要解释运动障碍的症状学，有必要了解 电机系统控制的层次结构。

  • 刚性
  • 肌张力障碍。
  • 痉挛。
金字塔主义。
19955111 {19955111:EGBWNQFK} 1 温哥华 50 默认 4970 https://neuropediatoolkit.org/wp-content/plugins/zotpress/
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1.
桑格 TD，德尔加多 MR，盖布勒-斯皮拉 D，哈雷特 M，明克 JW。导致儿童期肌张力增高的疾病的分类和定义。儿科[互联网]。 2003 年 1 月 1 日[引用于 2016 年 1 月 21 日]；111(1)：e89–97。可从： http://pediatrics.aappublications.org/cgi/doi/10.1542/peds.111.1.e89
探索技术。

为了评估高张关节，临床医生应询问父母对异常张力和不自主运动的描述，包括运动是在活动时还是在休息时发生，以及是否存在特定的触发运动或任务特异性。观察休息时的姿势以及四肢相对于重力的位置。如果可能的话，观察孩子躺着、坐着、走路和跑步的情况。如果投诉包括对特定活动或任务的反应异常表现或姿势，则应在执行受影响的任务时观察孩子。应注意任何异常固定、扭曲或重复的姿势，以及功能限制的程度。

应对每个待测试的接头进行以下观察。认识到焦虑对语气的影响，孩子在检查期间应尽可能放松，并且应支撑被检查的身体部位以抵抗重力。头部应保持在中线，以避免颈部强直反射影响音调。另外，如果仰卧，那么头部和躯干应该得到舒适的休息。

  1. 触诊肌肉以确定休息时是否发生收缩。
  2. 如果可能的话，在孩子仰卧、坐着、站立以及注意力分散的情况下测量受影响关节的运动阻力。
  3. 以极慢（3 秒完成运动）、中速（0.5 秒完成运动）和快速（尽可能快）的速度测量被动运动范围。注意运动开始时的阻力、运动开始后某个时间是否出现“卡住”，以及发生卡住的关节角度。
  4. 以慢、中、快的速度在运动方向上进行突然反转，并注意反转时（表明共同收缩）或之后一段时间（表明痉挛）是否存在阻力增加，以及任何速度依赖性。
  5. 指导孩子移动对侧的同一关节，观察是否有不自主的运动，然后测试对缓慢、被动运动的阻力的变化。指导儿童在对侧移动远处且不相关的关节（例如，通过打开和闭合 1 个拳头），然后在同侧移动，并观察是否有不自主运动或被动运动阻力的变化。
运动不足的症状。
  • 无力（肌肉激活不足）。区分不同的情况很重要 肌肉无力 的 锥体无力.
  • 选择性运动控制减少（无法激活特定的肌肉模式）。
  • 共济失调（运动过程中无法激活正确的肌肉模式）。
  • 发育性失用症和运用障碍（无法激活正确的肌肉模式来执行任务，以任务为导向）。
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1.
Sanger TD、Chen D、Delgado MR、Gaebler-Spira D、Hallett M、Mink JW 等。童年时期负面运动迹象的定义和分类。儿科[互联网]。 2006 年 11 月 1 日[引用于 2016 年 1 月 21 日]；118(5):2159–67。可从： http://pediatrics.aappublications.org/content/118/5/2159
疾病 多动症.
  • 肌张力障碍。
  • 韩国。
  • 手足徐动症。
  • 肌阵挛。
  • 摇晃。
  • 抽搐。
  • 刻板印象。
19955111 {19955111:3FZKVE28} 1 温哥华 50 默认 4970 https://neuropediatoolkit.org/wp-content/plugins/zotpress/
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1.
Sanger TD、Chen D、Fehlings DL、Hallett M、Lang AE、Mink JW 等。儿童期多动运动的定义和分类。莫夫混乱[互联网]。 2010 年 8 月 15 日[引用于 2015 年 6 月 15 日]；25(11):1538–49。可从： http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929378/
运动机能减退症（帕金森症）。
帕金森病亚型根据4轴定义

一、发病年龄a

二.临床特征

三．结果

四．病因学
发育性帕金森症I. 婴儿期或幼儿期

二.肌张力低下、运动功能减退、运动迟缓、姿势发育紊乱、GDD、静止性震颤或其他粗大振荡性抽搐、症状周期性波动、自主神经功能障碍、OGC、胎儿运动模式持续存在

三．对多巴胺能药物和/或生物胺前体的持续反应。早期治疗受试者的神经系统发育正常，晚期治疗受试者中不同程度的 ID（伴或不伴 MD），未治疗/晚期治疗受试者中的非退行性进展

四．原发性神经递质疾病（例如 TH、SR、AADC、PTPS 缺乏）
婴儿和幼儿期退行性帕金森病I. 婴儿期或幼儿期

二.严重僵硬性运动减退综合征、多灶性肌阵挛性抽搐或粗大振荡性抽搐、肌张力障碍、姿势发育缺乏、进行性 GDD、自主神经功能障碍、OGC

三．最初对多巴胺能药物产生剧烈反应，随后因WARS2缺陷而反应恶化。没有针对 DAT 缺乏症的治疗方法。 DaTSCAN 成像的显着变化也记录了进展过程

四．原发性或继发性神经递质疾病（例如 DAT、WARS2 缺乏症）
神经发育障碍背景下的帕金森症一、童年至青春期

二.早发性神经发育障碍（GDD、ID），随后随着时间的推移出现帕金森病特征。癫痫经常与

三．随着时间的推移没有明显的进展。可能出现回归稳定阶段

四．神经发育障碍（例如 MECP2)
多系统脑疾病背景下的帕金森症一、童年至青春期

二.与多系统大脑受累体征相关（痉挛、共济失调、肌阵挛、肌张力障碍、舞蹈症、认知衰退/痴呆、癫痫等）。表型可能由与帕金森病相关的其他特征主导

三．随着时间的推移，与特定脑成像异常或代谢改变相关的进展

四．涉及多系统的神经退行性或神经代谢性疾病（参见 表2, 表S1 获取条件列表）
青少年帕金森症和肌张力障碍帕金森症I. 童年（很少）、青春期

二.以帕金森病为主要表现，主要表现为非典型帕金森病，伴或不伴肌张力障碍、肌阵挛和认知能力下降

三．左旋多巴反应、运动并发症的发生和帕金森病体征的进展可能会根据特定的遗传状况而有所不同（例如，左旋多巴反应良好的患者） DNAJC6, 同步J1, 粉红1，无响应 PRKRA, ATP1A3; 早期发动机并发症 帕金 和 粉红1;进展缓慢 同步J1, 快速进展 DNAJC6)

四．原发性肌张力障碍或单基因帕金森症基因（例如 PRKRA, ATP1A3, 帕金, 粉红1, SYNJ1、DNAJC12、DNAJC6)
获得性帕金森病一、童年至青春期

二、三。临床特征和结果因病因而异

四．窒息、感染、免疫介导疾病、中毒、药物、肿瘤、甲状旁腺功能减退症和假性甲状旁腺功能减退症、脑积水（参见 表3, 表S2)
19955111 {19955111:34LMYZKM} 1 温哥华 50 默认 4970 https://neuropediatoolkit.org/wp-content/plugins/zotpress/
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