摘要
目的:在全面分析临床资料的基础上揭示注意缺陷多动障碍(ADHD)的中医证候规律和病机核心。方法:采取横断面回顾性研究方法,对符合研究标准的170例初次就诊的ADHD患儿进行6个方面的临床因素调查和分析。结果:中医证型分布显示以肾精不足、脑髓失养型为主,而无证可辨型与肾虚肝旺、阴虚阳亢型所占比例相当;中医证型分布与疾病严重程度呈显著正相关趋势(P<0.01);西医亚型与中医证型分布呈显著正相关趋势(P<0.01)。结论:ADHD病位在脑,核心病机是肾虚、脑髓不充、发育落后;中医证候分型可能与西医亚型有特定对应关系;在"肾系"辨证中,与先天不足关系最为密切的ADHD两类证型:肾精不足、脑髓失养型和肾虚肝旺、阴虚阳亢型之间可能并非是平行的关系,而是一种具有逻辑顺序的前后发展关系,而最早期有可能表现为无证可辨型,在同一脏腑体系中(本研究即"肾系")各证型间的转化趋势体现了本病的中医证候变化规律。
Objective: On the basis of comprehensive analysis of clinical data,TCM syndrome and pathogenesis of attention deficit hyperactivity disorder(ADHD) were revealed.Methods: Cross-sectional retrospective study method was used.6 aspects of clinical factors survey and analysis were used to 170 patients initially diagnosed as ADHD.Results: Distribution of TCM showed Syndromes of deficiency of the kidney essence,brain and marrow is not enough,and syndromeless differentiation and liver and kidney hyperactivity of yang due to yin deficiency type proportion quite;distribution of TCM syndromes and disease severity was positively related(P0.01);western medicine subtypes with Chinese medicine syndrome type distribution showed significant positive correlation(P0.01).Conclusion: ADHD disease lies in brain.The pathogenesis is hypokidney,brain and marrow are not enough,and the patients are not fully developed;the traditional Chinese medicine syndromes may be associated with western medicine subtype;in kidney system differentiation,there are two kinds of syndromes most closely related to ADHD: kidney essence deficiency,brain dystrophy type and hypokidney and hyperliver,hyperactivity of yang due to yin deficiency type may not have parallel relationship,but a logical time sequence,and may behave early as syndromeless type.In the same organ system(in this study"kidney"),various types of transformation trend reflected the change of TCM syndromes.
出处
《中医儿科杂志》
2012年第5期36-39,共4页
Journal of Pediatrics of Traditional Chinese Medicine
基金
天津市高等学校科技发展基金项目(20050316)
关键词
注意缺陷多动障碍
证候规律
病机
attention deficit hyperactivity disorder
rule of TCM syndrome
pathogenesis