Reading disorder (dyslexia)

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Disorders usually first diagnosed in infancy,
childhood, and adolescence

• Mental retardation
• Borderline intellectual function
• Learning disorders
• Reading, math, writing
• Motor skills disorder
• Communication disorders
• Elimination disorders
• Pervasive developmental disorders
• Attention deficit and disruptive behavior
  disorders
• ADHD
• ODD
• CD
• Tic disorder / Tourettes disorder
• Feeding and eating disorders
• Child abuse and neglect
• Temperament problems

• Anxiety disorders
• separation anxiety disorder
• selective mutism
• Specific phobia
• School phobia
• Social phobia
• OCD
• PTSD
• Eating disorders
• Schizophrenia
• Mood disorders
• Bipolar disorder
• Dysthymia
• major depression
• Substance abuse

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Disruptive behavior disorders

• Attention deficit hyperactive dsorder (ADHD)
• Oppositional-defiant disorder (ODD)
• Conduct disorder (CD)

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ADHD DSM-IV????

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• D. ??????????
• E. ??? ?????????

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ADHD DSM-IV ????

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• (?) Inattention(????)(6???)
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ADHD DSM-IV ????

• (?) Hyperactivity-impulsivity(6???)
• Hyperactivity (??)
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• ?????????? (??)
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• ??? Impulsivity (??)
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• 2. ??????
• 3. ?????

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Impulsivity

• Behavior that is swayed by emotional or
  involuntary impulses
• Behavior without adequate forethought
• Tendency ot choose immediate over long term
  rewards
• Engagement in behaviors that are likely to be
  punished.
• Persistent reward-seeking behaviors

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Type of ADHD

• Predominantly Inattentive Type (ADD)
• ???????
• Predominantly Hyperactive-Impulsive Type ?????
• Combined Type ??? (12)
• For individuals (especially adolescents and
  adults) who currently have symptoms that no
  longer meet full criteria, "In Partial Remission"
  should be specified. (adult ADD)

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ADHD????

• ????? (oppositional defiant disorder) 56
• ???????? (conduct disorder) 31
• ????? (learning disorder) 25
• ???? (communicative disorder) 20
• ??? (enuresis) 6
• ??? (anxiety disorder) 20
• ?????? (simple phobia) 9
• ????? (social phobia) 3
• ??? (major depressive disorder) 6
• ???????? (bipolar disorder) 6
• ???? (Tourettes disorder) 3

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Comorbidity of Psychiatric disorders in ADHD
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40/14
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ADHD vs. ADD

• Gender
• ADHD boys gt girls
• ADD girls gtboys
• Age of being detected ADHDltADD
• Clinical manifestation
• ADHD more behavior problem ODD or CD
• Self-regulation deficit selective attention
  problem
• ADD more academic problem LD
• selective attention problem
• more social withdrawn

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Self Regulation

• Sustained attention
• Inhibitory control over behavior
• Capacity to delay gratification
• Ability to suppress strong emotion

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Diagnosis of ADHD (I)

• Clinical interview (only way to establish
  Diagnosis)
• Hx from parents/caretakers
• Review school information
• School reports, LD?
• Rating scales (teacher)
• Explore parent teacher relationship
• Document signs symptoms
• Age of onset
• Duration
• Different settings
• Physical exam

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Diagnosis of ADHD (2)

• Meets DSM-IV or ICD-10 criteria
• Screen for comorbid disorders
• Psychological assessments
• IQ test, Attention test, Personality test
• For detect individual strength and weakness for
  counseling.

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Prevalence for ADHD in Children

• About 3 to 10
• Increasing prevalence from DSM-III (9.6)
• to DSM-III-R (10.9, 7.3)
• to DSM-IV (17.8, 11.4)
• More frequent in boys than in girls (3-41)

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Prevalence in adolescence adults

• No. and severity of symptoms declines with age.
• Prevalence in Adolescents 2-6
• No Gender difference
• The National Comorbidity Study (USA) suggest a
  prevalence of 4.7 or more in adults

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Prognosis of ADHD

• ADHD grown up
• 1/3 remission
• 1/3 adult ADD with residual symptom
• (inattentive, impulsive),
• 1/3 associated with conduct disorder
• (drug abuse, antisocial behavior, injuries
  of all sorts)
• poorer educational performance and were
  underachiever

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Age-Specific Prevalence of ADHD Remission
DSM-III-R ADHD
Biederman et al. 2001
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Adult ADHD Psychiatric Comorbidity
comorbid condition
Antisocial
Learning disabilities
Anxiety
Biederman, Am J Psychiatry, 1993 150(12)
1792-1798.
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Predictors of Persistence of ADHD
Risk Factors 1. Family History of
ADHD 2. Co-morbidity 3. Adversity
P lt 0.001
Beiderman et al, 1995 (N128)
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ADHD????????????????
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Etiologies of ADHDFrom Joel Nigg (2006), What
Causes ADHD?
Other
Perinatal
Smoking
Lead
FASD
LBW
Heritable (Genetics)
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Etiology of ADHD

• I. Genetic
• twin studies showing a mean heritability of 0.8
• polygenic disorder (catecholamine system)
• DRD4, DAT1, DRD5, DRD1,
• serotonin receptor (5HTR) 2A, 5HTR1B,
• synaptosomal associated protein of 25 kD
  (SNAP-25)
• Delay maturation of brain
• Minimal brain dysfunctions (MBD)
• Fetal exposure to Maternal abuse of alcohol,
  smoking, drug,
• Pregnancy complication or birth trauma
• Toxins (mercury, lead, manganese)

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ADHDMolecular Genetics

• Genes implicated by several studies
• DRD4, DRD5, 5HT1B
• No single gene causes ADHD
• The genes likely combine with each other and
  environmental risk factors to cause ADHD

Smalley, Am J Hum Genet. 200271(4)959-963.
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Etiology of ADHD

• II. Delay maturation of brain
• Minimal brain dysfunctions (MBD)
• Fetal exposure to Maternal abuse of alcohol,
  smoking, drug,
• Pregnancy complication or birth trauma
• Toxins (mercury, lead, manganese, PCB)

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Etiology of ADHD

• III. Gene Environment Interaction
• Chaotic family environments
• Poor parenting skills

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Pathophysiology of ADHD

• Dysfunction of the catecholamine system
• Wender P(1971) dysfunction in DA and NE
• Levy F (1991) dopamine deficit theory.
• Volkow et al (1998) methylphenidate blockade
  DA transporter. (PET)
• Pathophysiological findings
• No. of DAT binding sites is higher in drug-naive
  patients.
• Decrease in DOPA decarboxylase activity in the
  prefrontal cortex, primary deficits in
  subcortical dopamine systems.
• Complex dysregulation of DA neurotransmitter
  system

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• Both genetic and environmental risk factors have
  small, addictive and interactive effects on the
  probability a child will develop ADHD

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Brain imaging studies (Mid 1990s-)

• Anatomic abnormalities in specific brain regions
  where dopamine receptors are dense.
• reduced size of right frontal lobe and caudate
  nucleus
• A 10-year study by (NIMH)
• brains are 3-4 smaller than normal (
  pharmacologic treatment is not the cause)
• The more severe ADHD symptoms, the smaller
  frontal lobes, temporal gray matter, caudate
  nucleus, and cerebellum were.

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Grey Matter Difference Maps (A) and Statistical
Maps (B) in Children with ADHD and Controls
ADHD subjects show a 2030 increase in
grey-matter density in bilateral temporal
inferior parietal regions
Sowell et al., 2003
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Working Memory Related Changes In Adults with
ADHD Compensation?
HC gt ADHD
Control group demonstrates WM activation
associated with verbal rehearsal strategies
inhibitory control
ADHD gt HC
ADHD group demonstrates WM activation associated
with motor visual processing suggestive of
compensatory brain regions and strategies.
Schweitzer et al, Biological Psychiatry, 2004
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ADHD Delay in Cortex development
Shaw et al 2007 (NIMH)
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Children with ADHD Demonstrate Delayed Cortical
Maturation in Most Areas
An exception is in the primary motor cortex where
the ADHD group demonstrated earlier cortical
maturation
Shaw, P. et al. 2007, PNAS.
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• nigrostriatal dopamine pathway (from substantia
  nigra to caudate nucleus)
• mesolimbic dopamine pathway ( from ventral
  tegmentum to frontal cortex)
• The dopamine transporter density is more than an
  order of magnitude higher in the caudate nucleus
  than the prefrontal cortex , which is the reverse
  pattern of relative density of the D4 receptors,
  so the regulation of levels of synaptic dopamine
  by the reuptake process should differ
  dramatically in these two brain regions.
• the site of action of methylphenidate, which
  blocks the re-uptake process.

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ADHD????

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Treatments for ADHD

• Psychotropic medications (gt 4 years old)
• improve the core symptoms of ADHD in 70 of
  treated children
• Psychotherapy or psychosocial treatment
• Behavioral therapy or Cognitive-behavioral
  therapy
• Social skill / impulse control skill training
• Problem solving training
• Parental training
• Psychoeducation
• Other management, but no evidence of
  effectiveness
• Sensory intergration
• perceptual stimulation/training
• dietary management
• herbal and homeopathic treatments
• biofeedback
• meditation

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SNAP Inattention(Teacher)
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League Table of all Treatments in MTA Study
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psychotropic medications

• CNS stimulants (Short acting long acting)
• methylphenidate (MPH), Ritalin, Concerta
• D-amphetamine
• Pemoline (hepatic toxicity)
• Antidepressants
• TCA (severe CV side effects)
• SSRI (fluoxetine, sertrazline )
• Atomoxetine
• Clonidine (for severe aggressive cases,
  oversedation)
• Antipsychotics (oversedation)

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ADHD Pharmacotherapy Responsiveness
Methylphenidate
Amphetamine
Pemoline
Tricyclic antidepressants
Bupropion
MAOI
Clonidine/ Guanfacine
0
100
80
60
40
20
Responders
Wilens TE, Spencer TJ. Presented at Massachusetts
General Hospitals Child and Adolescent
Psychopharmacology Meeting, March 10-12, 2000,
Boston, MA.
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Mechanism of Action of Stimulants
Presynaptic Neurone
Amphetamine blocks
v
v
Storage vesicle
Cytoplasmic DA
Amphetamine blocks reuptake
DA Transporter
Methylphenidate blocks reuptake
Synapse
Wilens T, Spencer TJ. Handbook of Substance
Abuse Neurobehavioral Pharmacology. 1998501-513.
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Pervasive Developmental Disorders

• Autistic disorder
• Aspergers disorder
• ? ? ? ?
• The Story of Temple Grandin
• Rett disease
• PDD NOS

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Characteristics of Autistic disorder

• Diagnostic criteria (DSM-IV)
• Impaired social interaction (quality quantity)
• Impaired communication, usually severe
• Activities, behaviors and interest that are
• repetitive, Restricted and stereotype.
• Onset lt age 3 years
• diagnosis around age 2-3 years
• delayed or abnormal function development
• Male predominant

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Autistic disorder Associated features

• lt1gt 75 retarded level,
• lt2gt PIQgtVIQ
• lt3gt language expression below language
  comprehension
• lt4gt splinter ability hyperlexia, (able to read)
• good at puzzle, date,
• lt5gt odd response to stimuli
• oversensitive, exaggerated reaction,
  fascination to stimuli,
• hypo-sensitive
• lt6gt behavioral symptoms
• hyperactivity, inattention, aggression,
  temper tantrum
• stereotype behaviors, self-injury(head banging,
  biting),

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Autistic disorder

• Prevalence 2-5/10,000 , (severe autism)
• Male predominant
• Course life-long
• Prognosis
• depends on language skills (5y/o)
  overall intellectual level
• 1/3 partial independence
• highest functioning adult still had symptoms

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Aspergers disorder

• DSM-IV Diagnostic Criteria
• A. Qualitative impairment in social interaction,
• B. Restricted repetitive and stereotyped patterns
  of behavior, interests, and activities
• C. No delay in language
• D. No delay in cognitive development or in the
  development of age-appropriate self-help skills,
  adaptive behavior (other than in social
  interaction), and curiosity about the environment
  in childhood.
• F. Function impairment

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Comparison of Aspergers disorder with autistic
disorder (I)

• male gt female (both),
• prevalence 1-5/1000 (or higher)
• Age of diagnosis later, gt 5y/o
• Social and communication deficits are less
  severe.
• Normal curiosity about environment
• No delay in cognitive function, self-help skills,
  
• Language development normal
• lack of empathy
• problems with pragmatic responses difficulty
  with the emotional content of communication
• problem of integrating affective and social
  cognitive aspects of a situation.

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Comparison of Aspergers disorder with autistic
disorder (II)

• Difficulties with new environments and changes in
  their normal routine, but less severe than
  autism. (rigid stubborn)
• Special circumscribed interest are more
  prominent
• e.g. Train, Taiwan history, numerical,
• In autism Puzzle, date memorized, space,
  mechanical
• VIQ is usually gt PIQ (usually reverse in autism)
• Clumsiness is more frequently seen, but less
  severe.
• Outcome is usually more positive in aspergers.
• Go to college, get married, held a job, some
  social relation
• family history is more frequently positive

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PDDs (ASD) are lifelong disorders
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Etiology of Autistic disorder

• Non-psychogenic
• Generalized brain dysfunction
• Neurodevelopment disturbance (lt 30weeks
  pregnancy)
• seizure EEG abnormal (25)
• PKU, maternal rubella, fragile x syndrome (
  10 autism, mostly males), tuberous sclerosis
  (1/4 affected are autistic)
• hyperserotonin
• Imaging findings Reduced size of Corpus
  Callosum, Anterior Cingulate Gyrus , Cerebellum
• low activity in the parietal areas and the
  corpus callosum.

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Autism and Cerebral Hypoperfusion
fMRI Cerebellar Blood Flow and Activation
Allen et al., 2003 Am J Psychiatry 160(2)262-73
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Mirror Neuron ?????

• ?????? (anterior cingulate cortex)
• ????, ??????,????????
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• ??????(salience landscape theory)
• ??? (amygdala) ????????????,?????????
• ????????????

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Treatment (for autism Aspergers disorder)

• No specific treatment
• Behavioral therapy
• Speech, communication, cognitive social skill
  training
• Educational interventions
• Individual psychotherapy (for socially
  handicapped low esteem)
• Parent education and training

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Therapeutic Programs

• SI Sensory Integration/Occupational Therapy
• ABA Applied Behavior Analysis
• PRT Pivotal Response Training
• PECS Picture Exchange Communication System
• TEACCH Treatment and Education of Autistic and
  Communication Handicapped Children
• Floor time
• Social Stories
• Music therapy

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• (?) ?????Portage program

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Treatment (for autism Aspergers disorder)

• Medication can help with symptoms
• SSRI (stereotype, self-harm beh, depression,
  anxiety, withdraw),
• Antipsychotic (impulsive, psychotic)
• Depakene (mood stablizer, impulsive)
• Stimulants (for ADHD/ADD)

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The Ecology of Adolescent Behavior
Treatment Provider
Neighborhood
School
Peer Group
Extended
Parents
Child
Siblings
Family
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Tourettes disorder Multiple tics disorder

• Characteristic
• Multiple motor tics (Simple or complex)
• Vocal tics ( simple or complex, coprolalia)
• Wax Wine course
• Cephalic- caudal pattern, repetitive,
• Irresistible but able to be suppressed for some
  peiords.
• A history of motor tics before development of
  vocal tics.

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Characteristic of Tourettes disorder

• Prevalence0.05-5.2/10.000
• Malegtfemale 1.5-9 1
• Onset is almost always in childhood (age8-10
  years) or adolescence.
• Symptoms frequently worsen during adolescence,
• it is common to persist into adult life
• 50 remitted during adolescence

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Associated Features of Tourettes disorder

• Comborbid disorders
• ADHD
• Obsessive-compulsive disorder
• Depressed
• Pathophysiology
• Hypersensitivty of D2,
• Neuroimaging basal ganglia (volume reduction?)
• Autoimmune disease(? post streptoccocal
  infection)

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Treatment of Tics/TS

• A. Psychopharmacological management
• Antipsychotics
• First choice
• Atypical antipsychotics
• Clonidine
• For case of poor response to antipsychotics
• SSRI
• For case of combination with OCD
• Combing antipsychotics with CNS stimulant
• For comorbid ADHD if indicated.
• B. Psychoeducation Psychological support
• C. Parental/teacher psychoeducation

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Mental Retardation

• Diagnosis (Both IQ adaptive function)
• Mild ( FIQ lt 70, educable, grade 3 or 4),
• Moderate (FIQ lt 50/45 trainable),
• Severe (FIQ lt 35)
• Profound (FIQlt20)
• early intervention

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Mental retardation

• Special education training
• Strength weakness
• Practical, individualized
• Living skills, self help skills, Social
• Family attitude Guidance (Co-therapist)
• MR other psychiatric disorders
• Increase prevalence of psychiatric disorders
• Biological, psychological social factors
• Principle of Rx as other psychiatric disorder
  (drugsstart low, go slow)

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