跳转到内容

用户: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]

绝大多数注意力不足过动症（ADHD）的确切成因目前并没有定论，最有可能是基因和环境交互作用导致。.[1][2] 有些个案的成因可能与脑部的疾病感染和脑部创伤有关。[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]

       更进一步来说，双胞胎研究显示注意力不足过动症通常遗传自患者的父母。大约75%的患者的病因是基因因素。or 双胞胎研究显示注意力不足过动症通常遗传自患者的父母，这大约占所有病因的百分之七十五。[3][4][5]
       儿童青少年的手足（兄弟姊妹）比起非注意力不足过动症患者的手足多上三到四倍的机率带有注意力不足过动症的特征或也有注意力不足过动症。[8]基因可能也与注意力不足过动症是否从幼儿延续至成人有关联。[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]

       在一般的情况下，注意力不足过动症大多与数个影响多巴胺（大脑内一种神经传导物质）传递的基因有关[9][10]。这些基因分别是 多巴胺输送元（再摄取）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]

       其他基因分别是血清素输送元SERT, HTR1B（英语：HTR1B）, SNAP25（英语：SNAP25）, GRIN2A（英语：GRIN2A）, ADRA2A（英语：ADRA2A）, TPH2（英语：TPH2）, 和 脑源性神经营养因子（BDNF）[9][10]。

       一个名为LPN3（英语：LPN3）的基因，其变异体大约存在于9%的注意力不足过动症患者身上。而这9%的患者可能对于中枢神经兴奋剂特别有反应。[13]

       多巴胺输送元{{tsl|en|DRD4|DRD4}5}的七个重复存在的变异体DRD4-7R与注意力不足过动症有关。因为它放大了由多巴胺触发的抑制效果。DRD4的接收元是一个G蛋白偶联受体（G Protein-Coupled Receptors），作用是抑制腺苷酸环化酶（adenylyl cyclase）。DRD4的突变反映在许多行为表现上，包括注意力不足过动症的症状群，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过动症的盛行率中扮演一定的脚色，特别是有过动-冲动症状的男性患者。[15]

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

唐氏症患者可能有较高的机率出现注意力不足过动症。[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]

环境因素[编辑]

       除了基因外，一些环境因子也可能是注意缺陷多动障碍的致病因素。[21]例如：在怀孕期间摄取酒精可能导致包含类似注意缺陷多动障碍症状的胎儿酒精谱系障碍（fetal alcohol spectrum disorder）。暴露在特定有毒物质，例如：铅或多氯联苯、多氯联二苯或二联酚（polychlorinated biphenyls）等，可能会产生类似注意缺陷多动障碍的中毒症状。[22]暴露在磷酸酯（organophosphate）的杀虫剂、毒死蜱（chlorpyrifos）（一种晶体有机磷杀虫剂） 、Alkyl phosphate（英语：Alkyl phosphate） 或 dialkyl phosphate（英语：dialkyl phosphate）中，将提高致病率，虽然此结论尚未在学界中被广泛的认可。[25]在怀孕过程中接触到二手烟，将不利于胚胎的脑部神经发育，并将增加罹患注意缺陷多动障碍的机率。[23][26]

       新生儿严重早产、新生儿体重严重过轻（英语：low birth weight）、被极端疏于照料的儿童、遭受凌虐、严重地缺乏与社会的互动（英语：social deprivaton），也可能增加往后出现注意缺陷多动障碍的机率。[23][27]

       母亲在怀孕期间、儿童在出生时或成长初期遭受特定的感染都可能提高致病率。这些特定的感染包含但不限于：麻疹（measles）、 varicella zoster（英语：Varicella zoster virus）、 脑炎（encephalitis）、 风疹、德国麻疹或三日麻疹（rubella）, EV71（enterovirus 71）（肠病毒的一种）。[28]

       曾遭受 外伤性脑损伤（traumatic brain injury）（英语：外傷性腦損傷（traumatic brain injury））（英文）、外伤性脑损伤（traumatic brain injury）（日语：外傷性腦損傷（traumatic brain injury）） （日语）的儿童，其中至少30%将在往后的人生中发展出注意缺陷多动障碍[29]。因外力而导致脑部受损而致注意缺陷多动障碍大约占所有注意缺陷多动障碍所有个案的5%。[30]

       目前已有的证据无法支持减少食用特定食物来治疗注意缺陷多动障碍的疗法[32]减少食用有人工色素食品的儿童的相关研究，只有不到1/3的儿童在症状上有改善[32]，这方面的助益有可能只是对有食物过敏的儿童有帮助，也有可能是这些儿童同时也在接受注意缺陷多动障碍的治疗[32]

       截至2016年，研究并不支持“注意缺陷多动障碍是因为摄取过多的精致糖、看太多电视、贫穷或混乱、动荡不安、吵吵闹闹的家庭所致”。然而前述的这些项目可能会恶化一些注意缺陷多动障碍患者的注意缺陷多动障碍症状。[36] （详见本条目之饮食治疗一节）

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 病理生理学[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]

       截至目前为止，ADHD被认为是肇因于部分脑内的神经传导物质系统的损伤（特别是与多巴胺和正肾上腺素有关的神经传导系统），进而对患者的脑部执行功能产生不良的影响。[44][45]多巴胺与正肾上腺素的脑内通道大多起源自脑内的腹侧被盖区（ventral tegmental area） and 蓝斑核（locus coeruleus），并由此投射至不同的脑区且管理许多认知的流程（与认知功能相关的处理流程）。[44][46] 特别是那些投射至前额叶（prefrontal cortex）和纹状体（striatum）（英语：striatum）的脑内的多巴胺通道（dopaminergic pathway）们（群）和脑内的正肾上腺素通道/蓝斑核系统（norepinephrine pathway）（英语：norepinephrine pathway）们（群），它们主要的工作就是负责调节执行功能（executive function） (cognitive control of behavior)、动机（motivation）、 酬赏、报偿的感受能力（reward perception）、和运动神经的功能（motor function）。[44][45][46]以上是目前已知在ADHD的病理生理学（Pathophysiology）中扮演主要脚色的几条脑内通道（pathway）。对于ADHD更全面的概观以及更多可能与之相关的脑内通道也已经被提议。[45][47][48]

请参阅：Reward system、Incentive salience（英语：Incentive salience）、Reward dependence（英语：Reward dependence）、Brain stimulation reward（英语：Brain stimulation reward） 以了解关于大脑内回馈系统的运作机制。

Brain structure 大脑结构[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]

在儿童注意力不足过动症患者中，普遍存有一些脑部结构（特别是左侧的前额叶 prefrontal cortex、后顶叶皮质 posterior parietal cortex ）在体积上小于平均值的现象。[45][49]其他诸如ADHD患者的：前额 - 纹状体小脑（prefrontal-striatal-cerebellar）和前额叶纹状体丘脑回路（prefrontal-striatal-thalamic circuits）也被发现与非ADHD的人不同。[45][47][48]

Neurotransmitter pathways 神经传导物质的通道/路径[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]

       从前一些人倒果为因的以为ADHD患者脑部中偏多的多巴胺转运体（dopamine transporter）是ADHD的病因之一，然而后来经过研究证明，偏多的多巴胺转运体（dopamine transporter）是因为患者服用中枢神经兴奋剂治疗的关系。[50]

       目前的研究模型包含了 中脑皮质素-多巴胺通道（mesocorticolimbic dopamine pathway）（英语：mesocorticolimbic projection） 及 蓝斑核-去甲肾上腺素系统（locus coeruleus-noradrenergic system）（英语：locus coeruleus-noradrenergic system）。[44][45][46]用于治疗ADHD的中枢神经兴奋剂，其疗效可能是起因于它增进了神经传导物质在这些系统中的活动。[45][46][51] ADHD患者脑部中的 5-羟色胺能serotoninergic（与血清素serotonin有关）（英语：serotoninergic） 通道（=路径=pathway）、 谷氨酸能（glutamatergic）（一种神经传导物质）（英语：glutamate (neurotransmitter)）通道、 或 胆碱能（cholinergic） 通道可能也存有一些导致ADHD症状的原因。[51][52][53]

请参见：血清素。

Executive function and motivation 执行功能和动机[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的症状起因于某些执行功能上的缺陷，例如：注意力/专注力的控制（attentional control）、inhibitory control、及 工作记忆（working memory）。[54][45][46][55]执行功能简单来说就是一整群认知处理过程的集合。而这集合必须能够成功的帮助一个人选择并督促自己做出得以实现他那经过深思熟虑过后的目标之行为。[54][46][55]ADHD患者先天的执行功能损伤造成以下这些症状：难以维持有规划的、有组织性的（problems with staying organized）、缺乏时间观念（time keeping）、过度的拖延（excessive procrastination）、难以保持专注（maintaining concentration）、难以把注意力放对地方（ paying attention）、难以忽略与任务不相干的外务（ignoring distractions）、情绪管理的困难（regulating emotions）、难以把细节记起来（remembering details）。[54][45][46]ADHD患者在长期记忆的表现可看出ADHD患者的长期记忆是没有损伤的。ADHD患者在提取长期记忆时所产生的困难显然是肇因于工作记忆的受损[54][56]。

       端视一个ADHD患者其“脑部发展的程度”与其“所在环境对其执行功能要求的程度”的比例，因此有些ADHD患者可能直到青少年时期甚至是成年初期才开始显露出ADHD的症状。

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与“在儿童青少年时期缺乏动机”相关。儿童青少年ADHD患者会发现自己比起“眼前立即的回馈/酬赏”更难以专注在“长远的目标/回报/回馈/酬赏/满足”，并展现出对于“眼前立即的回馈/酬赏/满足”的冲动。[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）与哌甲酯（methylphenidate）并服的处方尚未经美国食品药物管理局核可，但医师会视个案的情况（如：共病、预后、......）以开仿单标示外使用（off-label use）的方式处方之。[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]

数种非中枢神经刺激剂，例如：阿托莫西汀（atomoxetine）、可乐定（clonidine）、安非他酮（bupropion）和guanfacine（英语：guanfacine），可与中枢神经刺激剂一起使用或作为中枢神经刺激剂的替代方案。[63][65][66]

2/9[编辑]

可乐定（clonidine）与胍法新（英语：guanfacine）（guanfacine）皆为非中枢神经兴奋剂，为alpha-2 肾上腺素受体（英语：alpha-2 adrenergic receptor）刺激剂/促进剂/活化剂 的一员，与哌甲酯（methylphenidate）并用或单独服用都有显著疗效其中两药物并服：

详阅：肾上腺素受体

2/12[编辑]

规律的运动，特别是有氧运动，也证实为一个有效的“附加疗法”（即表示可附加在现有具备科学实证且能在统计学上达到显著意义之有效改善症状的医学疗法）。Please update the three citations. =) [67][68][69]

2/15[编辑]

规律的运动，特别是有氧运动，也证实为一个有效的“附加疗法（英语：add-on treatment）”即表示可附加在现有具备科学实证且能在统计学上达到显著意义之有效改善症状的医学疗法）。

2/18[编辑]

  • 问题 Question:
“我的孩子就已经常常兴奋过头了，还让他吃兴奋剂？”
答复 Answer：
虽然这些药物被归纳为“兴奋剂”类，但是它们确实有帮助患者们保持平静的效果。[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]

美国一年因ADHD造成的损失是1200亿台币以上[75]。

未治疗的注意力不集中/过动症儿童会影响其学业表现，社会功能及生活品质，且将来容易因长期处在被指责，误解的情况下（如长期作业品质不佳被罚写甚至被记过），扭曲自尊及自信的人格发展，开始其他的问题，如反抗对立疾患 （易怒，指责他人，反抗规则），行为疾患（打架，说谎，偷窃，逃学等），药酒瘾及忧郁症等；长期对学业成绩，工作能力及工作维持均有负面影响。有注意力不集中/过动症儿童的家庭容易产生家人冲突及家庭压力，父母会因处理这些儿童产生的问题减少自己工作、社交或休息的时间，甚至因此影响父母自己的身心健康及婚姻状态。[76]

In respect of equipment warehouse[编辑]

值得注意的是，国际上通用的注意力不足过动症分类、治疗策略及描述并无区分所谓的普通‘注意力不足过动症’儿童和资优‘注意力不足过动症’儿童[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. ^ 示弱不只是弱者的权利，而且也是勇者的表现 陈永隆博士的6D思维，谈到“示弱，是来自坚强的内心”：‘示弱，是为了给别人自信；示弱，是看清世界有多大；示弱，是看懂自己有多小；示弱，是弱势时承认自己不完美；示弱，是优势时给旁人留点馀地。’示弱不只是弱者的权利，而且也是勇者的表现。
  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]. 坦诚示弱，你才会赢得更多 
  73. ^ 孫子兵法的智慧l. wikisource.org. 孙子兵法的智慧粉丝团 on Facebook. January 28, 2013 [February 2017]. 孙子兵法的智慧粉丝团\2013年1月28日\示弱不只是弱者的权利，而且也是勇者的表现\陈永隆博士的6D思维，谈到“示弱，是来自坚强的内心；示弱，是为了给别人自信；示弱，是看清世界有多大；示弱，是看懂自己有多小；示弱，是弱势时承认自己不完美；示弱，是优势时给旁人留点馀地。”示弱不只是弱者的权利，而且也是勇者的表现。 大家看《三国演义》第五十回，描写关公（云长）义释曹操的情节，故事虽属虚构，却令人动容。话说曹操舍大路不走，选择小路华容道，而小路山边有数处烟起，依照兵书所云“虚者实之，实者虚之”的原则，他认为诸葛亮足智多谋，故意使人于山僻处烧烟，使我军不敢从这条山路走，他却伏兵于大路等著。“吾料已定，偏不教中他计！”讵料，路途中遇到大将关云长帅军等候多时，关公提青龙刀，跨赤兔马，截住去路。操军见了，个个亡魂丧胆，面面相觑。如何是好？这时曹军将领程昱献计，建议曹操：“丞相旧日有恩于关云长，今只亲自告之，可脱此难。”曹操接纳建议。下面这段话就是当时处于弱势者的曹操的示弱故事。《三国演义》写道曹操马上纵马向前，与云长一阵寒暄以后，提起昔日礼遇关云长上马赠金、下马赠银之事。作者罗贯中这样写：“云长是个义重如山之人，想起当日曹操的许多恩义，与后来过关斩将之事，如何不动心？又见曹军惶惶皆欲垂泪，越发心中不忍。于是关云长把马头勒回，谓众军曰：‘四散摆开’。”曹操见关云长回马，认为机不可失，便和众将一齐冲将过去，冲出华容道免于此难。由于强势的人最怕示弱的人，弱者对强者最强有力的手腕就是“示弱”。关公见曹操泪眼求情，想起以前人家的礼遇，一时不知所措，让曹操有了逃脱间隙。各位看官，曹操的示弱行为换回了生命，也可能改写了三国历史。 孙子兵法势篇说：“乱生于治，怯生于勇，弱生于强。”这也是《老子‧七十八章》说：“弱之胜强，柔之胜刚”的道理。 企业、政治或人生经营实务上有关“乱生于治，怯生于勇，弱生于强”的实例特多。例如当年台湾南部某女乡长以哭穷闻名，某日省长（主席）出席地方会议，该女乡长报告乡治难题，当场难过痛哭流涕，省长印象特深，于是指示办理，使女乡长破涕为笑。这就是女乡长的示弱战略思维，你学到了吗？ 
  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]. 我们身边，有各种不同的“镜子”。有人在时间的流转中，从“它”照见了容颜的改变；有人在人生的戏局中，从“它”观看出真正的自我；但也有人不愿或不能面对“它”。试以“对镜”为题...... 
  75. ^ 陈锦宏 医师. 認識ADHD. 社团法人台湾心动家族儿童青少年关怀协会. [February 16th, 2017]. 美国一年因ADHD造成的损失是1200亿台币以上 
  76. ^ 陈锦宏 医师. 【誤解下的小孩】：談注意力不足/過動症 - 陳錦宏醫師. 社团法人台湾心动家族儿童青少年关怀协会. July, ninth, 2012 [February 16th, 2017]. 未治疗的注意力不集中/过动症儿童会影响其学业表现，社会功能及生活品质，且将来容易因长期处在被指责，误解的情况下（如长期作业品质不佳被罚写甚至被记过），扭曲自尊及自信的人格发展，开始其他的问题，如反抗对立疾患 （易怒，指责他人，反抗规则），行为疾患（打架，说谎，偷窃，逃学等），药酒瘾及忧郁症等；长期对学业成绩，工作能力及工作维持均有负面影响。有注意力不集中/过动症儿童的家庭容易产生家人冲突及家庭压力，父母会因处理这些儿童产生的问题减少自己工作、社交或休息的时间，甚至因此影响父母自己的身心健康及婚姻状态。研究显示美国一年因注意力不集中/过动症损失高达近40亿美金，其中即包括父母的工作损失。 
  77. ^ Choices, NHS. Attention deficit hyperactivity disorder (ADHD) - NHS Choices. 
取自“https://zh.wikipedia.org/w/index.php?title=User:It%27s_gonna_be_awesome/sandbox5&oldid=43701633”