跳转到内容

User:It's gonna be awesome/sandbox5

维基百科，自由的百科全书

Draft for ADHD topic

[编辑]
  • Merit points (pure ADHD without other associated illnesses)

Cause

[编辑]

The cause of most cases of ADHD is unknown; however, it is believed to involve interactions between genetic and environmental factors.[1][2] Certain cases are related to previous infection of or trauma to the brain.[1]

絕大多數注意力不足過動症（ADHD）的確切成因目前並沒有定論，最有可能是基因和環境交互作用導致。.[1][2] 有些個案的成因可能與腦部的疾病感染和腦部創傷有關。[1]

Genetics

[编辑]

Twin studies indicate that the disorder is often inherited from one's parents with genetics determining about 75% of cases.[3][4][5] Siblings of children with ADHD are three to four times more likely to develop the disorder than siblings of children without the disorder.[6] Genetic factors are also believed to be involved in determining whether ADHD persists into adulthood.[7]

       更進一步來說，雙胞胎研究顯示注意力不足過動症通常遺傳自患者的父母。大約75%的患者的病因是基因因素。or 雙胞胎研究顯示注意力不足過動症通常遺傳自患者的父母，這大約占所有病因的百分之七十五。[3][4][5]
       兒童青少年的手足（兄弟姊妹）比起非注意力不足過動症患者的手足多上三到四倍的機率帶有注意力不足過動症的特徵或也有注意力不足過動症。[8]基因可能也與注意力不足過動症是否從幼兒延續至成人有關聯。[7]

Typically, a number of genes are involved, many of which directly affect dopamine neurotransmission.[9][10] Those involved with dopamine include DAT, DRD4, DRD5, TAAR1, MAOA, COMT, and DBH.[10][11][12] Other genes associated with ADHD include SERT, HTR1B, SNAP25, GRIN2A, ADRA2A, TPH2, and BDNF.[9][10] A common variant of a gene called LPHN3 is estimated to be responsible for about 9% of cases and when this variant is present, people are particularly responsive to stimulant medication.[13] The 7 repeat variant of dopamine receptor D4 (DRD4–7R) causes increased inhibitory effects induced by dopamine and is associated with ADHD. The DRD4 receptor is a G protein-coupled receptor that inhibits adenylyl cyclase. The DRD4–7R mutation results in a wide range of behavioral phenotypes, including ADHD symptoms reflecting split attention.[14]

       在一般的情況下，注意力不足過動症大多與數個影響多巴胺（大腦內一種神經傳導物質）傳遞的基因有關[9][10]。這些基因分別是 多巴胺輸送元（再攝取）DAT, DRD4, DRD5（英语：DRD5）, TAAR1（英语：TAAR1）, MAOA（英语：MAOA）, catechol O-methyltransferase（COMT）, 和 Dopamine-beta-hydroxylase（DBH）.[10][11][12]

       其他基因分別是血清素輸送元SERT, HTR1B（英语：HTR1B）, SNAP25（英语：SNAP25）, GRIN2A（英语：GRIN2A）, ADRA2A（英语：ADRA2A）, TPH2（英语：TPH2）, 和 腦源性神經營養因子（BDNF）[9][10]。

       一個名為LPN3（英语：LPN3）的基因，其變異體大約存在於9%的注意力不足過動症患者身上。而這9%的患者可能對於中樞神經興奮劑特別有反應。[13]

       多巴胺輸送元{{tsl|en|DRD4|DRD4}5}的七個重複存在的變異體DRD4-7R與注意力不足過動症有關。因為它放大了由多巴胺觸發的抑制效果。DRD4的接收元是一個G蛋白偶聯受體（G Protein-Coupled Receptors），作用是抑制腺苷酸環化酶（adenylyl cyclase）。DRD4的突變反映在許多行為表現上，包括注意力不足過動症的症狀群，例如：分心。[14]

Evolution may have played a role in the high rates of ADHD, particularly hyperactive and impulsive traits in males.[15] Some have hypothesized that some women may be more attracted to males who are risk takers, increasing the frequency of genes that predispose to hyperactivity and impulsivity in the gene pool.[16] Others have claimed that these traits may be an adaptation that helped males face stressful or dangerous environment with, for example, increased impulsivity and exploratory behavior.[15][16] In certain situations, ADHD traits may have been beneficial to society as a whole even while being harmful to the individual.[15][16][17] The high rates and heterogeneity of ADHD may have increased reproductive fitness and benefited society by adding diversity to the gene pool despite being detrimental to the individual.[17] In certain environments, some ADHD traits may have offered personal advantages to individuals, such as quicker response to predators or superior hunting skills.[18]

演化可能在注意力不足過動症的盛行率中扮演一定的腳色，特別是有過動-衝動症狀的男性患者。[15]

People with Down syndrome are more likely to have ADHD.[19]

唐氏症患者可能有較高的機率出現注意力不足過動症。[20]


Environment

[编辑]
参见：Diet and attention deficit hyperactivity disorder

In addition to genetics, some environmental factors might play a role.[21] Alcohol intake during pregnancy can cause fetal alcohol spectrum disorders which can include ADHD or symptoms like it.[22] Children exposed to certain toxic substances, such as lead or polychlorinated biphenyls, may develop problems which resemble ADHD.[23][24] Exposure to the organophosphate insecticides chlorpyrifos and dialkyl phosphate is associated with an increased risk; however, the evidence is not conclusive.[25] Exposure to tobacco smoke during pregnancy can cause problems with central nervous system development and can increase the risk of ADHD.[23][26]

Extreme premature birth, very low birth weight, and extreme neglect, abuse, or social deprivation also increase the risk[23][27] as do certain infections during pregnancy, at birth, and in early childhood. These infections include, among others, various viruses (measles, varicella zoster encephalitis, rubella, enterovirus 71).[28] At least 30% of children with a traumatic brain injury later develop ADHD[29] and about 5% of cases are due to brain damage.[30]

Some studies suggest that in a minority of children, artificial food dyes or preservative may be associated with an increased prevalence of ADHD or ADHD-like symptoms[23][31] but the evidence is weak and may only apply to children with food sensitivities.[31][32][33] The United Kingdom and the European Union have put in place regulatory measures based on these concerns.[34] In a minority of children, intolerances or allergies to certain foods may worsen ADHD symptoms.[35]

Research does not support popular beliefs that ADHD is caused by eating too much refined sugar, watching too much television, parenting, poverty or family chaos; however, they might worsen ADHD symptoms in certain people.[36]

環境因素

[编辑]

       除了基因外，一些環境因子也可能是注意缺陷多动障碍的致病因素。[21]例如：在懷孕期間攝取酒精可能導致包含類似注意缺陷多动障碍症狀的胎兒酒精譜系障礙（fetal alcohol spectrum disorder）。暴露在特定有毒物質，例如：鉛或多氯聯苯、多氯聯二苯或二聯酚（polychlorinated biphenyls）等，可能會產生類似注意缺陷多动障碍的中毒症狀。[22]暴露在磷酸酯（organophosphate）的殺蟲劑、毒死蜱（chlorpyrifos）（一種晶體有機磷殺蟲劑） 、Alkyl phosphate（英语：Alkyl phosphate） 或 dialkyl phosphate（英语：dialkyl phosphate）中，將提高致病率，雖然此結論尚未在學界中被廣泛的認可。[25]在懷孕過程中接觸到二手菸，將不利於胚胎的腦部神經發育，並將增加罹患注意缺陷多动障碍的機率。[23][26]

       新生兒嚴重早產、新生兒體重嚴重過輕（英语：low birth weight）、被極端疏於照料的兒童、遭受凌虐、嚴重地缺乏與社會的互動（英语：social deprivaton），也可能增加往後出現注意缺陷多动障碍的機率。[23][27]

       母親在懷孕期間、兒童在出生時或成長初期遭受特定的感染都可能提高致病率。這些特定的感染包含但不限於：麻疹（measles）、 varicella zoster（英语：Varicella zoster virus）、 腦炎（encephalitis）、 風疹、德國麻疹或三日麻疹（rubella）, EV71（enterovirus 71）（腸病毒的一種）。[28]

       曾遭受 外傷性腦損傷（traumatic brain injury）（英语：外傷性腦損傷（traumatic brain injury））（英文）、外傷性腦損傷（traumatic brain injury）（日语：外傷性腦損傷（traumatic brain injury）） （日語）的兒童，其中至少30%將在往後的人生中發展出注意缺陷多动障碍[29]。因外力而導致腦部受損而致注意缺陷多动障碍大約占所有注意缺陷多动障碍所有個案的5%。[30]

       目前已有的證據無法支持減少食用特定食物來治療注意缺陷多动障碍的療法[32]減少食用有人工色素食品的兒童的相關研究，只有不到1/3的兒童在症狀上有改善[32]，這方面的助益有可能只是對有食物過敏的兒童有幫助，也有可能是這些兒童同時也在接受注意缺陷多动障碍的治療[32]

       截至2016年，研究並不支持「注意缺陷多动障碍是因為攝取過多的精緻糖、看太多電視、貧窮或混亂、動盪不安、吵吵鬧鬧的家庭所致」。然而前述的這些項目可能會惡化一些注意缺陷多动障碍患者的注意缺陷多动障碍症狀。[36] （詳見本條目之飲食治療一節）

Society

[编辑]

The diagnosis of ADHD can represent family dysfunction or a poor educational system rather than an individual problem.[37] Some cases may be explained by increasing academic expectations, with a diagnosis being a method for parents in some countries to get extra financial and educational support for their child.[30] The youngest children in a class have been found to be more likely to be diagnosed as having ADHD possibly due to their being developmentally behind their older classmates.[38][39] Behaviors typical of ADHD occur more commonly in children who have experienced violence and emotional abuse.[3]

The social construct theory of ADHD suggests that because the boundaries between "normal" and "abnormal" behavior are socially constructed, i.e. jointly created and validated by all members of society, and in particular by physicians, parents, and teachers, it then follows that subjective valuations and judgements determine which diagnostic criteria are used and, thus, the number of people affected.[40] This could lead to the situation where the DSM-IV arrives at levels of ADHD three to four times higher than those obtained with the ICD-10.[41] Thomas Szasz, a supporter of this theory, has argued that ADHD was "invented and not discovered."[42][43]

Pathophysiology 病理生理學

[编辑]

Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems, particularly those involving dopamine and norepinephrine.[44][45] The dopamine and norepinephrine pathways that originate in the ventral tegmental area and locus coeruleus project to diverse regions of the brain and govern a variety of cognitive processes.[44][46] The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behavior), motivation, reward perception, and motor function;[44][45][46] these pathways are known to play a central role in the pathophysiology of ADHD.[44][46][47][48] Larger models of ADHD with additional pathways have been proposed.[45][47][48]

       截至目前為止，ADHD被認為是肇因於部分腦內的神經傳導物質系統的損傷（特別是與多巴胺和正腎上腺素有關的神經傳導系統），進而對患者的腦部執行功能產生不良的影響。[44][45]多巴胺與正腎上腺素的腦內通道大多起源自腦內的腹側被蓋區（ventral tegmental area） and 藍斑核（locus coeruleus），並由此投射至不同的腦區且管理許多認知的流程（與認知功能相關的處理流程）。[44][46] 特別是那些投射至前額葉（prefrontal cortex）和紋狀體（striatum）（英语：striatum）的腦內的多巴胺通道（dopaminergic pathway）們（群）和腦內的正腎上腺素通道/藍斑核系統（norepinephrine pathway）（英语：norepinephrine pathway）們（群），它們主要的工作就是負責調節執行功能（executive function） (cognitive control of behavior)、動機（motivation）、 酬賞、報償的感受能力（reward perception）、和運動神經的功能（motor function）。[44][45][46]以上是目前已知在ADHD的病理生理學（Pathophysiology）中扮演主要腳色的幾條腦內通道（pathway）。對於ADHD更全面的概觀以及更多可能與之相關的腦內通道也已經被提議。[45][47][48]

請參閱：Reward system、Incentive salience（英语：Incentive salience）、Reward dependence（英语：Reward dependence）、Brain stimulation reward（英语：Brain stimulation reward） 以了解關於大腦內回饋系統的運作機制。

Brain structure 大腦結構

[编辑]

In children with ADHD, there is a general reduction of volume in certain brain structures, with a proportionally greater decrease in the volume in the left-sided prefrontal cortex.[45][49] The posterior parietal cortex also shows thinning in ADHD individuals compared to controls.[45] Other brain structures in the prefrontal-striatal-cerebellar and prefrontal-striatal-thalamic circuits have also been found to differ between people with and without ADHD.[45][47][48]

在兒童注意力不足過動症患者中，普遍存有一些腦部結構（特別是左側的前額葉 prefrontal cortex、後頂葉皮質 posterior parietal cortex ）在體積上小於平均值的現象。[45][49]其他諸如ADHD患者的：前額 - 紋狀體小腦（prefrontal-striatal-cerebellar）和前額葉紋狀體丘腦迴路（prefrontal-striatal-thalamic circuits）也被發現與非ADHD的人不同。[45][47][48]

Neurotransmitter pathways 神經傳導物質的通道/路徑

[编辑]

Previously it was thought that the elevated number of dopamine transporters in people with ADHD was part of the pathophysiology but it appears that the elevated numbers are due to adaptation to exposure to stimulants.[50] Current models involve the mesocorticolimbic dopamine pathway and the locus coeruleus-noradrenergic system.[44][45][46] ADHD psychostimulants possess treatment efficacy because they increase neurotransmitter activity in these systems.[45][46][51] There may additionally be abnormalities in serotoninergic, glutamatergic, or cholinergic pathways.[51][52][53]

       從前一些人倒果為因的以為ADHD患者腦部中偏多的多巴胺轉運體（dopamine transporter）是ADHD的病因之一，然而後來經過研究證明，偏多的多巴胺轉運體（dopamine transporter）是因為患者服用中樞神經興奮劑治療的關係。[50]

       目前的研究模型包含了 中腦皮質素-多巴胺通道（mesocorticolimbic dopamine pathway）（英语：mesocorticolimbic projection） 及 蓝斑核-去甲腎上腺素系統（locus coeruleus-noradrenergic system）（英语：locus coeruleus-noradrenergic system）。[44][45][46]用於治療ADHD的中樞神經興奮劑，其療效可能是起因於它增進了神經傳導物質在這些系統中的活動。[45][46][51] ADHD患者腦部中的 5-羥色胺能serotoninergic（與血清素serotonin有關）（英语：serotoninergic） 通道（=路徑=pathway）、 谷氨酸能（glutamatergic）（一種神經傳導物質）（英语：glutamate (neurotransmitter)）通道、 或 膽鹼能（cholinergic） 通道可能也存有一些導致ADHD症狀的原因。[51][52][53]

請參見：血清素。

Executive function and motivation 執行功能和動機

[编辑]

The symptoms of ADHD arise from a deficiency in certain executive functions (e.g., attentional control, inhibitory control, and working memory).[54][45][46][55] Executive functions are a set of cognitive processes that are required to successfully select and monitor behaviors that facilitate the attainment of one's chosen goals.[54][46][55] The executive function impairments that occur in ADHD individuals result in problems with staying organized, time keeping, excessive procrastination, maintaining concentration, paying attention, ignoring distractions, regulating emotions, and remembering details.[54][45][46] People with ADHD appear to have unimpaired long-term memory, and deficits in long-term recall appear to be attributed to impairments in working memory.[54][56] The criteria for an executive function deficit are met in 30–50% of children and adolescents with ADHD.[57] One study found that 80% of individuals with ADHD were impaired in at least one executive function task, compared to 50% for individuals without ADHD.[58] Due to the rates of brain maturation and the increasing demands for executive control as a person gets older, ADHD impairments may not fully manifest themselves until adolescence or even early adulthood.[54]

       ADHD的症狀起因於某些執行功能上的缺陷，例如：注意力/專注力的控制（attentional control）、inhibitory control、及 工作記憶（working memory）。[54][45][46][55]執行功能簡單來說就是一整群認知處理過程的集合。而這集合必須能夠成功的幫助一個人選擇並督促自己做出得以實現他那經過深思熟慮過後的目標之行為。[54][46][55]ADHD患者先天的執行功能損傷造成以下這些症狀：難以維持有規劃的、有組織性的（problems with staying organized）、缺乏時間觀念（time keeping）、過度的拖延（excessive procrastination）、難以保持專注（maintaining concentration）、難以把注意力放對地方（ paying attention）、難以忽略與任務不相干的外務（ignoring distractions）、情緒管理的困難（regulating emotions）、難以把細節記起來（remembering details）。[54][45][46]ADHD患者在長期記憶的表現可看出ADHD患者的長期記憶是沒有損傷的。ADHD患者在提取長期記憶時所產生的困難顯然是肇因於工作記憶的受損[54][56]。

       端視一個ADHD患者其「腦部發展的程度」與其「所在環境對其執行功能要求的程度」的比例，因此有些ADHD患者可能直到青少年時期甚至是成年初期才開始顯露出ADHD的症狀。

ADHD has also been associated with motivational deficits in children.[59] Children with ADHD find it difficult to focus on long-term over short-term rewards, and exhibit impulsive behavior for short-term rewards.[59]

ADHD與「在兒童青少年時期缺乏動機」相關。兒童青少年ADHD患者會發現自己比起「眼前立即的回饋/酬賞」更難以專注在「長遠的目標/回報/回饋/酬賞/滿足」，並展現出對於「眼前立即的回饋/酬賞/滿足」的衝動。[59]

MedlinePlus 3/3

[编辑]

https://medlineplus.gov/ency/article/001551.htm

https://medlineplus.gov/news/fullstory_162041.html

Mainland China's diagnosis procedure for ADHD 2/26

[编辑]

Put Schema here.

Q&A

[编辑]

Revision to present version

[编辑]

Let's practice to learn to stick to the schedule! =)

2/3's night

[编辑]

而阿托莫西汀（atomoxetine）與哌甲酯（methylphenidate）併服的處方尚未經美國食品藥物管理局核可，但醫師會視個案的情況（如：共病、預後、......）以開仿單標示外使用（off-label use）的方式處方之。[61] New citation is on the right. [62]

2/6

[编辑]

There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives, or added to stimulant therapy.[63][64]

數種非中樞神經刺激劑，例如：阿托莫西汀（atomoxetine）、可樂定（clonidine）、安非他酮（bupropion）和guanfacine（英语：guanfacine），可與中樞神經刺激劑一起使用或作為中樞神經刺激劑的替代方案。[63][65][66]

2/9

[编辑]

可樂定（clonidine）與胍法新（英语：guanfacine）（guanfacine）皆為非中樞神經興奮劑，為alpha-2 腎上腺素受體（英语：alpha-2 adrenergic receptor）刺激劑/促進劑/活化劑 的一員，與哌甲酯（methylphenidate）併用或單獨服用都有顯著療效其中兩藥物併服：

詳閱：腎上腺素受體

2/12

[编辑]

規律的運動，特別是有氧運動，也證實為一個有效的「附加療法」（即表示可附加在現有具備科學實證且能在統計學上達到顯著意義之有效改善症狀的醫學療法）。Please update the three citations. =) [67][68][69]

2/15

[编辑]

規律的運動，特別是有氧運動，也證實為一個有效的「附加療法（英语：add-on treatment）」即表示可附加在現有具備科學實證且能在統計學上達到顯著意義之有效改善症狀的醫學療法）。

2/18

[编辑]
  • 問題 Question:
「我的孩子就已經常常興奮過頭了，還讓他吃興奮劑？」
答覆 Answer：
雖然這些藥物被歸納為「興奮劑」類，但是它們確實有幫助患者們保持平靜的效果。[70]

2/21

[编辑]

Please reformat this citation. =) [71]

2/23

[编辑]

https://en.wikipedia.org/wiki/Attention_deficit_hyperactivity_disorder_management

And incorporate the subsequent citations into the article of ADHD_management. =) [72] [73] [74]

3/6

[编辑]

Re-format those un-formated citations. =)

3/9

[编辑]

Re-format those un-formated citations. =)

3/12

[编辑]

https://en.wikipedia.org/wiki/Attention_deficit_hyperactivity_disorder#Management

Commencement/inception of construction of social and cultural section for ADHD article on Chinese Wikipedia

[编辑]

美國一年因ADHD造成的損失是1200億台幣以上[75]。

未治療的注意力不集中/過動症兒童會影響其學業表現，社會功能及生活品質，且將來容易因長期處在被指責，誤解的情況下（如長期作業品質不佳被罰寫甚至被記過），扭曲自尊及自信的人格發展，開始其他的問題，如反抗對立疾患 （易怒，指責他人，反抗規則），行為疾患（打架，說謊，偷竊，逃學等），藥酒癮及憂鬱症等；長期對學業成績，工作能力及工作維持均有負面影響。有注意力不集中/過動症兒童的家庭容易產生家人衝突及家庭壓力，父母會因處理這些兒童產生的問題減少自己工作、社交或休息的時間，甚至因此影響父母自己的身心健康及婚姻狀態。[76]

In respect of equipment warehouse

[编辑]

值得注意的是，國際上通用的注意力不足過動症分類、治療策略及描述並無區分所謂的普通『注意力不足過動症』兒童和資優『注意力不足過動症』兒童[77]。

Reference

[编辑]
  1. ^ 1.0 1.1 1.2 1.3 Millichap, J. Gordon. Chapter 2: Causative Factors. Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD 2nd. New York, NY: Springer Science. 2010: 26. ISBN 978-1-4419-1396-8. LCCN 2009938108. doi:10.1007/978-104419-1397-5. 
  2. ^ 2.0 2.1 Thapar A, Cooper M, Eyre O, Langley K. What have we learnt about the causes of ADHD?. J Child Psychol Psychiatry. January 2013, 54 (1): 3–16. PMC 3572580 可免费查阅. PMID 22963644. doi:10.1111/j.1469-7610.2012.02611.x. 
  3. ^ 3.0 3.1 3.2 National Collaborating Centre for Mental Health. Attention Deficit Hyperactivity Disorder: Diagnosis and Management of ADHD in Children, Young People and Adults. British Psychological Society. 2009: 19–27, 38, 130, 133, 317. ISBN 9781854334718. 
  4. ^ 4.0 4.1 Neale, BM; Medland, SE; Ripke, S; et al. Meta-analysis of genome-wide association studies of attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. September 2010, 49 (9): 884–897. PMC 2928252 可免费查阅. PMID 20732625. doi:10.1016/j.jaac.2010.06.008. 
  5. ^ 5.0 5.1 Burt SA. Rethinking environmental contributions to child and adolescent psychopathology: a meta-analysis of shared environmental influences. Psychol Bull. July 2009, 135 (4): 608–637. PMID 19586164. doi:10.1037/a0015702. 
  6. ^ Nolen-Hoeksema S. Abnormal Psychology Sixth. 2013: 267. ISBN 9780078035388. 
  7. ^ 7.0 7.1 Franke B, Faraone SV, Asherson P, Buitelaar J, Bau CH, Ramos-Quiroga JA, Mick E, Grevet EH, Johansson S, Haavik J, Lesch KP, Cormand B, Reif A. The genetics of attention deficit/hyperactivity disorder in adults, a review. Mol. Psychiatry. October 2012, 17 (10): 960–987. PMC 3449233 可免费查阅. PMID 22105624. doi:10.1038/mp.2011.138. 
  8. ^ Nolen-Hoeksema S. Abnormal Psychology Sixth. 2013: 267. ISBN 9780078035388. 
  9. ^ 9.0 9.1 9.2 9.3 Gizer IR, Ficks C, Waldman ID. Candidate gene studies of ADHD: a meta-analytic review. Hum. Genet. July 2009, 126 (1): 51–90. PMID 19506906. doi:10.1007/s00439-009-0694-x. 
  10. ^ 10.0 10.1 10.2 10.3 10.4 10.5 Kebir O, Tabbane K, Sengupta S, Joober R. Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies. J Psychiatry Neurosci. March 2009, 34 (2): 88–101. PMC 2647566 可免费查阅. PMID 19270759. 
  11. ^ 11.0 11.1 Berry, MD. The potential of trace amines and their receptors for treating neurological and psychiatric diseases. Reviews on Recent Clinical Trials. January 2007, 2 (1): 3–19. PMID 18473983. doi:10.2174/157488707779318107. Although there is little direct evidence, changes in trace amines, in particular PE, have been identified as a possible factor for the onset of attention deficit/hyperactivity disorder (ADHD). … Further, amphetamines, which have clinical utility in ADHD, are good ligands at trace amine receptors. Of possible relevance in this aspect is modafanil, which has shown beneficial effects in ADHD patients and has been reported to enhance the activity of PE at TAAR1. Conversely, methylphenidate, …showed poor efficacy at the TAAR1 receptor. In this respect it is worth noting that the enhancement of functioning at TAAR1 seen with modafanil was not a result of a direct interaction with TAAR1. 
  12. ^ 12.0 12.1 Sotnikova TD, Caron MG, Gainetdinov RR. Trace amine-associated receptors as emerging therapeutic targets. Mol. Pharmacol. August 2009, 76 (2): 229–235. PMC 2713119 可免费查阅. PMID 19389919. doi:10.1124/mol.109.055970. 
  13. ^ 13.0 13.1 Arcos-Burgos M, Muenke M. Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD. Atten Defic Hyperact Disord. November 2010, 2 (3): 139–147. PMC 3280610 可免费查阅. PMID 21432600. doi:10.1007/s12402-010-0030-2. 
  14. ^ 14.0 14.1 Nikolaidis A, Gray JR. ADHD and the DRD4 exon III 7-repeat polymorphism: an international meta-analysis. Social Cognitive and Affective Neuroscience. Jun 2010, 5 (2-3): 188–193. PMC 2894686 可免费查阅. PMID 20019071. doi:10.1093/scan/nsp049. 
  15. ^ 15.0 15.1 15.2 15.3 Glover V. Annual Research Review: Prenatal stress and the origins of psychopathology: an evolutionary perspective. J Child Psychol Psychiatry. April 2011, 52 (4): 356–67. PMID 21250994. doi:10.1111/j.1469-7610.2011.02371.x. 
  16. ^ 16.0 16.1 16.2 Williams J, Taylor E. The evolution of hyperactivity, impulsivity and cognitive diversity. J R Soc Interface. June 2006, 3 (8): 399–413. PMC 1578754 可免费查阅. PMID 16849269. doi:10.1098/rsif.2005.0102. 
  17. ^ 17.0 17.1 Cardo E, Nevot A, Redondo M, et al. Trastorno por déficit de atención/hiperactividad: ¿un patrón evolutivo? [Attention deficit disorder and hyperactivity: a pattern of evolution?]. Rev Neurol. March 2010,. 50 Suppl 3: S143–7. PMID 20200842 （Spanish）. 
  18. ^ Adriani, Walter; Zoratto, Francesca; Laviola, Giovanni. Brain Processes in Discounting: Consequences of Adolescent Methylphenidate Exposure. Stanford, Clare; Tannock, Rosemary (编). Behavioral neuroscience of attention deficit hyperactivity disorder and its treatment. Current Topics in Behavioral Neurosciences. Volume 9. New York: Springer. 13 January 2012: 132–134. ISBN 978-3-642-24611-1. 
  19. ^ Ekstein, Sivan; Glick, Benjamin; Weill, Michal; Kay, Barrie; Berger, Itai. Down Syndrome and Attention-Deficit/Hyperactivity Disorder (ADHD). Journal of Child Neurology. 2011-10-01, 26 (10): 1290–1295. ISSN 0883-0738. PMID 21628698. doi:10.1177/0883073811405201. 
  20. ^ Ekstein, Sivan; Glick, Benjamin; Weill, Michal; Kay, Barrie; Berger, Itai. Down Syndrome and Attention-Deficit/Hyperactivity Disorder (ADHD). Journal of Child Neurology. 2011-10-01, 26 (10): 1290–1295. ISSN 0883-0738. PMID 21628698. doi:10.1177/0883073811405201. 
  21. ^ 21.0 21.1 CDC, Attention-Deficit / Hyperactivity Disorder (ADHD), Centers for Disease Control and Prevention, 16 Mar 2016 [17 Apr 2016] 
  22. ^ 22.0 22.1 Burger PH, Goecke TW, Fasching PA, Moll G, Heinrich H, Beckmann MW, Kornhuber J. [How does maternal alcohol consumption during pregnancy affect the development of attention deficit/hyperactivity syndrome in the child]. Fortschr Neurol Psychiatr (Review). September 2011, 79 (9): 500–506. PMID 21739408. doi:10.1055/s-0031-1273360 （German）. 
  23. ^ 23.0 23.1 23.2 23.3 23.4 23.5 NIMH. Attention Deficit Hyperactivity Disorder (Easy-to-Read). National Institute of Mental Health. 2013 [17 Apr 2016]. 
  24. ^ Eubig PA, Aguiar A, Schantz SL. Lead and PCBs as risk factors for attention deficit/hyperactivity disorder. Environ. Health Perspect. (Review. Research Support, N.I.H., Extramural. Research Support, U.S. Gov't, Non-P.H.S.). December 2010, 118 (12): 1654–1667. PMC 3002184 可免费查阅. PMID 20829149. doi:10.1289/ehp.0901852. 
  25. ^ 25.0 25.1 de Cock M, Maas YG, van de Bor M. Does perinatal exposure to endocrine disruptors induce autism spectrum and attention deficit hyperactivity disorders? Review. Acta Paediatr. (Review. Research Support, Non-U.S. Gov't). August 2012, 101 (8): 811–818. PMID 22458970. doi:10.1111/j.1651-2227.2012.02693.x. 
  26. ^ 26.0 26.1 Abbott LC, Winzer-Serhan UH. Smoking during pregnancy: lessons learned from epidemiological studies and experimental studies using animal models. Crit. Rev. Toxicol. (Review). April 2012, 42 (4): 279–303. PMID 22394313. doi:10.3109/10408444.2012.658506. 
  27. ^ 27.0 27.1 Thapar, A.; Cooper, M.; Jefferies, R.; Stergiakouli, E. What causes attention deficit hyperactivity disorder?. Arch Dis Child (Review. Research Support, Non-U.S. Gov't). March 2012, 97 (3): 260–5. PMID 21903599. doi:10.1136/archdischild-2011-300482. 
  28. ^ 28.0 28.1 Millichap JG. Etiologic classification of attention-deficit/hyperactivity disorder. Pediatrics (Review). February 2008, 121 (2): e358–65. PMID 18245408. doi:10.1542/peds.2007-1332. 
  29. ^ 29.0 29.1 Eme, R. ADHD: an integration with pediatric traumatic brain injury. Expert Rev Neurother (Review). April 2012, 12 (4): 475–83. PMID 22449218. doi:10.1586/ern.12.15. 
  30. ^ 30.0 30.1 30.2 Mayes R, Bagwell C, Erkulwater JL. Medicating Children: ADHD and Pediatric Mental Health illustrated. Harvard University Press. 2009: 4–24. ISBN 9780674031630. 
  31. ^ 31.0 31.1 Millichap, JG; Yee, MM. The diet factor in attention-deficit/hyperactivity disorder. Pediatrics. February 2012, 129 (2): 330–7. PMID 22232312. doi:10.1542/peds.2011-2199. 
  32. ^ 32.0 32.1 32.2 32.3 Sonuga-Barke EJ, Brandeis D, Cortese S, Daley D, Ferrin M, Holtmann M, Stevenson J, Danckaerts M, van der Oord S, Döpfner M, Dittmann RW, Simonoff E, Zuddas A, Banaschewski T, Buitelaar J, Coghill D, Hollis C, Konofal E, Lecendreux M, Wong IC, Sergeant J. Nonpharmacological interventions for ADHD: systematic review and meta-analyses of randomized controlled trials of dietary and psychological treatments. Am J Psychiatry. March 2013, 170 (3): 275–289. PMID 23360949. doi:10.1176/appi.ajp.2012.12070991. Free fatty acid supplementation and artificial food color exclusions appear to have beneficial effects on ADHD symptoms, although the effect of the former are small and those of the latter may be limited to ADHD patients with food sensitivities... 
  33. ^ Tomaska LD and Brooke-Taylor, S. Food Additives – General pp. 449–454 in Encyclopedia of Food Safety, Vol 2: Hazards and Diseases. Eds, Motarjemi Y et al. Academic Press, 2013. ISBN 9780123786135
  34. ^ FDA, Background Document for the Food Advisory Committee: Certified Color Additives in Food and Possible Association with Attention Deficit Hyperactivity Disorder in Children (PDF), U.S. Food and Drug Administration, March 2011 
  35. ^ 引用错误：没有为名为NiggHolton2014的参考文献提供内容
  36. ^ 36.0 36.1 CDC, Facts About ADHD, Centers for Disease Control and Prevention, 6 Jan 2016 [20 Mar 2016] 
  37. ^ Mental health of children and adolescents (PDF). 15 January 2005 [13 October 2011]. （原始内容 (PDF)存档于24 October 2009）. 
  38. ^ Elder TE. The importance of relative standards in ADHD diagnoses: evidence based on exact birth dates. J Health Econ. September 2010, 29 (5): 641–656. PMC 2933294 可免费查阅. PMID 20638739. doi:10.1016/j.jhealeco.2010.06.003. 
  39. ^ Parritz, R. Disorders of Childhood: Development and Psychopathology. Cengage Learning. 2013: 151. ISBN 9781285096063. 
  40. ^ Parens E, Johnston J. Facts, values, and Attention-Deficit Hyperactivity Disorder (ADHD): an update on the controversies. Child Adolesc Psychiatry Ment Health. 2009, 3 (1): 1. PMC 2637252 可免费查阅. PMID 19152690. doi:10.1186/1753-2000-3-1. 
  41. ^ 引用错误：没有为名为Singh的参考文献提供内容
  42. ^ Chriss, James J. Social control: an introduction. Cambridge, UK: Polity. 2007: 230. ISBN 0-7456-3858-9. 
  43. ^ Szasz, Thomas Stephen. Pharmacracy: medicine and politics in America. New York: Praeger. 2001: 212. ISBN 0-275-97196-1. 
  44. ^ 44.0 44.1 44.2 44.3 44.4 44.5 44.6 44.7 44.8 Chandler DJ, Waterhouse BD, Gao WJ. New perspectives on catecholaminergic regulation of executive circuits: evidence for independent modulation of prefrontal functions by midbrain dopaminergic and noradrenergic neurons. Front. Neural Circuits. May 2014, 8: 53. PMC 4033238 可免费查阅. PMID 24904299. doi:10.3389/fncir.2014.00053. 
  45. ^ 45.00 45.01 45.02 45.03 45.04 45.05 45.06 45.07 45.08 45.09 45.10 45.11 45.12 45.13 45.14 45.15 45.16 45.17 45.18 Malenka RC, Nestler EJ, Hyman SE. Chapters 10 and 13. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 266, 315, 318–323. ISBN 9780071481274. Early results with structural MRI show thinning of the cerebral cortex in ADHD subjects compared with age-matched controls in prefrontal cortex and posterior parietal cortex, areas involved in working memory and attention. 
  46. ^ 46.00 46.01 46.02 46.03 46.04 46.05 46.06 46.07 46.08 46.09 46.10 46.11 46.12 46.13 46.14 Malenka RC, Nestler EJ, Hyman SE. Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin. Sydor A, Brown RY (编). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 148, 154–157. ISBN 9780071481274. DA has multiple actions in the prefrontal cortex. It promotes the "cognitive control" of behavior: the selection and successful monitoring of behavior to facilitate attainment of chosen goals. Aspects of cognitive control in which DA plays a role include working memory, the ability to hold information "on line" in order to guide actions, suppression of prepotent behaviors that compete with goal-directed actions, and control of attention and thus the ability to overcome distractions. Cognitive control is impaired in several disorders, including attention deficit hyperactivity disorder. ... Noradrenergic projections from the LC thus interact with dopaminergic projections from the VTA to regulate cognitive control. ... it has not been shown that 5HT makes a therapeutic contribution to treatment of ADHD. 
    NOTE: DA: dopamine, LC: locus coeruleus, VTA: ventral tegmental area, 5HT: serotonin (5-hydroxytryptamine)
  47. ^ 47.0 47.1 47.2 47.3 47.4 Castellanos FX, Proal E. Large-scale brain systems in ADHD: beyond the prefrontal-striatal model. Trends Cogn. Sci. (Regul. Ed.). January 2012, 16 (1): 17–26. PMC 3272832 可免费查阅. PMID 22169776. doi:10.1016/j.tics.2011.11.007. Recent conceptualizations of ADHD have taken seriously the distributed nature of neuronal processing [10,11,35,36]. Most of the candidate networks have focused on prefrontal-striatal-cerebellar circuits, although other posterior regions are also being proposed [10]. 
  48. ^ 48.0 48.1 48.2 48.3 48.4 Cortese S, Kelly C, Chabernaud C, Proal E, Di Martino A, Milham MP, Castellanos FX. Toward systems neuroscience of ADHD: a meta-analysis of 55 fMRI studies. Am J Psychiatry. October 2012, 169 (10): 1038–1055. PMC 3879048 可免费查阅. PMID 22983386. doi:10.1176/appi.ajp.2012.11101521. 
  49. ^ 49.0 49.1 Krain AL, Castellanos FX. Brain development and ADHD. Clin Psychol Rev. August 2006, 26 (4): 433–444. PMID 16480802. doi:10.1016/j.cpr.2006.01.005. 
  50. ^ 50.0 50.1 Fusar-Poli P, Rubia K, Rossi G, Sartori G, Balottin U. Striatal dopamine transporter alterations in ADHD: pathophysiology or adaptation to psychostimulants? A meta-analysis. Am J Psychiatry. March 2012, 169 (3): 264–72. PMID 22294258. doi:10.1176/appi.ajp.2011.11060940. 
  51. ^ 51.0 51.1 51.2 51.3 引用错误：没有为名为cognition enhancers的参考文献提供内容
  52. ^ 52.0 52.1 Cortese S. The neurobiology and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD): what every clinician should know. Eur. J. Paediatr. Neurol. September 2012, 16 (5): 422–433. PMID 22306277. doi:10.1016/j.ejpn.2012.01.009. 
  53. ^ 53.0 53.1 Lesch KP, Merker S, Reif A, Novak M. Dances with black widow spiders: dysregulation of glutamate signalling enters centre stage in ADHD. Eur Neuropsychopharmacol. June 2013, 23 (6): 479–491. PMID 22939004. doi:10.1016/j.euroneuro.2012.07.013. 
  54. ^ 54.0 54.1 54.2 54.3 54.4 54.5 54.6 54.7 54.8 Brown TE. ADD/ADHD and Impaired Executive Function in Clinical Practice. Curr Psychiatry Rep. October 2008, 10 (5): 407–411. PMID 18803914. doi:10.1007/s11920-008-0065-7. 
  55. ^ 55.0 55.1 55.2 55.3 Diamond A. Executive functions. Annu. Rev. Psychol. 2013, 64: 135–168. PMC 4084861 可免费查阅. PMID 23020641. doi:10.1146/annurev-psych-113011-143750. EFs and prefrontal cortex are the first to suffer, and suffer disproportionately, if something is not right in your life. They suffer first, and most, if you are stressed (Arnsten 1998, Liston et al. 2009, Oaten & Cheng 2005), sad (Hirt et al. 2008, von Hecker & Meiser 2005), lonely (Baumeister et al. 2002, Cacioppo & Patrick 2008, Campbell et al. 2006, Tun et al. 2012), sleep deprived (Barnes et al. 2012, Huang et al. 2007), or not physically fit (Best 2010, Chaddock et al. 2011, Hillman et al. 2008). Any of these can cause you to appear to have a disorder of EFs, such as ADHD, when you do not. 
  56. ^ 56.0 56.1 Skodzik T, Holling H, Pedersen A. Long-Term Memory Performance in Adult ADHD: A Meta-Analysis. J. Atten. Disord. November 2013. PMID 24232170. doi:10.1177/1087054713510561. 
  57. ^ Lambek R, Tannock R, Dalsgaard S, Trillingsgaard A, Damm D, Thomsen PH. Validating neuropsychological subtypes of ADHD: how do children with and without an executive function deficit differ?. J Child Psychol Psychiatry. August 2010, 51 (8): 895–904. PMID 20406332. doi:10.1111/j.1469-7610.2010.02248.x. 
  58. ^ Nigg JT, Willcutt EG, Doyle AE, Sonuga-Barke EJ. Causal heterogeneity in attention-deficit/hyperactivity disorder: do we need neuropsychologically impaired subtypes?. Biol. Psychiatry. June 2005, 57 (11): 1224–1230. PMID 15949992. doi:10.1016/j.biopsych.2004.08.025. 
  59. ^ 59.0 59.1 59.2 Modesto-Lowe V, Chaplin M, Soovajian V, Meyer A. Are motivation deficits underestimated in patients with ADHD? A review of the literature. Postgrad Med. 2013, 125 (4): 47–52. PMID 23933893. doi:10.3810/pgm.2013.07.2677. Behavioral studies show altered processing of reinforcement and incentives in children with ADHD. These children respond more impulsively to rewards and choose small, immediate rewards over larger, delayed incentives. Interestingly, a high intensity of reinforcement is effective in improving task performance in children with ADHD. Pharmacotherapy may also improve task persistence in these children. ... Previous studies suggest that a clinical approach using interventions to improve motivational processes in patients with ADHD may improve outcomes as children with ADHD transition into adolescence and adulthood. 
  60. ^ 引用错误：没有为名为Pingtung Hospital的参考文献提供内容
  61. ^ Parent's Medication Guide: ADHD (PDF). American Psychiatric Association. American Psychiatric Association & American Academy of Child and Adolescent Psychiatry (AACAP). July 2013 [January 2017]. （原始内容存档于July 2013）. Though not FDA-approved for combined treatment, atomoxetine (Strattera) is sometimes used in conjunction with stimulants as an off-label combination therapy. 
  62. ^ Medical Encyclopedia → Attention deficit hyperactivity disorder. MedlinePlus.gov. 05 January 2017 [January 2017]. Medicine combined with behavioral treatment often works best. Different ADHD medicines can be used alone or combined with each other. The doctor will decide which medicine is right, based on the person's symptoms and needs. 
  63. ^ 63.0 63.1 Wigal SB. Efficacy and safety limitations of attention-deficit hyperactivity disorder pharmacotherapy in children and adults. CNS Drugs. 2009,. 23 Suppl 1: 21–31. PMID 19621975. doi:10.2165/00023210-200923000-00004. 
  64. ^ Childress, A. C.; Sallee, F. R. Revisiting clonidine: an innovative add-on option for attention-deficit/hyperactivity disorder. Drugs of Today (Barcelona, Spain: 1998). 2012, 48 (3): 207–217. ISSN 1699-3993. PMID 22462040. doi:10.1358/dot.2012.48.3.1750904. 
  65. ^ Castells X, Ramos-Quiroga JA, Bosch R, Nogueira M, Casas M. Castells X , 编. Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults. Cochrane Database Syst. Rev. 2011, (6): CD007813. PMID 21678370. doi:10.1002/14651858.CD007813.pub2. 
  66. ^ Childress, A. C.; Sallee, F. R. Revisiting clonidine: an innovative add-on option for attention-deficit/hyperactivity disorder. Drugs of Today (Barcelona, Spain: 1998). 2012, 48 (3): 207–217. ISSN 1699-3993. PMID 22462040. doi:10.1358/dot.2012.48.3.1750904. There are a number of non-stimulant medications, such as atomoxetine, bupropion, guanfacine, and clonidine that may be used as alternatives, or added to stimulant therapy. 
  67. ^ Den Heijer AE, Groen Y, Tucha L, Fuermaier AB, Koerts J, Lange KW, Thome J, Tucha O. Sweat it out? The effects of physical exercise on cognition and behavior in children and adults with ADHD: a systematic literature review. J. Neural. Transm. (Vienna). July 2016. PMID 27400928. doi:10.1007/s00702-016-1593-7. Beneficial chronic effects of cardio exercise were found on various functions as well, including executive functions, attention and behavior. 
  68. ^ Kamp CF, Sperlich B, Holmberg HC. Exercise reduces the symptoms of attention-deficit/hyperactivity disorder and improves social behaviour, motor skills, strength and neuropsychological parameters. Acta Paediatr. July 2014, 103 (7): 709–714 [14 March 2015]. PMID 24612421. doi:10.1111/apa.12628. We may conclude that all different types of exercise ... attenuate the characteristic symptoms of ADHD and improve social behaviour, motor skills, strength and neuropsychological parameters without any undesirable side effects. Available reports do not reveal which type, intensity, duration and frequency of exercise is most effective 
  69. ^ Rommel AS, Halperin JM, Mill J, Asherson P, Kuntsi J. Protection from genetic diathesis in attention-deficit/hyperactivity disorder: possible complementary roles of exercise. J. Am. Acad. Child Adolesc. Psychiatry. September 2013, 52 (9): 900–910. PMC 4257065 可免费查阅. PMID 23972692. doi:10.1016/j.jaac.2013.05.018. The findings from these studies provide some support for the notion that exercise has the potential to act as a protective factor for ADHD. 
  70. ^ Medical Encyclopedia → Attention deficit hyperactivity disorder. medlineplus.gov. 05 January 2017 [January 2017]. Psychostimulants (also known as stimulants) are the most commonly used medicines. Although these drugs are called stimulants, they actually have a calming effect in people with ADHD. 
  71. ^ 示弱不只是弱者的權利，而且也是勇者的表現 陳永隆博士的6D思維，談到「示弱，是來自堅強的內心」：『示弱，是為了給別人自信；示弱，是看清世界有多大；示弱，是看懂自己有多小；示弱，是弱勢時承認自己不完美；示弱，是優勢時給旁人留點餘地。』示弱不只是弱者的權利，而且也是勇者的表現。
  72. ^ 坦誠示弱，你才會贏得更多-李開復的故事. cheers.com.tw. August 2011 [January 2017]. 坦誠示弱，你才會贏得更多 
  73. ^ 孫子兵法的智慧l. wikisource.org. 孫子兵法的智慧粉絲團 on Facebook. January 28, 2013 [February 2017]. 孫子兵法的智慧粉絲團\2013年1月28日\示弱不只是弱者的權利，而且也是勇者的表現\陳永隆博士的6D思維，談到「示弱，是來自堅強的內心；示弱，是為了給別人自信；示弱，是看清世界有多大；示弱，是看懂自己有多小；示弱，是弱勢時承認自己不完美；示弱，是優勢時給旁人留點餘地。」示弱不只是弱者的權利，而且也是勇者的表現。 大家看《三國演義》第五十回，描寫關公（雲長）義釋曹操的情節，故事雖屬虛構，卻令人動容。話說曹操捨大路不走，選擇小路華容道，而小路山邊有數處煙起，依照兵書所云「虛者實之，實者虛之」的原則，他認為諸葛亮足智多謀，故意使人於山僻處燒煙，使我軍不敢從這條山路走，他卻伏兵於大路等著。「吾料已定，偏不教中他計！」詎料，路途中遇到大將關雲長帥軍等候多時，關公提青龍刀，跨赤兔馬，截住去路。操軍見了，個個亡魂喪膽，面面相覷。如何是好？這時曹軍將領程昱獻計，建議曹操：「丞相舊日有恩於關雲長，今只親自告之，可脫此難。」曹操接納建議。下面這段話就是當時處於弱勢者的曹操的示弱故事。《三國演義》寫道曹操馬上縱馬向前，與雲長一陣寒暄以後，提起昔日禮遇關雲長上馬贈金、下馬贈銀之事。作者羅貫中這樣寫：「雲長是個義重如山之人，想起當日曹操的許多恩義，與後來過關斬將之事，如何不動心？又見曹軍惶惶皆欲垂淚，越發心中不忍。於是關雲長把馬頭勒回，謂眾軍曰：『四散擺開』。」曹操見關雲長回馬，認為機不可失，便和眾將一齊衝將過去，衝出華容道免於此難。由於強勢的人最怕示弱的人，弱者對強者最強有力的手腕就是「示弱」。關公見曹操淚眼求情，想起以前人家的禮遇，一時不知所措，讓曹操有了逃脫間隙。各位看官，曹操的示弱行為換回了生命，也可能改寫了三國歷史。 孫子兵法勢篇說：「亂生於治，怯生於勇，弱生於強。」這也是《老子‧七十八章》說：「弱之勝強，柔之勝剛」的道理。 企業、政治或人生經營實務上有關「亂生於治，怯生於勇，弱生於強」的實例特多。例如當年台灣南部某女鄉長以哭窮聞名，某日省長（主席）出席地方會議，該女鄉長報告鄉治難題，當場難過痛哭流涕，省長印象特深，於是指示辦理，使女鄉長破涕為笑。這就是女鄉長的示弱戰略思維，你學到了嗎？ 
  74. ^ 中華民國九十一年大學入學指定科目考試作文題. wikisource.org. July 2002 [February 2017]. 我們身邊，有各種不同的「鏡子」。有人在時間的流轉中，從「它」照見了容顏的改變；有人在人生的戲局中，從「它」觀看出真正的自我；但也有人不願或不能面對「它」。試以「對鏡」為題...... 
  75. ^ 陳錦宏 醫師. 認識ADHD. 社團法人台灣心動家族兒童青少年關懷協會. [February 16th, 2017]. 美國一年因ADHD造成的損失是1200億台幣以上 
  76. ^ 陳錦宏 醫師. 【誤解下的小孩】：談注意力不足/過動症 - 陳錦宏醫師. 社團法人台灣心動家族兒童青少年關懷協會. July, ninth, 2012 [February 16th, 2017]. 未治療的注意力不集中/過動症兒童會影響其學業表現，社會功能及生活品質，且將來容易因長期處在被指責，誤解的情況下（如長期作業品質不佳被罰寫甚至被記過），扭曲自尊及自信的人格發展，開始其他的問題，如反抗對立疾患 （易怒，指責他人，反抗規則），行為疾患（打架，說謊，偷竊，逃學等），藥酒癮及憂鬱症等；長期對學業成績，工作能力及工作維持均有負面影響。有注意力不集中/過動症兒童的家庭容易產生家人衝突及家庭壓力，父母會因處理這些兒童產生的問題減少自己工作、社交或休息的時間，甚至因此影響父母自己的身心健康及婚姻狀態。研究顯示美國一年因注意力不集中/過動症損失高達近40億美金，其中即包括父母的工作損失。 
  77. ^ Choices, NHS. Attention deficit hyperactivity disorder (ADHD) - NHS Choices. 
检索自“https://zh.wikipedia.org/zhwiki/w/index.php?title=User:It%27s_gonna_be_awesome/sandbox5&oldid=43701633”