motor delay

电机延迟
  • 文章类型: Journal Article
    帕金森病(PD)是一种普遍的神经退行性疾病,由于多巴胺的减少而发生在老年,导致神经细胞破坏.这种疾病很难诊断,因为它的症状与衰老过程的症状相似。患有PD的人的运动控制和功能受损,运动障碍,和颤抖。为了治疗PD,增加给予大脑多巴胺量的药物用于缓解症状。本调查检查了罗替戈汀的处方以实现这一目标。这篇综述的主要目的是研究罗替戈汀在PD晚期和早期的使用。审查中使用的统计模型发现,晚期和早期PD患者的罗替戈汀处方剂量没有显着差异,然而,有一些混杂变量可能扭曲了这一结果;因此,需要进一步的研究来验证或取消这一假设。
    Parkinson\'s disease (PD) is a prevalent neurodegenerative disorder that occurs in old age due to a decrease in dopamine, which causes nerve cell destruction. This disease is difficult to diagnose since its symptoms are similar to those of the aging process. Those with PD have impaired motor control and function, dyskinesia, and tremors. To treat PD, drugs that enhance the amount of dopamine given to the brain are administered to alleviate symptoms. This inquiry examines the prescription of rotigotine to achieve this objective. The primary objective of this review is to examine the usage of rotigotine in both the late and early stages of PD. The statistical model utilized in the review found that there was not a significant difference in the dosage of rotigotine prescribed to late and early-stage PD patients, however, there were some confounding variables that may have skewed this result; therefore, further research is necessary to validate or nullify this hypothesis.
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  • 文章类型: Systematic Review
    UNASSIGNED:系统研究早期运动干预对1岁以下有运动发育障碍或有运动延迟风险的婴儿运动和运动发育的影响。
    UNASSIGNED:2000年1月至2021年9月的相关文献是通过搜索PubMed,Embase,科克伦,Pedro和WebofScience数据库。选择标准包括在12个月校正年龄之前开始的干预措施。方法学质量采用AACPDM标准进行评估,Mallen评分和Cochrane偏倚风险方法。使用PRISMA方案(PICO方法)和AMSTAR-2进行评价程序。这篇综述已在PROSPERO(CRD42021286445)中预先注册。
    UNASSIGNED:十篇文章符合纳入标准;七篇文章具有中等到强的方法学质量。干预措施包括跑步机训练(n=3),爬行训练(n=1),“肚子时间”(n=1),采用新生儿发育计划(n=1)或Bobath方法(n=1)进行物理治疗,跑步机训练结合积极的腿部运动(n=2)或Bobath理疗(n=1)。从该综述中得出的有效干预措施的三个关键特征是:(1)婴儿残疾或延迟风险明确;(2)该方案是标准化的,易于复制;(3)婴儿需要主动运动。
    UNASSIGNED:迫切需要进行更多高质量的研究,研究早期运动干预对有一系列残疾或延迟风险的婴儿的粗大运动和运动发育的影响。概述了未来研究的建议。
    UNASSIGNED: To systematically examine the effect of early motor interventions on motor and locomotor development in infants <1 year of age with motor developmental disability or at risk of motor delay.
    UNASSIGNED: Pertinent literature from January 2000 to September 2021 was identified by searching the PubMed, Embase, Cochrane, Pedro and Web of Science databases. Selection criteria included interventions starting before 12 months corrected age. Methodological quality was assessed with AACPDM criteria, Mallen score and Cochrane risk of bias methodology. Evaluation procedure was performed using PRISMA protocol (PICO approach) and AMSTAR-2. This review was preregistered in PROSPERO (CRD42021286445).
    UNASSIGNED: Ten articles met the inclusion criteria; seven had moderate to strong methodological quality. The interventions included treadmill training (n = 3), crawling training (n = 1), \"tummy time\" (n = 1), physical therapy with neonatal developmental program (n = 1) or Bobath approach (n = 1), treadmill training combined with active leg movements (n = 2) or Bobath physiotherapy (n = 1). The three key characteristics of effective interventions that emerged from the review were: (1) the infants\' disability or risk of delay was well-defined; (2) the protocol was standardized and easy to replicate; (3) infants were required to make active movements.
    UNASSIGNED: There is an urgent need for additional high-quality studies on the effects of early motor interventions on the gross motor and locomotor development of infants with a range of disabilities or risks for delay. Suggestions for future research are outlined.
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  • 文章类型: Case Reports
    Cutis laxa is a set of genetically heterogeneous conditions with phenotypes ranging from progeria-like appearance, corneal clouding, clenched fingers with marked retardation of growth both pre and postnatal growth to very mild phenotypes with skin laxity becoming evident in 2nd or 3rd decade. A child who presents with predominant motor delay is written off with a clinical diagnosis of rickets in the absence of any clinical sign of lax skin. Here, we report a 2-year-old child who presented with motor delay and joint hyperlaxity. Mutation analysis demonstrated a heterozygous mutationc.G1867A in the exon 15 of ALDH18A1 gene known to cause autosomal dominant cutis laxa.
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