Post on 04-Jun-2018
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Advances in the
Neurobiology of ADHD
Joseph Biederman, M.D.
Professor of Psychiatry,
Massachusetts General Hospitaland Harvard Medical School
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Disclosures 2009-2011
n Research Support:
q Eliminda, J&J, Shire, NIH, Philanthropy
n Honoraria:
q Fundacion Areces, Medice, Spanish ChildPsychiatry Association, Fundacion Cabral,
Monterey Mexico, MGH Academy
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0 5 10 15 20Prevalence of ADHD (%)
Puerto Rico
New York City
Pittsburgh
Iowa
TennesseeMinnesota
Oregon
Missouri
Virginia
North Carolina
N.Y., Mich., Wis.
IndiaChina
NetherlandsNew Zealand
JapanBrazil
UkraineGermany
Netherlands/BelgiumSwitzerland
IsraelUnited Kingdom
IrelandCanada
New ZealandSpain
0 5 10 15 20Prevalence of ADHD (%)
Worldwide Prevalence of ADHD in Children
Faraone SV et al. (2003), World Psychiatry 2(2):104-113
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ADHD: Etiology
ADHD is a heterogeneous behavioral disorder
with multiple possible etiologies
ADHD
Neuroanatomic
Neurochemical
CNSinsults
Genetic
origins
Environmentalfactors
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Inattention
Impulsivity/Hyperactivity
ADHD: Core Symptom Areas
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%
78%
Persistence of ADHD into Young Adult Years
Biederman et al. Psychological Medicine, 2006, 36, 167–179;
Biederman et al Psychiatric Research In Press 2010.
0
20
40
60
80
100
Syndromatic Remission Persistence
65%
SyndromaticRemission
8%Medicated
13%
FunctionalPersistence22%
SymptomaticPersistence
35% SyndromaticPersistence
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Faraone et al. Psychol Med. 2006;36:159-165.
Full Diagnosis
Residual Diagnosis
0
10
20
30
40
50
60
70
80
90
100
12 15 17 21 26
Age at Follow-up
P e r s i s t e n c e R a t e
Loss of full diagnostic status is not equivalent to remission.
Persistence of Full and Residual Diagnoses
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ADHD: Course of the Disorder
Inattention
Time
Hyperactivity
Impulsivity
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Kessler et al. Am J Psychiatry 2006; 163:716-723
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ADHD as a Brain Disorder:
Neuroimaging Findings
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Brain Imaging and ADHD
n Magnetic Resonance Imaging (MRI) Anomalies(N= >25 studies):
q Asymmetry of the Caudate Nucleus
q Corpus Callosum size and shape
q Smaller Right Frontal area
q Smaller Right Basal Ganglia
q Cerebellum (vermis)
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Regions of Interest With Large
Standardized Mean Difference Scores (N=2)
0 0.2 0.4 0.6 0.8 1 1.2 1.4 1.6
Prefrontal Cortex
Frontal Lobe
Total Deep FrontalWhite Matter
Left Deep Frontal
White Matter
Right Deep Frontal
White Matter
P <0.001
Standardized Mean Difference Score
P <0.001
P <0.001
P <0.001
P <0.001
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Developmental Trajectories of Brain
Volume Abnormalities in Youth
w/ADHD
n Design: MRI case control studyn N=152 youth w/ ADHD and 139 controls of
both gendersn Objective: assess volumetric changes
over time in medicated vs unmedicated youthw/ADHD and controls
Castellanos et al. JAMA. 2002 Oct;288(14):1740-8
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Brain Volumes and ADHD
M i l l i l i t e r s
Non-ADHD
Controls
Unmedicated Medicated
Unadjusted Total Cerebral Brain Volume for Unmedicated and
Medicated Children and Adolescents With ADHD and Controls
N=103
N=49
N=139
*p=0.001 by 2-way analysis of variance (group [medicated vs. unmedicated vs. control] by sex);
Castellanos FX et al. (2002), JAMA 288(14):1740-1748
1,000
1,020
1,040
1,060
1,080
1,100
1,120
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Developmental Trajectories of Brain
Volume Abnormalities in Youth
w/ADHD
n Conclusions:
q Genetic and or early environmental influences on
brain development in ADHD are fixed,
nonprogressive and unrelated to stimulanttreatment
Castellanos et al. JAMA. 2002 Oct;288(14):1740-8
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ADHD: Neurobiologic Basis
ALERTING
EXECUTIVE CONTROL
ORIENTING (SELECTIVE ATTENTION)
Posner and Raichle. Images of M ind.Scientific American Books; 1996.
Attention Networks
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Seidman et al, Biological Psychiatry. 2006; In Press
MRI findings in Adult with ADHD
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Volume Reductions in Adult ADHD
Biederman, Makris, Valera et al. Psychol Med. In Press.
Volumetric reductions
in light blue (frontal and
cerebellar regions)
Superior frontal
gyrus Anteriorcingulate
gyrus
Cerebellar cortex
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Smaller Dorsal and Rostral ACC in ADHD
Seidman et al, Biological Psychiatry. 2006; 60: 1071-1080
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Cortical Volume
Cortical Thickness
Vogt, 2005
Cerebral Cortex
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•Dorsolateral FrontalCortex (BA 8, 9)
•Supramarginal Gyrus
(BA 40)
•Superior Temporal Gyrus
(BA 22)
•Angular Gyrus
(BA 39)
•Middle Temporal Gyrus
(BA 21)
Makris et al. Cerebral Cortex June 2007; 17:1364-1375
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•Anterior CingulateGyrus (BA 24)
•Orbital Frontal Cortex
((BA 11, 12, 13, 14)•Orbital Frontal Cortex((BA 11, 12, 13, 14)
Makris et al. Cerebral Cortex June 2007; 17:1364-1375
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Reproduced from Makris N, et al. Cerebral Cortex. 2007; doi:10.1093/cercor/bhm156.
A DT-MRI Study of Connections in
ADHD
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Makris et al. Cerebral Cortex 2008 in press
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cccc
70 60 50 40 30 20 10 070
60
50
40
30
20
10
0
10
20
30
COGNITIVE TASK
EMOTIONALTASK
Counting Stroop(Bush et al. 1998)
Counting Stroop
(Bush et al. 1999)Emotional Counting
Stroop(Whalen et al.
1998)
Cognitive
Division
Affective
Division
Bush,
Luu &
Posner
(2000)
Trends in
Cognitive Sciences
4:215-222
Anterior Cingulate Cortex: Increases
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MGH-NMR Center & Harvard- MIT CITP Bush et al, Biological Psychiatry 1999
1 x 10-3
1 x 10-2y = +21 mm
Normal Controls
1 x 10-2
1 x 10-3
y = +21 mm
ADHD
Dorsal Anterior Cingulate Cortex (Cognitive
Division) Fails to Activate in ADHD
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Methylphenidate Activates Dorsal
Anterior Midcingulate Cortex
Bush et al. Arch Gen Psychiatry. 2008:65:102-114.
0
0.5
1
1.5
2
2.5
Baseline 6 Weeks
OROS MPH
Placebo
• fMRI at baseline and again at week 6• OROS MPH group showed higher daMCC activation at 6 weeks vs placebo
• N=21 adults with ADHD; dosing to 1.3 mg/kg/day OROS MPH or placebo
P = 0.02 vs PBO
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Cortical Thickness Differences
Functional ROI
DTI ROI
Volumetric ROI
Dorsal ACC (dACC)
“Cognition”
Perigenual ACC (pACC)
“Emotion”
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Makris et al. Dev Neurosci 2009;31:36-49
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ADHD
Imaging Studies Summary
• Neuroimaging studies confirm that brainabnormalities in fronto-subcortical networksare associated with ADHD
• But neuroimaging techniques are not valid
tools for ADHD diagnosis; imaging measuresare not sensitive or specific enough to be usedfor diagnostic purposes
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Directed Attention Fascination
Executive circuit
§ Inhibitory deficits
§ Executive dysfunction
Reward circuit
§ Reduce time to reward
§ Delay aversion
ADHD
Toward a Dual Pathway Model
Sonuga-Barke. Neurosci Biobehav Rev. 2003;27:593.
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Frontosubcortical Networks and
Catecholamines
n Dopaminergic and noradrenergic dysregulation
abnormalities in fronto subcortical pathways
n Medications that are effective in ADHD are eitherdopaminergic or noradrenergic
Zametkin. J Am Acad Child Adolesc Psychiatry. 1987;26(5):676-686.
Zametkin. J Am Acad Child Adolesc Psychiatry. 1987;26(5):676-686
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Brain Stem
MESENCEPHALON
PONS
MEDULLARaphe nuclei(serotonin)
Substantia nigrategmentum(dopamine)
Locus ceruleus(norepinephrine)
to cerebellum
to cord
to diencephalon and
cerebrum
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GeneticBasis
of ADHD
ADHD: Genetics
Twin Studies Family Studies
Adoption Studies Molecular Genetics
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Mean heritability of ADHD = .75Faraone et al. Biol Psychiatry . 2005;57:1313-23.
ADHD
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Matheny 1971
Willerman 1973
Goodman 1989
Gillis 1992
Edelbrock 1992
Stevenson 1992
Schmitz 1995
Thapar 1995
Gjone 1996
Silberg 1996
Sherman 1997
Levy 1997
Nadder 1998
Hudziak 2000
Willcutt 2000
Thapar 2000
Coolidge 2000
Kuntsi 2001
Martin 2002
Rietveld 2003
Laarson 2004
Heritability
Panic Disorder SchizophreniaHeight
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Dopamine Transporter(DAT)
DopamineReceptor
(DRD4)
Presynaptic Neuron
Methylphenidate
(MPH)
Dopamine
The Dopamine Story...
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Williams et al. Lancet 2010; 376 (9750): 1401-8.
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ADHD Genetics
n The literature is predominated by
candidate gene studies
n Genome-wide association studies
are emerging
n These studies will lead to greater
progress as they do not assume
we know more than we do about
the etiology of ADHD
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Maternal Smoking During Pregnancy:
Results in Children
0
5
10
15
20
25
H i s t o r y o f M
a t e r n a l
S m o k i n g
( % )
* P =0.04, controlling for
SES, parental ADHD, and
parental IQ
P =0.00222%
ADHD( N=140)
8%
Controls( N=120)
Milberger et al. Am J Psychiatry 1996;153:1138.
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ADHD
Diagnostic Considerations
Inattention
Impulsivity/Hyperactivity
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0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
M D D
B P D A g o r
a p h o b i a
S o c i a l p h o b i a
S i m p
l e p h o b i a
O C D O D D
C D T i c s / T o u r e t t e ' s
E n u r e s i s
N i c o t i n e d e p e n d e n c e
A l c o
h o l d e p e n d e n c e
C u m u l a t i v e M o r b i d i t y R i s k
Control ADHD
P .009 for all categories
Biederman et al. Psychological Medicine, 2006, 36, 167–179.
Cumulative Morbidity Risks for Psychiatric
Disorders in ADHD and Control Probands
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Biederman et al.
AJP. April 2010
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Kessler et at. Am J Psychiatry. 2006; 163:4
Patterns of Comorbidity in ADHD Adults
0 1 2 3 4 5 6 7 8
Social phobia
PTSD
Panic disorder
Obsessive-compulsive disorder
Major depressive disorder
intermittent explosive disorder
Dysthymia
Drug dependence
Bipolar disorder
Any substance use disorder
Any mood disorder
Any anxiety disorder
Alcohol dependence
Odds Ratio
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Cocaine and Methylphenidate (COC and
MPH )block the Dopamine Transporter
DA
DA
DA
DA DA
MAO A
DA
DA
signal
DA
DA
DA
DA DA
MAO A
DA
DA
signal
DA
DA
DA
DADA
DADA
DA
DA DA
DA
DA
DA
coc or MPH
Volkow, Swanson. Am J Psychiatry. 2003 Nov;160(11):1909-18
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0
0.01
0.02
0.03
0.04
0.05
0.06
0 20 40 60 80 100 120
U p t a k e i n s t r i a t u m ( % / c c )
Time (min)
0
0.01
0.02
0.03
0.04
0.05
0.06
0 20 40 60 80 100 120
U p t a k e i n s t r i a t u m ( % / c c )
Time (min)
0
0.0005
0.001
0.0015
0.002
0.0025
0.003
0.0035
0 20 40 60 80 100 120
U p t a k e i n s t r i a t u m ( n C i / c c )
Time (min)
iv cocaine iv MPH oral MPH
Rate of Drug Uptake Into the Brain
RapidRapid Slow
Volkow et al. Arch Gen Psych1995;52. J Neurosci 2001.
§ Cocaine (iv) and methylphenidate (iv) produce a
“high” but methylphenidate (oral) does not
§ The slow brain uptake of oral methylphenidate
permits effective treatment without a “high”
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SUD in ADHD Youth Growing Up:
Overall Rate of Substance Use Disorder
Biederman, Wilens, Mick et al., Pediatric 1999
0
5
10
15
20
25
30
35
Control(n=344)
Medicated(n=117)
Unmedicated(n = 45)
P e r c e n t o f G r o u p
p < 0.001
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0 10 3020
25
50
75
100
Age
*p<0.05 vs. Controls
%
Biederman et al. Am J Psychiatry. 2008 Mar 3
Stimulant Therapy and Subsequent Risk
for Substance Dependence Disorders
No Stimulant
Therapy*
Controls
Stimulant
Therapy**p<0.05 vs. Controls
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Biederman et al.
Pediatrics 2009
Jul;124(1):71-8.
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Protective Effect of Stimulants on Comorbidity
Biederman et al. Pediatrics in press 2009
c2(1) =19.7, p<0.001 c2
(1) =17.8, p<0.001
c2(1) =3.5, p=0.063
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Functional Impairments
Results of A Survey of 1000 Subjects with and
without ADHD
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Educational Impairment in High School
*
*
*
*
* p .001
Percentage of Those Who Attended High School
52%
27%
37%
13%
37%
10%
30%
8%
"C" average or lower
Had a tutor
Had special classes
Had to repeat a grade
ADHD (N=464)
Non-ADHD (N=487)
Biederman et al. J Clin Psychiatry. 2006 Apr; 67(4):524-40
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Relationship Problems as AdultsPercentage of Each Group
28%
10%
15%
5%
ADHD (N=500)
No ADHD (N=501)
**
*
Percent "Strongly Agree"
47%
40%
70%
70%
**
**
Ever divorced
Ever separated
Good relationship with parents
Fits in well with peers
* P 0.01, ** P 0.001Biederman et al. J Clin Psychiatry. 2006 Apr; 67(4):524-40
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Current Employment Status
*
*
*
*
* p .001
Percentage of Each Group
52%
72%
34%57%
48%
27%
14%5%
Currently employed
Employed full time
Not currently employed
Looking for work ADHD (N=500)Non-ADHD (N=501)
Biederman et al. J Clin Psychiatry. 2006 Apr; 67(4):524-40
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Average Household Income by
Education Level Attained
$23,859
$29,577
$46,471$38,733
$66,683$63,086
$52,404
$91,316
$0
$10,000
$20,000
$30,000
$40,000
$50,000$60,000
$70,000
$80,000
$90,000
$100,000
Less than High
School
High
School/Some
College
College/Some
Post-Grad
Post-graduate
Degree
Control ADHD
Education (Highest Degree Obtained)Biederman and Faraone. Medscape General Medicine 2006; 8:12.
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Traffic Accidents and Violations
0
10
20
30
40
50
60
70
P e r c e n t a g e
Drove
before
licensed
12 or more
traffic
citations
5 or more
speeding
citations
License
suspended
or revoked
ADHD (n = 105)
Control (n = 64)
3 or more
vehicular
crashes
P = 0.003
P = 0.001 P = 0.002P = 0.001
P = 0.007
Negative Driving Outcomes From Driving History Interviews
With Young Adults Aged 17-28
Barkley et al. J Int Neuropsychol Soc . 2002;8:655-672.
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Summary
n ADHD is a neurobehavioral disorder with a:
q Complex etiology
q Neurobiologic basis
q Strong genetic component
n ADHD
q Affects millions of people of both gendersq Persists through adolescence and adulthood in a high
percentage of cases
q Can have negative impact on multiple areas of functioning