, Burns, Schmitt, Epstein, & Tamm (2017), Assessment, Epub ahead of print
• 1. Behavior is slow (e.g., sluggish) (Factor loading = 0.92) ✔
• 2. Lost in a fog (0.89) ✔
• 3. Stares blankly into space (0.96) ✔
• 4. Drowsy or sleepy (yawns) during the day (0.95) ✔
• 5. Daydreams (0.88) ✔
• 6. Loses train of thought (0.86) ✖
• 7. Low level of activity (e.g., underactive) (0.97) ✔
• 8. Gets lost in own thoughts (0.81) ✔
• 9. Easily tired or fatigued (1.02) ✔
• 10. Forgets what was going to say (0.94) ✖
• 11. Easily confused (0.91) ✔
• 12. Lacks motivation to complete tasks (e.g., apathetic) (0.27) ✖
• 13. Spaces or zones out (0.82) ✔
• 14. Gets mixed up (0.85) ✖
• 15. Thinking is slow (0.87) ✔
• 16. Difficulty expressing thoughts (e.g., gets “tongue-tied”) (0.78) ✖
ADHD Varies by Setting; ASD Far Less So
Better Here: Worse Here:
• Fun Boring
• Immediate Delayed Consequences
• Frequent Infrequent Feedback
• High Low Salience
• Early Late in the Day
• Supervised Unsupervised
• One-to-one Group Situations
• Novelty Familiarity
• Fathers Mothers
• Strangers Parents
• Clinic Exam Room Waiting Room
 Prevalence (United States)
• 2-5% of children (using DSM-III or III-R)
• 5.5-8% of children (using DSM-IV or 5)
– Adding Inattentive Type nearly doubles prevalence over III-R
• 4-5% of adults (~12 million in US)
• Varies by sex, age, social class, & urban-rural
– 3:1 Males to females in children (5:1 in clinical samples)
– 1.5:1 males to females in adults
– More common in children; less so in adults
– Somewhat more common in middle to lower-middle classes
– More common in population dense areas
– For instance, 12-15% of U.S. military dependents (DSM-III-R)
– No evidence for ethnic differences to date that are independent of
social class and urban-rural
• For ASD, prevalence < 1%, sex ratio = 4:1
 Persistence to Adulthood
• 70-80% ADHD persistence into adolescence
• Young Adulthood ADHD (age 20-26)
– 3-8% Full disorder (self-report using DSM3R)
– 46% Full disorder (parent reports using DSM3R)
– 66% - Using 98th percentile of severity (parent report)
– 85-90% remain functionally impaired
• Adulthood ADHD (mean age 27)
– 14-35% recovered from disorder
– 44-55% still fully disordered (diagnosable)
– 15-30% highly symptomatic but not diagnosable
• ASD is far more persistent (95%+)
Impairments Associated with Child ADHD

Health Risks (sleep, migraines, obesity, dental, etc.)

Accidental Injuries, TBI, ER visits

Antisocial Behavior in 25-40%

Comorbid Psychiatric Disorders

(ODD, CD, ASD, Anxiety, etc.)

Peer Relationship Problems (50-70%)

LDs, Low Academic Achievement,

School Maladjustment

Greater Family Conflict/Stress

Developmental Delays
(motor, speech, adaptive skills, etc.)
 Life Course Impaired Parenting Behavior
Impairments Marital/Cohabiting Problems & Violence*
Linked to Poorer Health – Obesity, CHD Risk
ADHD Occupational & Financial Difficulties
Delayed Transition to Independence
Driving Risks (speeding, crashes, DUI)

Accidental Injuries, Suicide

Risky Sexual Behavior – Early pregnancy

More Smoking, Marijuana & Alcohol Use and SUDs

Antisocial Behavior/Legal Problems

Peer Relationship Problems

Greater Family Conflict/Stress

Limited Educational Success

 Comorbid Disorders with ADHD
• Autistic Spectrum Disorders (22%)
– 28-52% of ASD cases have ADHD
• Oppositional Defiant Disorder (40-84%; Mean = 65%)
• Conduct Disorder (15-56%; Mean = 45%)
– Predicts personality disorders by age 27 - 10-21%; antisocial & borderline mostly
• Anxiety Disorders (20-35%; odds = 3.0): increases with age
• Major Depression (25-35%; odds = 5.5)
– Suicidal ideation & attempts increase during high school; decrease by age 27
• Risk for substance use disorders (20-30%) by adolescence
• Bipolar Disorder (0-27%; likely 6-10% max.)
– A one-way comorbidity? (80-97% BPDs have ADHD but only 2-3% of ADHD
cases have BPD)
• Females have risk for bulimia – binge eating pathology
(16%) and somewhat elevated risk for anorexia
• Personality Disorders by adulthood (related to CD):
- Antisocial (11-21%) - Passive Aggressive (18%)
- Histrionic (12%) - Borderline (14%)
 Etiologies
• Disorder arises from multiple causes
• All currently recognized causes fall in the realm of
biology (neurology, genetics)
• But there are gene x environment interactions
• Causes may compound each other (genetics & TBI)
• Final common pathway for ADHD appears to be the
fronto-striatal-cerebellar circuits in the brain
• Solely social causes lack credibility
• But early severe social conditions (neglect, physical
abuse, malnutrition) may interact with genetics to
increase risk for disorder
 Etiologies of ADHD
Adapted from Joel Nigg (2006), What Causes ADHD? New York: Guilford Press.

Other
Perinatal
Complications
Smoking
ADHD risk genes
Lead & Other Toxins can interact with
Fetal Alcohol these other causes
Exposure to further increase
risk for the disorder
Prematurity & Heritable (Genetics) Some ADHD is due
Low Birth Weight
to new genetic
mutations occurring
in the child but not
the parent
The Ideal Treatment Package for ADHD
 Advances in Medications
• Stimulants: Methylphenidate and
Amphetamines
– New stimulant delivery systems
• Pills, pump, pellets, patch and pro-drug, liquids, oral
dissolving tablets, delayed activation system
– Better understanding of preschooler stimulant
response
• Atomoxetine and viloxazine– highly
selective NE reuptake inhibitors
• Guanfacine XR and clonidine ER- alpha-2
agonists (formerly anti-hypertensives)
 ADHD Psychosocial Treatments
• Parent education about ADHD changes families
• Learning the value and limitations of parent training
– Changes mainly defiance and parent-child conflict, less so ADHD
– Works best in younger children
• (<11 yrs., 65-75% respond; falls to 25-35% for teens)

• Effectiveness of classroom behavior management is

now solidly established but is time, setting, and person
limited
• Routine physical exercise (for coping not curing)
• Improving sleep (duration)
– some impact on next day inattention
• Effectiveness of cognitive behavioral training of EF
deficits in adults with ADHD
– Safren (Harvard Medical School), Ramsay & Rostain (Univ. of Pennsylvania), Solanto (Mt.
Sinai Medical Center, NYC)
 Experimental ADHD Psychosocial Treatments
• Friendship Coaching – training parents as social skills
therapists for their ADHD children – good evidence to date
• Challenging Horizons Program – good evidence to date
– after school supplemental training for teens focusing on social, recreational,
and academic remediation
• Time Management and Organization Training
– Equivalent to standard behavior management training
• Preschool play curriculum -- for kids at-risk for EF deficits
– Two separate curricula & studies: Adele Diamond & Jeffrey Halperin
• Mindfulness meditation training
– Mixed results, some promising, but most studies are not rigorously done
• Transcranial magnetic stimulation (noninvasive)
– Mixed effects in only a few studies to date (Rubio, B et al., Journal of Child Neurology,
Dec. 2015, Epub ahead of print.
• Omega 3 or 3/6 Fatty Acids (Fish Oil)
– studies show mixed results (effects aon parent ratings, not teacher ratings);
Cochrane 2012 meta-analysis finds no effects. Effects found are small in
magnitude, more for omega 3s, and mainly on inattention for a minority of
inattentive only cases (25%), if any effects are found at all
 Unproven/Disproven Therapies
• Elimination Diets – removal of sugar, additives, etc. (Some
evidence for food colorings – effect sizes of .23 or lower)
• Megavitamins, Anti-oxidants, Minerals (No compelling proof or
have been disproved)
• Sensory Integration Training (disproved)
• Chiropractic Skull Manipulation (no proof)
• Play Therapy, Psycho-therapy (disproved)
• Self-Control (Cognitive) Therapies for Children (disproved)
• Social Skills Therapies for Children (in clinic)
– Better for Inattentive (SCT) Type and Anxious Cases
• Neurofeedback (EEG)*
– Numerous positive clinical studies but all suffer serious flaws in their methods; 5
randomized placebo-controlled trials find no benefit
• Training of executive functions (espec. working memory)
– CogMed, Nintendo with Brain Age game, Lumosity.com,
mybraintrainer.com, e-mindfitness.com, happyneuron.com,
positscience.com
 Conclusions
• ADHD is a disorder of self-regulation and executive
functioning; ASD is a disorder of social communication and
interaction coupled with restricted/repetitive behavior patterns
• Though distinct they ca be comorbid in a substantial
percentage of cases of each
• A new attention disorder (SCT/CDD) has been identified that
is distinct from ADHD but overlaps with it and especially with
ASD
– Probably requires a distinct set of treatments than those for ADHD
• Several advances in medication delivery systems and in new
medication options occurred in the past decade
– The most remarkable advance may be in discovering a
neuroprotective effect of long-term medication use that facilitates
brain development and functioning
• Some advances have been made in modifying previous
psychosocial treatments and in developing new ones
• ADHD is among the most treatable psychiatric disorders