注意（力）缺陷多动障碍

本页使用了标题或全文手工转换
维基百科，自由的百科全书
注意力缺陷多动障碍
Attention deficit hyperactivity disorder
同义词注意力不足疾患、多动障碍（ICD-10）
注意力缺陷多动障碍的常见症状
注意力缺陷多动障碍的常见症状
症状不容易专注、过度活动、不易控制行为[1][2]
常见始发于在6至12岁之前[3]
病程超过六个月[3]
肇因遗传（英语：Genetic disorder）和环境因素（英语：environmental factors）[4][5]
诊断方法排除其他疾病后，依症状进行诊断[1]
相似疾病或共病行为规范障碍、对立反抗症、学习障碍、躁郁症[6]
治疗心理治疗、生活方式调整、药物[1]
药物中枢神经刺激剂、阿托莫西汀、胍法辛[7][8]
患病率5110万人（2015年）[9]
分类和外部资源
医学专科精神病学、儿童与青少年精神医学
[编辑此条目的维基数据]
“ADHD”的各地常用译名
中国大陆注意力缺陷多动障碍
台湾注意力不足过动症
香港专注力失调或过度活跃症
澳门专注力失调/过度活跃症
日本注意欠陥・多动性障害
大韩民国注意力缺乏过多行动障碍
注意力缺乏 过剩行动 综合症
越南𦇒乱增动减注意

注意力缺陷多动障碍（Attention deficit hyperactivity disorder）简称ADHD，是神经发展障碍的精神疾患[10][11]，其特点是注意力不足、活动过度或是冲动，而且不符合患者年龄该有的情形[1][2]。症状会在12岁以前出现，持续超过六个月，而且其症状已造成至少二个情境（例如学校、家庭或是交友休闲）的问题[3][12]。对于儿童而言，注意力不集中可能会造成课业成绩不佳的情形[1]。有时注意力缺陷多动障碍也会和其他心理疾患或是物质滥用有关[13]。注意力缺陷多动障碍会对患者造成不便，不过许多患有ADHD的人在其有兴趣的事物上可以有持续性的专注力（称为过度专注）[5][14]。

注意力缺陷多动障碍是目前诊断最多，也有最多研究的儿童及青少年精神疾病，不过对于大部分的案例而言，还不确定确切的致病原因[4]。依照《精神疾病诊断与统计手册》第四版（DSM-IV）的判据，约有5–7%的儿童诊断为注意力缺陷多动障碍[2][15]，若依照《世界通用疾病分类手册》第十版ICD-10的判据，则有1–2%诊断为注意力缺陷多动障碍[16]。2015年估计全球有5110万人受到注意力缺陷多动障碍的影响[9]。患病率主要会受到诊断方式及判断基准不同所影响[17]，男孩诊断出ADHD的比例是女孩的二倍以上[2]，不过因为ADHD女孩的症状和男孩不同，因此常被忽略[18][19][20]。儿童期诊断到的注意力缺陷多动障碍，约到30–50%会持续到成年，成年人约有2–5%会有成人注意力缺陷多动障碍[21][22][23]。在成人注意力缺陷多动障碍中，过动的情形可能会被“内在的不安宁”所取代[24]。ADHD的症状可能不太容易和其他疾病的症状区分，也不太容易区分正常范围的活力充沛以及过动的分界点在哪里[12]。

注意力缺陷多动障碍的治疗的建议方式依各国而不同，一般都会以心理治疗、生活方式调整以及药物，这三种中的一种或多种方式来进行治疗[1]。英国的医学指南建议针对儿童，只有在症状严重时，才建议使用药物为第一线的疗法，若儿童拒绝接受心理治疗，或是接受治疗后进展不大，需考虑用药物进行治疗，若针对成人，药物为第一线的治疗方式[25]。加拿大及美国则是建议第一线的治疗应该是合并药物治疗及行为治疗，只有一些学龄前的儿童例外[26][27]。在所有的医学指南中，都不建议针对学龄前的儿童用兴奋剂作为第一线的治疗方式[25][27]。用兴奋剂治疗，在前十四个月的疗效有研究数据可供佐证，不过不确定长期使用的疗效[28][29][30]。患有ADHD的成人可能会发展出应对方法（英语：Coping_(psychology)），来处理因ADHD症状造成的部分或所有影响[31]。

18世纪起的医学文献中就有描述过类似注意力缺陷多动障碍的症状[32]。自1970年起，就有出现有关注意力缺陷多动障碍疾病本身、其诊断及治疗方式的争议[33]，争议和临床医生、教师、政策订定者、家长及媒体有关。争议焦点包括ADHD的病因，以及是否要用兴奋剂来治疗ADHD[34]。目前大部分的医疗人员都接受ADHD是儿童及成人的遗传性疾病，科学界的争议点则是在其诊断方式及治疗方式[35][36][37]。此疾病在1980年至1987年的正式名称是注意力缺失症（attention-deficit disorder，简称ADD），在更早期的名称是儿童过度活跃的反应（hyperkinetic reaction of childhood）[38][39]。

名称[编辑]

注意力缺陷多动障碍也译作注意力不集中/过动症（英语：Attention Deficit/Hyperactivity Disorder，简称AD/HD）、过度活跃症（英语：Hyperkinetic Disorder；于ICD 10中的名称），俗称有多动症、多动障碍及大雄·胖虎综合症（日本）等。此病患的儿童习称过动儿，也有医疗人士建议改称为心动儿。[40]

症状及体征[编辑]

ADHD的症状[41]
专注力失调 过动-冲动
  • 很难注意事情的细节
  • 不容易专注在一件事情上
  • 不容易针对事物或是活动进行规划组织
  • 会遗忘一些需要的物品
  • 在日常活动中比较健忘
  • 注意力持续时间较短，较容易分心
  • 不容易处理较具结构性的学校功课
  • 难以完成繁琐或需要花时间的任务
  • 没办法好好坐着
  • 在座位上坐立不安、动来动去
  • 会在不适当的时间点离开座位
  • 从事具风险性的事物，不太考虑后果
  • 时常处于活跃状态、精力充沛、停不下来
  • 说话的频率及时间会比其他人要多
  • 问题未说完就抢着说答案
  • 不容易轮流等候
  • 在对话中常常插嘴或是打断别人说话

注意力缺陷多动障碍的常见情形有不专心、过动（在成人则会以不安来表现）、破坏行为及冲动[42][43]。在人际关系及学业上都容易出现问题[42]，不过其症状不容易定义，因为很难介定一般情形下的不专心、过动及冲动会到什么程度，到什么情形下才需要介入治疗[44]。

依照《精神疾病诊断与统计手册》（DSM）第五版（DSM-5）的定义，注意力缺陷多动障碍的症状需出现超过六个月，或是其情形要比同年龄的要明显很多[2]，而且其症状已造成至少二个情境（例如社交、学校/工作、家庭）的问题[2]，这些条件需在12岁以前就出现[2]，若是17岁以下的，在专注力失调或是过动/冲动上的症状，至少需要有五项符合[2]。

子类型[编辑]

注意力缺陷多动障碍可分为三个子类型：ADHD注意力不足为主型（英语：Attention deficit hyperactivity disorder predominantly inattentive）（ADHD-PI或ADHD-I）、ADHD过动为主型（ADHD-PH或ADHD-HI）以及混合型（ADHD-C）[2][44]。

若是以注意力不足（专注力失调）为主的儿童或青少年，会有以下大部分甚至全部的症状，且非由其他医学疾病或药物直接造成[2][45]：

  • 容易分心、粗心、忘记事情、且经常从一件事情切换至另一件事情。
  • 很难持续专注在同一件事情上。
  • 除非进行自身有兴趣的事务，不然进行几分钟后就觉得无聊。
  • 难以对组织（规划）事情、完成一个任务保持专注。
  • 很难完成回家作业，或是如期缴交，常会遗失一些要完成作业或是其他活动需要的东西（例如铅笔、玩具、作业等）*
  • 当别人在和患者说话时，似乎没有在听对方说话。
  • 作白日梦、很感到困惑、动作缓慢。
  • 不容易像其他非注意力缺陷多动障碍患者一样，快速且准确的处理信息。
  • 难以遵从指示
  • 不容易认知细节，常忽略细节。

若是以过动为主的儿童或青少年，会有以下大部分甚至全部的症状且非由其他医学疾病或药物直接造成[2][45]：

  • 常常烦躁及坐立不安
  • 不停地讲话
  • 四处东奔西跑、碰触或玩弄视野内的任一或每一个物体。
  • 难以在上课时间、吃饭时间、做功课的时间乖乖坐好。
  • 一直在动来动去。
  • 不容易进行安静的活动或是工作。
  • 没有耐心
  • 脱口说出不恰当的话语、毫无掩饰地流露内心的想法，且行事不顾后果。
  • 难耐在游戏中因轮流所产生的等待时间。
  • 经常打断他人的对话或活动。

若注意力缺陷多动障碍患者的症状符合上述二类，则属于合并型的注意力缺陷多动障碍。

ADHD的女性比较不会有过动及冲动的症状，比较会有注意力不集中及分心的症状[46]。注意力缺陷多动障碍中有关过动的症状，可能会随着年龄增长而渐渐消退，而转变为青少年及成人阶段的“内在不安宁”[21]。

注意力缺陷多动障碍的儿童、青少年及成年比较容易有社交技巧上的问题，例如社交互动、发展友谊及建立友谊。有半数的注意力缺陷多动障碍患者曾受到同侪社会排斥的情形，而没有注意力缺陷多动障碍的人被社会排斥的比例约为10%至15%。患有注意力缺陷多动障碍的人比较不容易处理口语及非语言的讯息，比较容易在社交互动上有负面的影响，也比较容易在对话时离题、忽略到一些社交的信息、也比较不容易学习社交技能[47]。

注意力缺陷多动障碍的儿童比较常有不容易控制情绪的问题[48]，其写字（英语：handwriting）能力也比较弱[49]，在语言、说话及运动上的发展都比较晚[50][51]。虽然注意力缺陷多动障碍会造成许多的不便，不过若注意力缺陷多动障碍的儿童针对有兴趣的主题及事物，其专注力持续时间和其他儿童相当，甚至比其他儿童要好[14]。

可能有关的疾病[编辑]

在注意力缺陷多动障碍患者中，大约会有三分之二的概率会伴随其他的疾病或特征[14]。常见的共病或特征如下：

  • 癫痫[52]
  • 妥瑞症[52]
  • 自闭症谱系（ASD）：此疾病会影响社交技巧、沟通能力，也会出现固定兴趣和重复行为[52]。
  • 在注意力缺陷多动障碍患者中，较常出现有焦虑症的情形[53]。
  • 间歇性暴怒（英语：Intermittent explosive disorder）[2]
  • 在注意力缺陷多动障碍的儿童中，有20%至30%有学习障碍的情形。学习障碍可能包括发展障碍、语言障碍以及学习技巧的障碍[54]。注意力缺陷多动障碍本身不是一种学习障碍，不过常常会造成其他学业上的困难[54]。
  • 强迫症（OCD）常和注意力缺陷多动障碍一起出现，其中也有许多相同的特征[55]。
  • 智能障碍[2]
  • 反应性依附疾患（英语：Reactive attachment disorder）[2]
  • 物质使用疾患。注意力缺陷多动障碍的儿童及成人在物质滥用上的风险较高[21]。最常见的是酒或是大麻[21]。物质使用疾患的原因可能和注意力缺陷多动障碍造成的大脑回馈酬赏回路（英语：reward pathway）改变有关[21]。若注意力缺陷多动障碍和物质使用疾患一起出现，这会让注意力缺陷多动障碍的评估及治疗更加困难。如果ADHD合并“严重的”物质滥用问题，基于往后衍生的风险大小之考量，会优先治疗物质滥用问题[56][57]
  • 睡眠障碍常和ADHD一起出现。这也可能是治疗ADHD的副作用。对于注意力缺陷多动障碍的儿童而言，失眠是最常见的睡眠障碍，一般会用行为疗法来进行治疗[58][59]。 ADHD患者常伴随着不容易入睡的问题，而他们也会睡的比较熟，因此早上不容易起床[60]，有时会针对不容易入睡的儿童用褪黑素治疗[61]。
  • ADHD的患者约有50%有对立反抗症（ODD），有20%有行为规范障碍（CD）[62]，其特性是反社会的行为，例如心态固执、有攻击性、常常闹脾气（英语：temper tantrums）、说谎和偷窃等[55]。若有对立反抗症或行为规范障碍的ADHD患者，长大成人后出现反社会人格障碍的概率约有一半[63]。根据脑部造影，可确认ADHD和行为规范障碍是两种不同的疾病[64]。
  • 有关注意力的原发型疾病，其症状是注意力不佳，不容易专注，也不容易维持清醒。这类儿童常会坐立不安、打呵欠及伸展身体，这些动作看似过动，但其实是为了让自己维持警觉以及有活力的状态[65]。
  • 迟缓的认知速率（英语：Sluggish cognitive tempo）（SCT）是许多症状的总称，其中不少症状可能也包括了注意力不足的问题。在ADHD的个案中，不论其子类型如何，有30%至50%符合这些症状[66]。
  • 刻板的惯性动作症（英语：Stereotypic movement disorder）[2]
  • 情感障碍（特别是躁郁症及重度抑郁症）。诊断患有混合子类型ADHD的男孩较容易有情感障碍[53]。有ADHD的成人有时也会有躁郁症，需要很仔细的评估来诊断及治疗这两种疾病[67]。
  • 注意力缺陷多动障碍的患者较常有不宁腿综合症，一般是因为缺铁性贫血所造成[68][69]。不过不宁腿综合症也可能是注意力缺陷多动障碍症状的一部分，因此需要进行详细的诊断，区分不宁腿综合症和注意力缺陷多动障碍[70]。
  • 注意力缺陷多动障碍的患者出现夜遗尿的风险较高[71]。

有一个2016年的系统回顾发现注意力缺陷多动障碍和肥胖、哮喘及睡眠障碍有有着直接的关联，和乳糜泻和偏头痛也有一些关系[72]。不过同一年的另一篇系统回顾认为注意力缺陷多动障碍和乳糜泻没有明确关系[73]。

智力[编辑]

有研究发现患有注意力缺陷多动障碍的人其智商（IQ）测试的结果会比没有注意力缺陷多动障碍的人要低[74]，不过有关此研究结果的重要性，目前仍有争议，因为很难区分影响是因为ADHD的症状（例如分心）所造成还是ADHD本身对于智力有影响[74]。

有一份成人ADHD的研究指出有关ADHD患者在智力上的差异，没有统计上的意义，也可以用其他相关的疾病来解释[75]。

病因[编辑]

大多数注意力缺陷多动障碍（ADHD）的确切成因目前并没有定论[76][77]，目前认为最有可能是基因、环境和社会等因素相互作用导致[76][77]。有些则是因为之前孕妇或是婴儿的感染，或是婴儿脑部创伤而引起[76]。

基因遗传[编辑]

双生子研究指出此疾病常常是遗传得来的，占了所有案例的75%[78][79][80]。若一儿童的兄弟姊妹中有患有ADHD，其自己身罹患ADHD的概率，是兄弟姊妹都没有ADHD的儿童的三至四倍[81]。一般也认为基因因素会决定ADHD的症状是否会持续到成年[82]。

一般来说，ADHD和许多基因有关，特别是和会影响多巴胺神经传导的基因有关[83][84]。和多巴胺有关的有多巴胺转运体（DAT）、多巴胺受体D4（DRD4）、多巴胺受体D5（英语：DRD5）、痕量胺相关受体1（英语：TAAR1）、单胺氧化酶A（英语：MAOA）、儿茶酚-O-甲基转移酶（COMT）及多巴胺β羟化酶（DBH）[84][85][86]，其他和ADHD有关的有血清素转运体（SERT）、HTR1B（英语：HTR1B）、SNAP25（英语：SNAP25）、GRIN2A（英语：GRIN2A）、ADRA2A（英语：ADRA2A）、TPH2（英语：TPH2）及脑源性神经营养因子（BDNF）[83][84]。有一种常见的Latrophilin 3（英语：Latrophilin 3）基因变异，估计造成9%的ADHD，若有这种变异时，会对兴奋剂药物格外有反应[87]。DRD4 7R变体基因会增强多巴胺造成的抑制作用，也和ADHD有关。DRD4受体是G蛋白偶联受体，会抑制腺苷酸环化酶。DRD4-7R变异会造成许多行为上的表型，包括反映了注意力分散的ADHD症状[88]。

演化也可能是造成ADHD高比率的原因，特别是男性过动以及冲动的倾向[89]，有人曾提出假说，认为女性比较容易被会冒险的男性所吸引，因此增加了基因库中爱好冲动及冒险的基因的比率[90]。其他人则认为这种倾向有助于男性面对有压力或是危险的环境（例如更有冲劲，从事探索行为）[89][90]。在特定情境下，ADHD倾向虽然对个体是有害的，但是对群体是有益的[89][90][91]。ADHD虽然对个体可能不利，但其高比例以及异质性也有利于群体的生殖健康，并且可以增加基因库的多样性，对群体有益[91]。在特定环境下，ADHD也可能对个体有利，例如对捕食者的反应更快，以及较好的狩猎技巧（英语：Hunter vs. farmer hypothesis）等[92]。

患有唐氏综合症的人比较容易患有ADHD[93]。

环境因素[编辑]

除了基因外，一些环境因子也可能是注意力缺陷多动障碍的致病因素[94]。例如：在怀孕期间摄取酒精可能导致胎儿酒精谱系障碍，可能包括了注意力缺陷多动障碍，或是有类似症状[95]。暴露在特定有毒物质，例如：铅或多氯联苯等，可能会产生类似注意力缺陷多动障碍的中毒症状[4][96]。暴露在磷酸酯的杀虫剂毒死蜱及烷基磷酸酯（英语：Alkyl phosphate）中，也可能会增加患病的风险，不过此一论点尚未受到广泛认可[97]。在怀孕过程中吸烟，将不利于胚胎的脑部神经发育，并将增加罹患注意力缺陷多动障碍的概率[4][98]。

新生儿极度早产、体重过轻、极端疏于照料、遭受凌虐、缺乏社会的互动也会增加ADHD的风险[4][99]。母亲在怀孕期间、儿童在出生时或成长初期遭受一些疾病的感染都可能提高致病率（例如麻疹、带状疱疹、脑炎、风疹、EV71等）[100]。长时间于妊娠期间使用对对乙酰氨基酚与孩子出生后带有ADHD，有统计上的相关性[101][102]。创伤性脑损伤的儿童中，后来至少有30%有ADHD的症状[103]，其中约有5%是因为脑部损伤[104]。

一些研究发现，人工食用色素或防腐剂可能与少部分儿童出现类似ADHD的症状，或者是与ADHD的流行率增加有关[4][105]，但是这些研究的证据力薄弱，而且可能只适用于有食物敏感的孩子[105][106][107]。英国及欧洲联盟已针对这些疑虑发布相关食品管理措施[108]。对于某些食物的食物过敏或食物不耐症，可能会恶化少数孩子既有的ADHD症状[109]。

截至2018年11月，研究并不支持注意力缺陷多动障碍是因为摄取过多的精致糖、看太多电视、教养方式（英语：parenting）、贫穷或家庭吵吵闹闹所造成，不过这些可能会让一些注意力缺陷多动障碍的症状更加恶化[43]。

社会[编辑]

有些情形下，ADHD的患者不是其自身的问题，而是反映了家庭机能不全或是教育系统的不足[110]。也有一种情形，诊断出ADHD表示其他人对其课业期待的增加，因为在一些国家，诊断是一种让家长取得更多对小孩经济及教育支持的方式[104]。一般有经历过暴力或是情感虐待的儿童比较容易出现ADHD的行为[78]。

ADHD的社会建构理论（英语：social construct theory of ADHD）认为评断正常及异常的标准是社会建构的（是由社会中的所有人建立并且使其有效的，特别是医生、病患、家长、教师等），然后再主观的评估及判断要使用哪一种判据，以及有多少人会因此受到影响[111]。他们认为这是依DSM-IV标准诊断到的ADHD人数会是由ICD-10标准所诊断人数三至四倍的原因[20]。汤玛士·萨斯是ADHD社会建构理论的支持者，他认为ADHD是“发明出来的，之后取了这个名字”[112]。

班上里年龄最小的儿童比较容易诊断为ADHD，原因可能是他们的发展本来就比其他年龄略长几个月到一年的同学要晚一些[113][114][115]，在许多国家都有出现这种情形[115]，他们使用ADHD药物的比例也是其他同学的两倍左右[116]。

病理生理学[编辑]

现今的ADHD病理生理学模型认为ADHD和脑内的神经递质系统的功能障碍有关（特别是与多巴胺和去甲肾上腺素有关的部分）[117][118]。多巴胺及去甲肾上腺素的神经通道起源于腹侧被盖区及蓝斑核，投射到大脑中的不同部位，管理许多不同的认知流程[117][119]。投射到前额叶皮质及纹状体的多巴胺通道（英语：dopamine pathway）及蓝斑核-去甲肾上腺素系统（LC-NA system）会调节执行功能（认知和行为的功能与管理）、动机、酬赏的感受能力，以及运动机能[117][118][119]。这些传导通道在ADHD的病理生理学中的功能非常重要[117][119][120][121]。目前也已提议针对ADHD其他可能的神经通道建立更大规模的模型[118][120][121]。

大脑结构[编辑]

ADHD的左前额叶通常与控制组有显著不同

在儿童注意力缺陷多动障碍患者中，普遍存有一些左侧的前额叶皮质在体积上小于平均值的现象[118][122]。注意力缺陷多动障碍患者的后顶叶皮层（英语：posterior parietal cortex）也比控制组要薄[118]。其他诸如注意力缺陷多动障碍患者的：前额-纹状体-小脑和前额叶-纹状体-丘脑回路也与非注意力缺陷多动障碍患者不同[118][120][121]。

ADHD儿童的伏隔核、杏仁核、尾状核、海马体及壳核（英语：putamen）的皮质下体积都比非ADHD儿童的要小[123]。在ADHD青年的大脑中也有发现在左右半大脑中，白质径的不对称，认为颞叶整合的中断可能和ADHD的行为特征有关[124]。

神经递质的通道[编辑]

之前一度认为ADHD患者其多巴胺转运体的增加是其病理生理学的一部分，不过后来发现这可能是为了适应暴露在兴奋剂下的调整[125]，目前的模式包括了中脑皮质素-多巴胺通道（英语：mesocorticolimbic projection）及蓝斑核-去甲肾上腺素系统[117][118][119]，用于治疗注意力缺陷多动障碍的兴奋剂，其疗效可能是起因于它增进了神经递质在这些系统中的活动[118][119][126]。注意力缺陷多动障碍患者脑部中的5-羟色胺能（英语：serotoninergic）通道（与血清素有关）、谷氨酸能（英语：glutamate (neurotransmitter)）通道或是胆碱能（英语：cholinergic）通道也可能有些异常造成ADHD的症状[126][127][128]。

执行功能和动机[编辑]

注意力缺陷多动障碍的症状起因于某些执行功能上的缺陷（例如专注力、抑制控制及工作记忆等）[60][118][119][129]。执行机能是一整组的认知处理机能，这些机能是要成功选择及控制行为以达到其设定目标所必需的[60][119][129]。ADHD患者的执行机能障碍也会造成其难于维持整齐、不容易守时、过度延宕、不容易维持注意力、难以保持专注、难以忽略不相干的事物、不容易管理情绪，以及难以记住细节等问题[60][118][119]。ADHD的患者的长期记忆部分似乎没有受损，长期记忆的缺陷可能是因为工作记忆部分的受损[60][130]。ADHD的儿童及成人中，有30至50%的患者符合执行机能障碍的判据[131]。有项研究指出ADHD患者中，有80%有至少一项的执行机能不足，而没有ADHD的人只有50%有此情形[132]。由于当人成长时，大脑的成熟速度以及需要的执行机能可能会渐渐的不协调，因此有些注意力缺陷多动障碍患者可能直到青少年时期甚至是成年期（特别是成年初期）才开始显露出注意力缺陷多动障碍的症状[60]。

注意力缺陷多动障碍也与患者在儿童时期的缺乏动机相关[133]。患有ADHD的儿童常难以专注在长期的酬赏，比较容易专注在短期酬赏，而且会因为短期酬赏出现冲动的行为[133]。

诊断[编辑]

有关儿童ADHD的诊断会依照儿童的行为发展及心智发展进行评估，并且排除药物、毒品的影响，以及其他疾病及精神问题可以解释的症状[56]，一般也会考虑家长以及老师的回馈意见[12]，大多数的诊断都是因为个案的教师首先对于孩子的健康提出关切，经转介后而成[104]。注意力缺陷多动障碍可以视为是在一些所有人都有的连续性心理特征中，这些人其中有一项或几项是处于较极端的状态[134]。对于ADHD的药物反应结果，无法就此确认诊断或排除诊断。脑部影像的研究还不能在每一个人身上有一致性的结果，因此目前只用于研究用途，不用在诊断上[135]。

在美国会用《精神疾病诊断与统计手册》第五版（DSM-5）中的判据来进行诊断，欧洲国家则是用《世界通用疾病分类手册》第十版（ICD-10）的判据，若是由DSM-IV的判据进行诊断，ADHD的人数会是用ICD-10诊断人数的三至四倍[20]。注意力缺陷多动障碍分类为神经发展障碍中的一种[11][21]，也属于紊乱行为综合症（英语：disruptive behavior disorder），同属于紊乱行为综合症的疾病还有对立反抗症、行为规范障碍、反社会人格障碍[136]。若确认有注意力缺陷多动障碍，不代表有神经功能障碍（英语：neurological disorder）[78]。在诊断时，需要一并筛检其他的情形，包括焦虑、抑郁、对立反抗症、行为规范障碍、学习及语言障碍等。其他也需要评估的有其他神经发展障碍、抽动综合症及睡眠呼吸暂停等[137]。

用量化脑波（英语：quantitative electroencephalography）（QEEG）诊断超声波是目前正在研究的领域之一，然而迄今为止，脑波经过量化后的数值与ADHD之间的关系仍然不明[138][139]。美国美国食品药品监督管理局已核可用QEEG来评估是否有ADHD[140]，评估的检查用脑波中Theta波（英语：Theta wave）活动和Beta波（英语：Beta wave）活动的比例来做为诊断的基准；不过至少有五个研究都无法重现前人发现的结果[141][142]。

在诊断和评估ADHD的过程中中，也会用到自我评量表，例如ADHD评量表（英语：ADHD rating scale）及Vanderbilt ADHD诊断评量表（英语：Vanderbilt ADHD diagnostic rating scale）[143]。

诊断与统计手册（DSM）[编辑]

注意力缺陷多动障碍的诊断需由有资格的精神医学专科医生，依照一系列的判据评估后提出。在美国使用的判据是由美国精神医学学会所定义，列在精神疾病诊断与统计手册（DSM）。在DSM的判据中，注意力缺陷多动障碍可以分为以下三个子类型[2][41]：

  1. ADHD注意力不足为主型（英语：ADHD predominantly inattentive）（ADHD-PI或ADHD-I），其症状是容易分心、健忘、作白日梦、不善计划、很难专心、不容易完成一个任务[3][2]。
  2. ADHD过动为主型（ADHD-PH或ADHD-HI）的症状是过度的烦躁不安、过动、无法等待、很难一直坐在座位上、不成熟的行为，也会有破坏性的行为[3][2]。
  3. ADHD混合型（ADHD-C），混合了上述二种子类型的症状[3][2]。

上述子类型是以至少六个月出现注意力不足、过动－冲动及混合型的症状为判断基准[144]。这些症状需要在六到十二岁时就出现，而且在至少二个的环境出现（例如家庭、学校、工作）[3]。而且不符合此儿童年龄该有的情形[3][145]，而且需要有实际证据说明这已造成社交、学校或工作的相关问题[144]。

国际疾病分类（ICD）[编辑]

在世界卫生组织的《世界通用疾病分类手册》第十版（ICD-10）中，过度活跃症（hyperkinetic disorder）的症状类似DSM-5里的ADHD。若也有出现（ICD-10所定义的）行为规范障碍情形[50]，则会称为是“过度活跃行为障碍”（hyperkinetic conduct disorder）。否则，会分类为“活力和注意力的紊乱”（disturbance of activity and attention）、“其他的过度活跃症”（other hyperkinetic disorders）或“过度活跃症，无特殊症状”（hyperkinetic disorders, unspecified），后者也称为是“过度活跃综合症”（hyperkinetic syndrome）[50]。

在ICD-11的版本中，此疾病分为在6A05（注意力缺陷多动障碍）中，不再使用过度活跃症的名称[146]。

成人的注意力缺陷多动障碍[编辑]

主条目：成人注意力缺陷多动障碍

成人注意力缺陷多动障碍的诊断标准和注意力缺陷多动障碍相同，包括症状需在六岁至十二岁之间就已出现。会针对家长或监护人询问，当事人还是儿童时的行为或发展情形，也可以作为评估的参考。ADHD的家族史也对诊断有帮助[21]。成人注意力缺陷多动障碍的核心症状和儿童的相同，但其表现的方式会和儿童的不同，例如儿童时的过度身体活动，在成人时会转变成不安的感觉，以及持续性的心理活动[21]。

估计成人中有2–5%有注意力缺陷多动障碍[21]，患有注意力缺陷多动障碍的儿童，约有25–50%会持续到成人，其他的儿童在长大后症状较轻微，甚至没有症状[2][21]，据最近的研究，大部分的在成人时没有接受治疗[147]。许多有ADHD，但没有诊断出来的成年人，其生活可能会比较混乱，也有可能喝酒或是使用非处方的药品或，这些是他们适应机制的一部分[31]。其他的问题可能包括关系或是工作上的困难、以及较高的犯罪风险[21]。相关的心理健康问题包括：抑郁、焦虑症及学习障碍[31]。

有些成人ADHD的症状会和儿童的不同。例如患有ADHD的儿童可能会有过度攀爬奔跑的情形，成年人的症状可能是感觉无法放松休息，或是在社交场合中一直说话。ADHD的成人可能会出现一些寻求感官的行为，以及脾气不好。也可能会出现像物质滥用或是赌博之类的行为。DSM-IV判据没有特别为成人ADHD订定，因此受到批评，而DSM-V有专门针对成人ADHD的判据[21]。

鉴别诊断[编辑]

和ADHD症状有关的其他疾病[148]
抑郁 焦虑症 躁郁症
  • 感到无助、低自尊或不快乐
  • 对于喜好事物
    或是日常活动失去兴趣
  • 疲劳
  • 睡眠相关问题
  • 很难维持注意力
  • 食欲改变
  • 易怒及敌意
  • 对心理压力的容忍度低
  • 会想到死亡
  • 无理由的疼痛
亢奋期
抑郁期
  • 和抑郁症的症状相同

注意力缺陷多动障碍的症状，包括情绪及自尊低落、情绪波动以及易怒，类似持续性抑郁症、循环性情感症、躁郁症及边缘性人格障碍的症状[21]。有些因为焦虑症、反社会人格综合症、发展性障碍、智能迟滞或的症状也会注意力缺陷多动障碍混淆。而物质滥用造成的中毒及戒断的症状也类似ADHD的症状。有时这些疾病也可能和ADHD一起出现。另外会造成ADHD症状的疾病有甲状腺功能亢进症、癫痫、铅中毒、听觉障碍、肝病、睡眠呼吸暂停、药物相互作用、未治疗的乳糜泻、头部外伤[31][73]。

原发性的睡眠障碍可能会影响注意力及行为，而ADHD的症状也可能会影响睡眠[149]，一般会建议有ADHD的儿童也要定期评估是否有睡眠问题[150]。儿童想睡时会出现的情形从打呵欠、揉眼睛之类，也可能有过动或注意力不集中的情形[151]。阻塞性睡眠呼吸暂停也可能会有类似ADHD的症状[151]。

生物标记研究[编辑]

数篇关于ADHD生物标记的回顾性研究指出，ADHD患者的血小板单胺氧化酶表现型（expression）、尿液中的去甲肾上腺素、MHPG（英语：3-Methoxy-4-hydroxyphenylglycol）及苯乙胺浓度都和都与由“非ADHD患者”组成的对照组不同[152][153]检测上述这些项目可能可以作为是否有ADHD的诊断生理标记（diagnostic biomarkers），用来诊断ADHD，不过还需要更多研究与实验来确立这方面利用的可行性[153]。ADHD患者在尿液及血浆中的苯乙胺浓度比对照组要低，已知苯丙胺和哌甲酯会增加苯乙胺在体内的合成。特别是那些对苯丙胺和哌甲酯有反应的ADHD患者[85][152][153]。ADHD患者尿液中偏低的苯乙胺浓度与其不专心的症状相关[153]。当今的脑波检测（EEG）还不够精准，还无法用来当作诊断依据[154]。

治疗[编辑]

主条目：注意力缺陷多动障碍的治疗

注意力缺陷多动障碍的治疗方式包括心理治疗、行为治疗及药物，也有可能是用几种方式一起进行。治疗对病症会有长期的改善，但是无法完全根除病症的影响[155]。药物包括有兴奋剂、阿托莫西汀、肾上腺素受体α2（英语：alpha-2 adrenergic receptor）拮抗剂，有时也会包括抗抑郁药物[53][126]。若时无法专注在长期奖励上的人，有许多的正增强方式可以提升其工作表现[133]。ADHD药物中的兴奋剂也可以提升患者的毅力及工作表现[118][133]。

行为治疗[编辑]

有关行为治疗在ADHD上的应用，有许多良好的循证，若是针对学龄前，或是症状轻微的病患，一般会建议用行为治疗为第一线的疗法[156][157]。心理疗法包括有心理教育、行为治疗、认知行为疗法（CBT）、人际取向心理治疗、家庭治疗（英语：family therapy）、学校介入、社交技巧训练、行为方面的同侪介入、机构培训[158]、父母管理训练[78]及神经反馈（英语：neurofeedback）训练[159]。父母管理训练可以改善包括反对行为以及不合常规行为在内的一些行为问题[160]。目前还不清楚神经反馈训练是否有效[161]。

有关家庭治疗的效果，目前还很少足够品质的证据可以佐证。目前证据认为家庭治疗的效果类似群体照顾（community care），效果比安慰剂要好[162]。有许多注意力缺陷多动障碍支持组织可以提供相关信息，并且协助家庭适应ADHD的情形[163]。

有关社交技巧的训练、行为调整以及药物的对病患的好处可能有限。要减少后续心理及精神问题（例如重度抑郁症、犯罪、学校学习失败、物质使用疾患）的主要因素是和没有从事偏差行为的人建立友谊[164]。

规律的体能锻炼，特别是有氧运动，对于患有ADHD的儿童及成人而言也是有效的副加疗法（英语：adjunct therapy），特别是配合兴奋剂药物治疗时更是如此，不过针对改善症状，最理想的运动种类及强度还不清楚[165][166][167]。长期规律有氧运动对ADHD患者的好处是提升行为及运动能力、提升管控功能（包括专注、抑制控制、计划等）、较快的信息处理速度，记忆力也会比较好[165][166][167]。家长及教师针对ADHD儿童规律有氧运动对行为及以社交-情绪上的改善有：全身整体机能较佳、减少ADHD症状、自尊感较好、减少焦虑及抑郁的程度、较少身体症状、课业成绩及教室行为较佳，社交行为也有改善[165]。若在有使用兴奋剂治疗时进行运动，会增加兴奋剂药物对执行功能的影响[165]，一般认为运动的短期效果是因为运动时大脑突触多巴胺和去甲肾上腺素浓度的增加所造成[165]。

药物[编辑]

针对注意力缺陷多动障碍，可以用中枢神经刺激剂（也称为兴奋剂）药物进行治疗[168][169][已过时]，对于症状至少会有一些效果，短期而言，约有80%会有效果[34][170][169]。家长及教师反应哌甲酯比较可以改善其症状[170][34][171]，中枢神经刺激剂也可以减少ADHD儿童意外事故的风险[172]。针对ADHD的中枢神经刺激剂药物除了哌甲酯外，还有苯丙胺、甲基苯丙胺等。

针对ADHD的非中枢神经刺激剂药物有许多种，包括阿托莫西汀、安非他酮、胍法辛及可乐定，这些可以作为主要药物治疗，或是配合中枢神经刺激剂药物一起使用[168][173]。目前有关各药物之间的比较，还没有说服力足够的研究结果可以佐证，不过在副作用上似乎差不多[174]。中枢神经刺激剂药物比较可以提升课业表现，阿托莫西汀则无此效果[175]。阿托莫西汀比较不会有成瘾问题，因此若有娱乐性药物或是强迫性药物使用风险的人，比较建议使用阿托莫西汀[21]。有关药物对社交行为上的影响，目前的数据也还不充份[174]。截至2015年6月年 (2015年6月-Missing required parameter 1=month!)，还没有完全确定ADHD药物的长期影响[176][177]。核磁共振成像 研究推测长期用苯丙胺或哌甲酯治疗，会减少因为ADHD造成的大脑功能及结构异常[178][179][180]。2018年的文献回顾发现若考虑短期效果，哌甲酯对儿童最有效，苯丙胺对成人最有效[181]。

什么情形要用胍法辛治疗会依国家而不同，英国国家健康照护专业组织（英语：National Institute for Health and Care Excellence）（NICE）针对成人是第一线药物，若针对儿童，只建议在病情严重时才使用，而大部分美国的医学指南会建议可以针对各年龄层使用[26]。针对学龄前的儿童，一般不建议用药物治疗[78][182]。若治疗用的中枢神经刺激剂剂量不足，可能会有没有药效的情形[183]，这尤其常出现在青少年及成人身上，因为核可的剂量是针对学龄儿童的，因此有些医疗人员会依体重或是依其他因素给药[184][185][186]

一般而言，在正常治疗剂量的哌甲酯及中枢神经刺激剂是安全的，不过有其副作用以及禁忌症[168]。若哌甲酯给儿童及青少年使用，有研究发现这和一些严重或不严重的有害副作用有关，不过证据品质还不充份[187]。若针对儿童开立这类药物，需仔细的监测儿童的情形[187]。若ADHD的中枢神经刺激剂严重过量，可能会和兴奋性精神病（英语：stimulant psychosis）或是狂躁的症状[188]。若是治疗用的剂量，出现类似情形的概率非常低，只有0.1%，会在开始用中枢神经刺激剂药物治疗后的前几周出现[188][189][190]，若也使用抗精神病药，可以有效缓解急性苯丙胺精神病的症状[188]，若长期治疗，需要定期的监测[191]。兴奋剂的药物治疗需要定期停药，评估是否还需要用药、减少发育迟缓的情形，并且减低抗药性[192][193]。若是长期使用超过ADHD治疗剂量的兴奋剂药物滥用，一般会和成瘾及物质依赖有关[194][195]。不过未治疗的ADHD，会提高物质滥用以及行为规范障碍的风险[194]。兴奋剂药物的使用，可能可以降低风险，但也有可能没有此效果[21][176][194]。还不清楚怀孕时服用这些药物是否安全[196]。

饮食[编辑]

饮食的调整可能对少部分的ADHD儿童有帮助[197]一份2013年的元分析针对有ADHD症状，而且有补充游离脂肪酸或是减少食用有人工色素食品的儿童的相关研究发现，只有不到三分之一的儿童在症状上有改善[106]。这方面的助益有可能只是对有食物敏感的儿童有帮助，也有可能是因为这些儿童同时也在接受ADHD的治疗[106]。这些已发表的文献也发现目前已有的证据无法支持减少食用特定食物来治疗ADHD的疗法[106]。2014年发表的文献也发现排除饮食在治疗ADHD上的成效有限[109]。另一篇2016年文献回顾指出，根据研究结果，“无麸质饮食在未来成为ADHD的标准疗法”之概率是微乎其微[73]。

2017的文献回顾指出有一些排除饮食的方式对于非常小，无法用药的幼童，以及对药物没有反应的患者可能有用，不过不鼓励用补充游离脂肪酸或是减少食用有人工色素食品作为ADHD的正规治疗方式[198] 。长期铁、镁及碘等矿物质的不足可能可以让ADHD的症状加剧[199]，也有少数证据指出组织内锌含量过低和ADHD有关[200]。不过除非证实有锌不足（英语：zinc deficiency）的情形（除了发展中国家外，很少有锌不足的情形），一般不建议用锌补充剂（英语：zinc supplementation）治疗[201]。不过若锌矿物质和苯丙胺类药物同时使用的话，可以减低苯丙胺药物的最小有效剂量，也就是可以服用较少的药物而达到相同的效果[202]。另有证据指出Ω-3脂肪酸对于病情会有些许的改，不过不建议取代医学治疗[203][204]。

预后[编辑]

孩童的ADHD有30–50%的概率持续到其成人时期[22]，那些持续被ADHD影响的成人可能会在成长过程中发展出一些技巧，弥补部分ADHD的症状[31]。有ADHD的儿童与青少年相较于其他没有ADHD的儿童与青少年，其发生意外受伤等事故的风险较高[172]。ADHD药物能改善患者在生活中许多方面的功能性不足，也可以提升生活品质（英语：Quality of life (healthcare)）（例如减少意外受伤的风险），不过[205]。

流行病学[编辑]

主条目：注意力缺陷多动障碍的流行病学

注意力缺陷多动障碍是童年阶段最常见的发育疾患[206]。根据2015年发表的研究，依照DSM-III, DSM-III-R及DSM-IV的标准，国际ADHD流行率中位数，儿童为6-8%[207][15]。若使用ICD-10的标准，同年龄儿童的流行率则为1–2% [16]。

美国的成人注意力缺陷多动障碍的流行率为4-5%[208][209]。成人ADHD在台湾的流行率推估为3-4%[210]:24-25。ADHD是全球性的[211][212]。世界各地ADHD流行率的差异主要是因为世界各地使用的ADHD诊断方法不同[213]。若使用相同的诊断方法，则世界各地所得出的ADHD流行率将介于伯仲之间[214]。

在亚洲，台湾[215]、日本[216]、韩国[217]、越南[218]、中国大陆[219]、港澳[220][221]等地的未成年之ADHD流行率均介于6-8%之间。

英国和美国的ADHD诊断率和治疗率自1970年代起逐年增加至今[222]。学界的共识认为这个现象是因为诊断方法的变迁[222]以及人们逐渐愿意利用药物来治疗ADHD所致[16]，并非ADHD的流行率真的增加了[213][223]。学界共识认为，2013年起，DSM的版本从DSM 4TR 推进到 DSM 5 会使得ADHD的诊断数增加（特别是成人注意力缺陷多动障碍的诊断数） [224]。

历史及社会文化[编辑]

注意力缺陷多动障碍诊断判据、患病率及治疗的时间轴

在人类历史中很早就有出现过动的情形。1798年时苏格兰医生亚历山大·克里奇顿（英语：Alexander Crichton）在其著作《对精神紊乱的性质和起源的探究》（An inquiry into the nature and origin of mental derangement）中提到了精神不安[225][226][页码请求]。1902年，英国儿科医生George Still（英语：George Frederic Still）首次描述一项与注意力缺陷多动障碍近似的病征，出现在一系列给伦敦皇家内科医学院的教材中[227][222]。他也注意到先天及后天因素都可能会影响此疾病[228]。

Tredgold提出了脑损伤和行为问题或是学习问题之间的关联性，这种关联可以由1917年至1928年的昏睡性脑炎流行病得到验证[228][229][230]。

不同的时期，描述注意力缺陷多动障碍的名词也有所不同：在1952年的DSM-I称为微细脑功能失常（minimal brain dysfunction），在1968年的DSM-II则称为儿童活动亢进（hyperkinetic reaction of childhood），在1980年的DSM-III称为“注意力不足症，可能伴随过动，也可能没有”（attention-deficit disorder (ADD) with or without hyperactivity）[222]。在1987年的DSM-III-R更名为注意力缺陷多动障碍，，在1994年的DSM-IV将注意力缺陷多动障碍分为注意力散涣主导型（英语：Attention deficit hyperactivity disorder predominantly inattentive）、过动—冲动型以及混合型[231]。在2013年的DSM-5仍保留这三个名称[2]。其他的名词有在1930年代使用的微细脑创伤（minimal brain damage）[232]。

1934年时，Benzedrine是第一个美国许可使用，治疗注意力缺陷多动障碍的苯丙胺药物[233]哌甲酯在1950年代开始使用，而对映异构的右旋苯丙胺则是在1970年代开始使用[222]。1937年时，兴奋剂开始用在注意力缺陷多动障碍的治疗[234]。Charles Bradley给行为障碍的儿童服用Benzedrine，发现可以改善行为，也提升其课业表现[235][236]。

到1990年时，许多研究“隐约提到ADHD儿童其前额-纹状体网络较小”[237]，同一时期识别出ADHD在遗传上的特点，也认为ADHD是持续性、长期的疾病，会从儿童持续到成人时期[238]。ADHD分为目前三类的原因是因为Lahey和其同事完成的现场实验[2][239]。

在2004年时，美国参议院提出了注意力缺陷多动障碍意识之日（ADHD Awareness Day），后来演变成每年十月为注意力缺陷多动障碍意识之月（ADHD Awareness Month）[240][241]。

争议[编辑]

主条目：注意力缺陷多动障碍的争议

自1970年代开始，注意力缺陷多动障碍疾病本身、其诊断及医疗在欧美就已经是有争议性的议题[33][34][242]。争议和临床医生、教师、政策订定者、家长及媒体有关。有的观点认为注意力缺陷多动障碍是正常行为的范围内[56][243]，也有些是假定注意力缺陷多动障碍属于遗传疾病[244]。其他有关注意力缺陷多动障碍的争议包括是否可以在合理剂量范围内，对儿童用兴奋剂药物进行治疗[34][245]、诊断的方式、以及过度诊断（英语：overdiagnosis）的可能性[245]。英国国家健康照护专业组织（英语：National Institute for Health and Care Excellence）（NICE）在2009年发表声明，声明中有提及目前存在的争议，也表示：目前的治疗及诊断方式都是依照学术文献中的主流学术观点为基础[134]。2014年时，基思·康纳斯（早期推动美国大众认知注意力缺陷多动障碍的人士之一）在《纽约时报》提出他认为注意力缺陷多动障碍在美国有过度诊断的情形[246]，不过同年有一篇经过同侪审查的医学回顾性文献，表明ADHD在美国成人种群中其实有诊断不足（诊断率低于实际的患病率）的情形[23]。

ADHD的诊断率在各国家、同一国家的不同地区、种族及种群之间有着相当的差异，因此除了ADHD的患病率外，可能也有其他因素影响ADHD的诊断[247]。部分社会学家认为ADHD是将“不常见且不被广泛接受的行为”医疗化的例子，也就是将一些以往认为和医学无关的学校表现问题，用医疗的方式来处理[33][104]。在美国，大部分的医疗人员认为ADHD是真正的疾病，至少在症状较明显的人身上是这样没错[104]。而医疗人员之间仍存在的争议主要是在那些较多数，症状较轻微的病症的诊断及治疗方式[36][248][249]。有些宗教对治疗方式也会有不同的认知，例如公民人权委员会（山达基在1969年成立的反精神医学团体）曾在1980年代提出反对使用利他林的运动，目前该组织的立场仍是不主张用中枢神经刺激剂处方治疗ADHD[250]

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  185. ^ Biederman, Joseph. New-Generation Long-Acting Stimulants for the Treatment of Attention-Deficit/Hyperactivity Disorder. Medscape. 2003 [19 June 2016]. （原始内容存档于7 December 2003）. As most treatment guidelines and prescribing information for stimulant medications relate to experience in school-aged children, prescribed doses for older patients are lacking. Emerging evidence for both methylphenidate and Adderall indicate that when weight-corrected daily doses, equipotent with those used in the treatment of younger patients, are used to treat adults with ADHD, these patients show a very robust clinical response consistent with that observed in pediatric studies. These data suggest that older patients may require a more aggressive approach in terms of dosing, based on the same target dosage ranges that have already been established – for methylphenidate, 1–1.5–2 mg/kg/day, and for D,L-amphetamine, 0.5–0.75–1 mg/kg/day....
    In particular, adolescents and adults are vulnerable to underdosing, and are thus at potential risk of failing to receive adequate dosage levels. As with all therapeutic agents, the efficacy and safety of stimulant medications should always guide prescribing behavior: careful dosage titration of the selected stimulant product should help to ensure that each patient with ADHD receives an adequate dose, so that the clinical benefits of therapy can be fully attained.     
  186. ^ Kessler S. Drug therapy in attention-deficit hyperactivity disorder. Southern Medical Journal. January 1996, 89 (1): 33–8. PMID 8545689. doi:10.1097/00007611-199601000-00005. 
  187. ^ 187.0 187.1 Storebø OJ, Pedersen N, Ramstad E, Kielsholm ML, Nielsen SS, Krogh HB, Moreira-Maia CR, Magnusson FL, Holmskov M, Gerner T, Skoog M, Rosendal S, Groth C, Gillies D, Buch Rasmussen K, Gauci D, Zwi M, Kirubakaran R, Håkonsen SJ, Aagaard L, Simonsen E, Gluud C. Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents – assessment of adverse events in non-randomised studies. The Cochrane Database of Systematic Reviews. May 2018, 5: CD012069. PMID 29744873. doi:10.1002/14651858.CD012069.pub2. 
  188. ^ 188.0 188.1 188.2 Shoptaw SJ, Kao U, Ling W. Shoptaw SJ, Ali R , 编. Treatment for amphetamine psychosis. The Cochrane Database of Systematic Reviews. January 2009, (1): CD003026. PMID 19160215. doi:10.1002/14651858.CD003026.pub3. A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. In such cases, symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention ...
    About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) ...
    Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis.     
  189. ^ Adderall XR Prescribing Information (PDF). United States Food and Drug Administration. Shire US Inc. December 2013 [30 December 2013]. （原始内容存档 (PDF)于2013-12-30）. Treatment-emergent psychotic or manic symptoms, e.g., hallucinations, delusional thinking, or mania in children and adolescents without prior history of psychotic illness or mania can be caused by stimulants at usual doses. ... In a pooled analysis of multiple short-term, placebo controlled studies, such symptoms occurred in about 0.1% (4 patients with events out of 3482 exposed to methylphenidate or amphetamine for several weeks at usual doses) of stimulant-treated patients compared to 0 in placebo-treated patients. 
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  194. ^ 194.0 194.1 194.2 Malenka RC, Nestler EJ, Hyman SE. Sydor A, Brown RY , 编. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience 2nd. New York: McGraw-Hill Medical. 2009: 323, 368. ISBN 978-0-07-148127-4. supervised use of stimulants at therapeutic doses may decrease risk of experimentation with drugs to self-medicate symptoms. Second, untreated ADHD may lead to school failure, peer rejection, and subsequent association with deviant peer groups that encourage drug misuse. ... amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy (Chapter 12). Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction 
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  216. ^ Domenic Greco, PhD. Is Prevalence of ADD/ADHD the Same in the U.S., Europe, and Japan?. 2012-09-10 [2017-04-22]. （原始内容存档于2012-09-10）. Japan reports a 7% of school-aged children have ADD/ADHD. 
  217. ^ Park, Subin; Cho, Maeng Je; Chang, Sung Man; Jeon, Hong Jin; Cho, Seong-Jin; Kim, Byung-Soo; Bae, Jae Nam; Wang, Hee-Ryung; Ahn, Joon Ho; Hong, Jin Pyo. Prevalence, correlates, and comorbidities of adult ADHD symptoms in Korea: Results of the Korean epidemiologic catchment area study. Psychiatry Research (Elsevier BV). 2011, 186 (2-3): 378–383 [2017-04-21]. doi:10.1016/j.psychres.2010.07.047. In the National Comorbidity Survey Replication, 4.4% of 3199 subjects aged 18 to 44 years met the DSM-IV criteria for ADHD (Kessler et al., 2006). The acceptance of ADHD symptoms in adults, because the prevalence rates of ADHD in Korean school-age children are similar to the rates reported in Western countries (Kim, 2002). 
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  250. ^ 亚洲不应使用西方精神科对于注意力缺陷多动障碍（ADHD）的诊断，及兴奋剂处方的治疗 互联网档案馆的存档，存档日期2017-09-02.

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