Update on Treating ADHD

52 Pages·2017·1.53 MB·English

by  Laura Hullfish

Update on Treating ADHD
ASCP Annual Meeting
Miami Beach, FL May 31, 2018
Anthony L. Rostain, M.D., M.A
Professor of Psychiatry and Pediatrics
University of Pennsylvania Perelman School of Medicine
Co-Director, Developmental Neuropsychiatry Program
The Children’s Hospital of Philadelphia
Medical Director, Adult ADHD Treatment & Research Program
PENN Behavioral Health
Disclosures
Book royalties (Routledge/Taylor Francis Group, St. Martin’s Press)
•
Scientific advisory board honoraria (Shire, Ironshore, Arbor)
•
Consultant honoraria for MLB, NFL, SUNY/Upstate (AHRQ grant)
•
CME presentations for WebMD, NACE, Global Medical Education,
•
American Psychiatric Association
Learning Objectives
To review
• Current understandings about the neurobiology of ADHD
• Mechanisms of action of commonly prescribed ADHD medications
• Practical tips for prescribing and monitoring medications
• New medication options currently under investigation
Neurobiology of ADHD
Symptoms
Predominantly Predominantly
ADHD Combined
inattentive hyperactive–impulsive
Executive Function Motivation
Basic
Working Behavioral Delay
Processes Reinforcement
memory inhibition aversion
PFC Basal ganglia Cerebellum
Neural
Mechanisms
Noradrenalin Dopamine Serotonin
Genes
DBH HTR1B DAT1 D4 D5 SER T SNAP-25
PFC = prefrontal cortex.
Tripp G, et al. Neuropharmacology. 2009;57(7-8):579-589.
n
Behavioral disinhibition, emotional ability
o
Full expression of Inattention persists and hyperactive–
and emergence of diagnosis in preschool it
ADHD, psychiatric ai impulsive symptoms wane
years t
i
comorbidity, school failure, n
i
peer rejection g
Prodrome: hyperactivity; and speech, n
and neurocognitive ik Substance abuse, low self-esteem
language and motor coordination o
dysfunction m and social disability
problems
S
In utero Childhood Adolescence Adulthood
Genetic Psychosocial influences, chaotic family environments, peer influences and mismatch with
predisposition school and/or work environments
Different genetic risk factors affect the course of ADHD at different stages of the lifespan
Fetal exposures
and
epigenetic changes
Frontal–subcortical–cerebellar dysfunction via structural and functional brain abnormalities and
downregulation of catecholamine systems that regulate attention, reward, executive control and
motor functions
Persistence of cortical thickness,
Clinical Progression Etiology Pathophysiology
default-mode network and white matter
tract abnormalities
Faraone SV, et al. Nat Rev Dis Primers. 2015;1:15020.
Schematic
representation
of functional
circuits involved
in the
pathophysiology
of ADHD
Purper-Ouakil D, et al. Pediatr Res. 2011;69(5 Pt 2):69R-76R.
Regulation of Attention and Emotion
Arnsten AF, et al. J Am Acad Child Adolesc Psychiatry. 2012;51(4):356-367.
Regulation of Attention and Emotion
Arnsten AF, et al. J Am Acad Child Adolesc Psychiatry. 2012;51(4):356-367.
The Prefrontal Cortex Requires a Proper Level
of Catecholamines for Optimal Function
Guided attention and responses
Focused, organized and flexible
(eg, Optimally treated ADHD)
NE a
2A
Moderate D
1
Unguided attention / responses Misguided attention / responses
Distracted, poor impulse control Mental inflexibility, stimulus bound
Too little NE a , b
(eg, Untreated ADHD) (eg, Excessive dose of stimulant)
1 1
a /D Excess D
2A 1 1
Drowsy Alert Stressed
Increasing Levels of Catecholamine Release
Arnsten AF. J Pediatr. 2009;154(5):I-S43.
Treatment Modalities for ADHD
Educational / Workplace
Interventions
Psychosocial
Medical
Interventions
Interventions
Dulcan M. J Am Acad Child Adolesc Psychiatry. 1997;36(10 Suppl):85S-121S.