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兒童青少年精神疾病

兒童青少年精神疾病. 台北榮民總醫院 精神部兒童青少年精神科主任 陳映雪醫師. Mental retardation Borderline intellectual function Learning disorders Reading, math, writing Motor skills disorder Communication disorders Elimination disorders Pervasive developmental disorders

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兒童青少年精神疾病

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  1. 兒童青少年精神疾病 台北榮民總醫院 精神部兒童青少年精神科主任 陳映雪醫師

  2. 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 / Tourette’s 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 Disorders usually first diagnosed in infancy, childhood, and adolescence

  3. Disruptive behavior disorders Attention deficit hyperactive dsorder (ADHD) Oppositional-defiant disorder (ODD) Conduct disorder (CD)

  4. ADHD DSM-IV診斷標準 A.核心症狀 1.注意力差　　 學習問題 2.好動 3.衝動 ＊持續六個月以上 B.於七歲之前就有的症狀 C.至少在兩種情境呈現症狀 D.造成社會生活功能障礙 E.無法由 其它精神疾病來解釋 行為問題、人際衝突、易發生意外、青少年時期車禍多

  5. ADHD DSM-IV 診斷標準 • 具有下列(一)或(二)之一達六個月以上 與發展程度比較的不適應症狀 (一) Inattention（無法專心）(6項以上) • 常粗心大意或無法注意細節（功課或工作上） • 工作或遊戲注意力無法持久 • 別人跟他講話，經常不注意聽 • 無法遵守指示完成功課或工作 • 安排工作或活動常發生困難 • 常常逃避或拒絕需要持續精神（用功）的工作 • 遺忘帶需要的東西 • 容易被外界轉移注意力 • 日常生活中經常遺忘每天該作的事

  6. ADHD DSM-IV 診斷標準 (二) Hyperactivity-impulsivity：(6項以上) Hyperactivity (過動) • 手腳亂動, 坐著也扭來扭去 • 無法安靜坐著或常離座 (教室) • 常過度的跑來跑去，或爬上爬下 • 無法安靜遊戲 • 不停的動，精力過盛 • 話很多Impulsivity (衝動) 1.話未問完，就搶著回答 2.缺乏耐心等待 3.常干擾別人

  7. 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

  8. Type of ADHD • Predominantly Inattentive Type (ADD) 注意力不集中型 • Predominantly Hyperactive-Impulsive Type 過動衝動型 • Combined Type 結合型 (1+2) • For individuals (especially adolescents and adults) who currently have symptoms that no longer meet full criteria, "In Partial Remission" should be specified. (adult ADD)

  9. ADHD共病疾病 • 對立異常症 (oppositional defiant disorder) 56% • 反社會規範異常症 (conduct disorder) 31% • 學習障礙症 (learning disorder) 25% • 溝通障礙 (communicative disorder) 20% • 遺尿症 (enuresis) 6% • 焦慮症 (anxiety disorder) 20% • 單純性畏懼症 (simple phobia) 9% • 社會畏懼症 (social phobia) 3% • 重鬱症 (major depressive disorder) 6% • 雙相性情感性疾患 (bipolar disorder) 6% • 托倫氏症 (Tourette’s disorder) 3%

  10. Comorbidity of Psychiatric disorders in ADHD 4% 40%/14% 11% 34%

  11. ADHD vs. ADD • Gender : • ADHD: boys > girls • ADD: girls >boys • Age of being detected: ADHD<ADD • 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

  12. Self Regulation • Sustained attention • Inhibitory control over behavior • Capacity to delay gratification • Ability to suppress strong emotion

  13. 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

  14. 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.

  15. 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 boysthan in girls (3-4:1)

  16. Prevalence inadolescence & 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

  17. 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

  18. Age-Specific Prevalence of ADHD Remission : DSM-III-R ADHD Biederman et al. 2001

  19. Adult ADHD: Psychiatric Comorbidity % comorbid condition Antisocial Learning disabilities Anxiety Biederman, Am J Psychiatry, 1993; 150(12): 1792-1798.

  20. Predictors of Persistence of ADHD Risk Factors: 1. Family History of ADHD 2. Co-morbidity 3. Adversity P < 0.001 Beiderman et al, 1995 (N=128)

  21. 生物性因素 無 藥 物 治 療 父母管教方式 環境因素 對立異常症 注意力缺損過動症 行為障礙症 學習問題 人際互動問題 ADHD發展成對立異常症或行為障礙症因素

  22. Etiologies of ADHDFrom Joel Nigg (2006), What Causes ADHD? Other Perinatal Smoking Lead FASD LBW Heritable (Genetics)

  23. 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)

  24. ADHD:Molecular 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. 2002;71(4):959-963.

  25. 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)

  26. Etiology of ADHD • III. Gene – Environment Interaction • Chaotic family environments • Poor parenting skills

  27. 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

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

  29. 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.

  30. Grey Matter Difference Maps (A) and Statistical Maps (B) in Children with ADHD and Controls ADHD subjects show a 20–30% increase in grey-matter density in bilateral temporal & inferior parietal regions Sowell et al., 2003

  31. Working Memory Related Changes In Adults with ADHD – Compensation? HC > ADHD Control group demonstrates WM activation associated with verbal rehearsal strategies & inhibitory control ADHD > HC ADHD group demonstrates WM activation associated with motor & visual processing suggestive of compensatory brain regions and strategies. Schweitzer et al, Biological Psychiatry, 2004

  32. ADHD: Delay in Cortex development Shaw et al 2007 (NIMH)

  33. 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.

  34. 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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