Article(id=1322912262389891696, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.01.005, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793336461874, onlineDateStr=2026-10-30, pubDate=1736438400000, pubDateStr=2025-01-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793336461874, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793336461874, creator=13701087609, updateTime=1793336461874, updator=13701087609, issue=Issue{id=1322912162913596032, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='1', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1736438400000', pubDateStr='2025-01-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793336438157, creator='13701087609', updateTime=1793340633627, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322929760048906989, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322929760048906990, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322912162913596032, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=24, endPage=34, ext={EN=ArticleExt(id=1322912262909985393, articleId=1322912262389891696, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Acupuncture Syncope’s Neural Mechanism,Classification and the Tradeoff of Its Safety and Efficacy, columnId=1317115241041875867, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Overseas Qihuang Forum, runingTitle=null, highlight=null, articleAbstract=

Acupuncture syncope(commonly know as needle fainting),long considered an adverse event to be prevented,has been found to result in rapid recovery for almost all patients with appropriate management. Some patients even experience“significant”therapeutic effects after fainting. Though the mechanism of acupuncture syncope and its potential benefits have not been thoroughly investigated,this article,based on reviews of extensive literature on acupuncture syncope(case reports,surveys,and systematic reviews)and recent research on vasovagal syncope,supports the notion that acupuncture syncope is not harmful. It raises a novel point that acupuncture syncope is actually a form of vasovagal syncope rather than shock. The pathophysiological basis of acupuncture syncope includes patientsusceptibility to syncope,arterial baroreflex dysfunction or instability,and vasovagal responses triggered by psychological stress,postural stress,and particularly acupuncture(somatic nerve stimulation). Based on its neurological mechanism,acupuncture syncope can be classified into three types. Type Ⅰ(psychological stress type)occurs immediately before and after the needle is inserted. Type Ⅱ(sympathetic triggering type)is further divided into progressive sympathetic activation type(Type Ⅱ a)and inhibitory type(Type Ⅱ b). The sympathetic excitability of this type is initially high,which further increases under needle stimulation before suddenly or gradually decreasing,leading to fainting. Type Ⅲ(vagus-triggered type)is induced by directly stimulating vagalafferentatsome special parts of the body (e.g.,the auricular region). The article proposes that the significant therapeutic effects experienced by some fainting patients(mainly Types Ⅱ and Ⅲ)are related to the strong stimulation of acupuncture and the fainting itself,which strongly activate the hypothalamic-pituitary-adrenal axis,cholinergic vagal anti-inflammation pathways,and reset disease homeostasis. For patients susceptible to syncope,clinicians should mitigate psychological stress and administer light acupuncture stimulation in the supine position when needed. When pre-syncope symptoms occur,preventing falls and should be the first priority. Unless syncope persists,additional needle insertion is unnecessary,though existing needles may be retained for the duration of treatment. For patients who have not responded to previous acupuncture treatments,clinicians might consider intentionally selecting more sensitive acupoints and applying more intensive stimulation at an orthostatic posture to induce syncope. This approach aims to achieve a more effective treatment outcome. In essence,clinical management should consider the trade off between ensuring patient safety and maximizing treatment efficacy.

, authors=Guanyuan JIN, authorsList=Guanyuan JIN, authorCompany=null, correspAuthors=null, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1322912265724363386, articleId=1322912262389891696, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=晕针的神经机制、分型与利弊权衡, columnId=1317115241377420189, journalTitle=中华中医药学刊, columnName=海外岐黄论坛, runingTitle=null, highlight=null, articleAbstract=

长期以来,晕针一直被视作不良事件加以防范,但几乎所有患者在适当处置后都会快速复原,而且部分患者甚至晕针后“获大效”,对晕针及其起效的机制未曾深究。通过回顾迄今为止的大量晕针文献(个案、调查与系统评论)及血管迷走性晕厥的最新研究,支持晕针虽属不良反应但“不伤人”的认知,赞同晕针属于血管迷走性晕厥,而非休克。患者的晕厥易感性,动脉压力感受性反射障碍或不稳定性,心理应激、体位应激尤其合并针灸(躯体神经刺激)激发的血管迷走性反应,是晕针的病理生理学基础。按其神经机制,晕针可分为三种类型:Ⅰ型(心理应激型),在进针前后立即发生。Ⅱ型(交感触发型),它进而分为渐进性交感神经激活型(Ⅱa型)与抑制型(Ⅱb型)。该型的交感兴奋性较高,在针刺作用下进一步提高再突然或逐渐下降,导致晕针。Ⅲ型(迷走触发型),针刺一些特殊部位(如耳甲区)激发迷走传入诱导的晕针。进一步提出晕针患者(主要是Ⅱ、Ⅲ型)“获大效”的原理离不开针灸刺激(多半为强刺激)乃至晕针本身强烈激发下丘脑-垂体-肾上腺轴、胆碱能迷走抗炎机制,以及对疾病稳定态的再设置。由此,一方面对晕针易感人群可特别关注,包括消除紧张情绪,治疗取卧位,轻刺激;出现晕针先兆时,以防范跌倒损伤为首位;除非晕厥持续,无须再施针,但也可以继续留针。另一方面,对于敏感性低、久治无效的患者,则可以有意在身体敏感部(穴)位采取较强的刺激手段,同时取容易晕针的直立(坐)体位,寻求转机。换言之,应该在保证晕针“不伤人”与期待“获大效”目标之间作出临床权衡。

, authors=金观源, authorsList=金观源, authorCompany=null, correspAuthors=null, authorNote=

金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

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金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

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金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

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注:PVN:室旁核;NTS:孤束核;CVLM:尾侧腹外侧延髓;RVLM:头端腹外侧延髓;DMNX:迷走神经背侧运动核;NM:疑核;IX:舌咽神经;Xa:迷走神经传入;Xe:迷走神经传出;Symp.N:交感神经。

, figureFileSmall=4cWoC9cmm2s47Bom96AOpw==, figureFileBig=+phJnLeqggGppnrJTynLNA==, tableContent=null), ArticleFig(id=1322912550911877349, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=EN, label=null, caption=null, figureFileSmall=DInAkx0fDGOsnZe+6S9fDA==, figureFileBig=04lTiTniUnMJiNHc3+DI8g==, tableContent=null), ArticleFig(id=1322912551033512166, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=CN, label=图2, caption=晕针的应激刺激与压力感受性反射的调制, figureFileSmall=DInAkx0fDGOsnZe+6S9fDA==, figureFileBig=04lTiTniUnMJiNHc3+DI8g==, tableContent=null), ArticleFig(id=1322912551150952679, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=EN, label=null, caption=null, figureFileSmall=4ZOTR7iPnC+5eABU8XVGug==, figureFileBig=On+LHLl3H6grb+Q1ROhWsQ==, tableContent=null), ArticleFig(id=1322912551264198888, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=CN, label=图3, caption=晕针的临床及机制分型, figureFileSmall=4ZOTR7iPnC+5eABU8XVGug==, figureFileBig=On+LHLl3H6grb+Q1ROhWsQ==, tableContent=null), ArticleFig(id=1322912551436165353, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=EN, label=null, caption=null, figureFileSmall=shYI1O9H6fkB5+c0dAHXMA==, figureFileBig=olWtkuupk0nNGvwE2H/EgA==, tableContent=null), ArticleFig(id=1322912551595548906, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=CN, label=图4, caption=浮针皮下扫散刺激穿支血管(改画自陶凯,2016), figureFileSmall=shYI1O9H6fkB5+c0dAHXMA==, figureFileBig=olWtkuupk0nNGvwE2H/EgA==, tableContent=null), ArticleFig(id=1322912551750738155, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
作者作者所在地研究时间(年.月)研究方法晕针场合针刺次数/研究人数/文献数目晕针例数晕针发生率/(%)危及生命例数文献来源发表年
金观源中国1972—1977回顾研究针刺治疗30 000次310.10[7]1981
金观源美国1990—2000前瞻研究针刺治疗30 000次30.010[45]2003
CHEN F P等中国台北1988.8—1989.4回顾研究针刺治疗28 385次/2855人54次/520.190[12]1990
罗致宁等中国2011.3—9回顾研究体检采血6157人230.370[43]2013
2012.3—9前瞻研究6519人30.050
LIN J T等美国1973—1977.6回顾研究献血262 935人8240.350[42]1982
1977.6—1978.5前瞻研究70 000人840.120
UMLAUF R捷克1975—1988业者调查针刺治疗140 000次0.280[35]1988
YONG D等新加坡1995.9—1996.5回顾研究针刺治疗12 172次/1128人20.02/0.180[31]1999
ERNSR E等英国—1997系统评论针刺治疗9项调查0~0.30[37]2001
MACPHERSON H等英国2000业者调查针刺治疗34 407次120.030[34]2001
LAO L等美国1972—1991系统评论针刺治疗英文文献60[38]2003
MELCHART D等德国,瑞士2001.7—2002.4前瞻研究针刺治疗97 733人10[32]2004
XU G P等中国1998.4—2007.4回顾研究针刺治疗820[33]2007
HE W等中国1956—2010系统评论针灸拔罐28篇中文文献4680[39]2012
ZHANG J H等中国1980—2009系统评论针刺治疗6篇中文文献1890[40]2014
WU J Y等中国1980—2013系统评论针刺治疗12篇文献180[36]2015
ZHANG Y等莱索托王国2017.10—2018.4回顾研究针刺治疗2050人20.100[13]2020
XU M等中国—2022.6映射评论针刺治疗86项系统评论0[41]2023
), ArticleFig(id=1322912551918510316, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322912262389891696, language=CN, label=表1, caption=

1956年至今世界各地报道的晕针发生率与结局

, figureFileSmall=null, figureFileBig=null, tableContent=
作者作者所在地研究时间(年.月)研究方法晕针场合针刺次数/研究人数/文献数目晕针例数晕针发生率/(%)危及生命例数文献来源发表年
金观源中国1972—1977回顾研究针刺治疗30 000次310.10[7]1981
金观源美国1990—2000前瞻研究针刺治疗30 000次30.010[45]2003
CHEN F P等中国台北1988.8—1989.4回顾研究针刺治疗28 385次/2855人54次/520.190[12]1990
罗致宁等中国2011.3—9回顾研究体检采血6157人230.370[43]2013
2012.3—9前瞻研究6519人30.050
LIN J T等美国1973—1977.6回顾研究献血262 935人8240.350[42]1982
1977.6—1978.5前瞻研究70 000人840.120
UMLAUF R捷克1975—1988业者调查针刺治疗140 000次0.280[35]1988
YONG D等新加坡1995.9—1996.5回顾研究针刺治疗12 172次/1128人20.02/0.180[31]1999
ERNSR E等英国—1997系统评论针刺治疗9项调查0~0.30[37]2001
MACPHERSON H等英国2000业者调查针刺治疗34 407次120.030[34]2001
LAO L等美国1972—1991系统评论针刺治疗英文文献60[38]2003
MELCHART D等德国,瑞士2001.7—2002.4前瞻研究针刺治疗97 733人10[32]2004
XU G P等中国1998.4—2007.4回顾研究针刺治疗820[33]2007
HE W等中国1956—2010系统评论针灸拔罐28篇中文文献4680[39]2012
ZHANG J H等中国1980—2009系统评论针刺治疗6篇中文文献1890[40]2014
WU J Y等中国1980—2013系统评论针刺治疗12篇文献180[36]2015
ZHANG Y等莱索托王国2017.10—2018.4回顾研究针刺治疗2050人20.100[13]2020
XU M等中国—2022.6映射评论针刺治疗86项系统评论0[41]2023
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晕针的神经机制、分型与利弊权衡
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中华中医药学刊 | 海外岐黄论坛 2025,43(1): 24-34
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晕针的神经机制、分型与利弊权衡
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金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

"}, bioImg=null, bioContent=

金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

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金观源
作者信息
  • 美国国际系统医学研究所,美国 威斯康星州 53045
作者简介:

金观源(1949-),男,浙江杭州人,教授,威州执照针灸师,神经生理学家,美国中医博士班导师,博士,研究方向:系统医学、针灸基础及临床。

Acupuncture Syncope’s Neural Mechanism,Classification and the Tradeoff of Its Safety and Efficacy
Guanyuan JIN
Affiliations
  • International Institute of Systems Medicine, WI 53045, USA
出版时间: 2025-01-10 doi: 10.13193/j.issn.1673-7717.2025.01.005
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长期以来,晕针一直被视作不良事件加以防范,但几乎所有患者在适当处置后都会快速复原,而且部分患者甚至晕针后“获大效”,对晕针及其起效的机制未曾深究。通过回顾迄今为止的大量晕针文献(个案、调查与系统评论)及血管迷走性晕厥的最新研究,支持晕针虽属不良反应但“不伤人”的认知,赞同晕针属于血管迷走性晕厥,而非休克。患者的晕厥易感性,动脉压力感受性反射障碍或不稳定性,心理应激、体位应激尤其合并针灸(躯体神经刺激)激发的血管迷走性反应,是晕针的病理生理学基础。按其神经机制,晕针可分为三种类型:Ⅰ型(心理应激型),在进针前后立即发生。Ⅱ型(交感触发型),它进而分为渐进性交感神经激活型(Ⅱa型)与抑制型(Ⅱb型)。该型的交感兴奋性较高,在针刺作用下进一步提高再突然或逐渐下降,导致晕针。Ⅲ型(迷走触发型),针刺一些特殊部位(如耳甲区)激发迷走传入诱导的晕针。进一步提出晕针患者(主要是Ⅱ、Ⅲ型)“获大效”的原理离不开针灸刺激(多半为强刺激)乃至晕针本身强烈激发下丘脑-垂体-肾上腺轴、胆碱能迷走抗炎机制,以及对疾病稳定态的再设置。由此,一方面对晕针易感人群可特别关注,包括消除紧张情绪,治疗取卧位,轻刺激;出现晕针先兆时,以防范跌倒损伤为首位;除非晕厥持续,无须再施针,但也可以继续留针。另一方面,对于敏感性低、久治无效的患者,则可以有意在身体敏感部(穴)位采取较强的刺激手段,同时取容易晕针的直立(坐)体位,寻求转机。换言之,应该在保证晕针“不伤人”与期待“获大效”目标之间作出临床权衡。

晕针  /  血管迷走性晕厥  /  神经机制  /  分型  /  不良反应  /  安全性  /  疗效  /  临床权衡

Acupuncture syncope(commonly know as needle fainting),long considered an adverse event to be prevented,has been found to result in rapid recovery for almost all patients with appropriate management. Some patients even experience“significant”therapeutic effects after fainting. Though the mechanism of acupuncture syncope and its potential benefits have not been thoroughly investigated,this article,based on reviews of extensive literature on acupuncture syncope(case reports,surveys,and systematic reviews)and recent research on vasovagal syncope,supports the notion that acupuncture syncope is not harmful. It raises a novel point that acupuncture syncope is actually a form of vasovagal syncope rather than shock. The pathophysiological basis of acupuncture syncope includes patientsusceptibility to syncope,arterial baroreflex dysfunction or instability,and vasovagal responses triggered by psychological stress,postural stress,and particularly acupuncture(somatic nerve stimulation). Based on its neurological mechanism,acupuncture syncope can be classified into three types. Type Ⅰ(psychological stress type)occurs immediately before and after the needle is inserted. Type Ⅱ(sympathetic triggering type)is further divided into progressive sympathetic activation type(Type Ⅱ a)and inhibitory type(Type Ⅱ b). The sympathetic excitability of this type is initially high,which further increases under needle stimulation before suddenly or gradually decreasing,leading to fainting. Type Ⅲ(vagus-triggered type)is induced by directly stimulating vagalafferentatsome special parts of the body (e.g.,the auricular region). The article proposes that the significant therapeutic effects experienced by some fainting patients(mainly Types Ⅱ and Ⅲ)are related to the strong stimulation of acupuncture and the fainting itself,which strongly activate the hypothalamic-pituitary-adrenal axis,cholinergic vagal anti-inflammation pathways,and reset disease homeostasis. For patients susceptible to syncope,clinicians should mitigate psychological stress and administer light acupuncture stimulation in the supine position when needed. When pre-syncope symptoms occur,preventing falls and should be the first priority. Unless syncope persists,additional needle insertion is unnecessary,though existing needles may be retained for the duration of treatment. For patients who have not responded to previous acupuncture treatments,clinicians might consider intentionally selecting more sensitive acupoints and applying more intensive stimulation at an orthostatic posture to induce syncope. This approach aims to achieve a more effective treatment outcome. In essence,clinical management should consider the trade off between ensuring patient safety and maximizing treatment efficacy.

acupuncture syncope  /  vasovagal syncope  /  neural mechanism  /  classification  /  adverse event  /  safety  /  efficacy  /  trade off
金观源. 晕针的神经机制、分型与利弊权衡. 中华中医药学刊, 2025 , 43 (1) : 24 -34 . DOI: 10.13193/j.issn.1673-7717.2025.01.005
Guanyuan JIN. Acupuncture Syncope’s Neural Mechanism,Classification and the Tradeoff of Its Safety and Efficacy[J]. Chinese Archives of Traditional Chinese Medicine, 2025 , 43 (1) : 24 -34 . DOI: 10.13193/j.issn.1673-7717.2025.01.005
晕针现象在针灸临床上并不罕见。因为它发生突然,来势似乎凶险,自古至今大多数针灸学教材一直把晕针放置在针灸异常情况或者说不良反应范畴,加以防范。虽然对其发生机制的认识及处置措施已有一个逐步深化的过程,但仍不能适应发展现代针灸的需要。
据明代《针灸大成》记载:“凡针晕者,神气虚也,不可起针,急以别针补之,用袖掩病人口鼻回气,内与热汤饮之即苏,良久再针。甚者,针手膊上侧筋骨陷中,即虾蟆肉上惺惺穴,或足三里穴,即苏。若起针,坏人”[1],这反映了古人对晕针机制的原始认知,并且以“气之补泻”论述其处置措施。其中“不可起针,急以别针补之,用袖掩病人口鼻回气”多与现代针灸临床认知与所为相悖。
20世纪50年代承澹盦已经认识到晕针是一种神经反射导致的“急性脑贫血”,多见于“神经质、腺病质之患者或身体衰弱者”,但基于那时对晕针的神经机制理解甚少,他把晕针等同于休克,认为“危险殊甚”“救治之法,则不外重复刺激其知觉神经,再反射脑皮,唤醒其机能作用……亦可注射樟脑强心注射剂”[2]。当代针灸学教科书基本延续承氏认知,把晕针作为针灸异常情况的首位而防范;虽根据临床观察,进一步提出晕针是因为“病人体质虚弱,精神过度紧张,或当劳累、大汗出、空腹、大泻、大出血后。或因施术时手法太重”[3-4],但对晕针的发生机制,一直缺乏深入的研究,也没有把晕针与休克或其他晕厥区别开来,以至于对晕针的处置措施,也没有比承氏有明显的进步,依然只强调预防与急救。
清代李守先是第一位提出晕针无害而有益的古代医学家,他在《针灸易学》书中写道“然晕针者,必获大效,以血气交泰之故。俗云针不伤人,此之谓也”[5]。20世纪50年代初朱琏在其《新针灸学》书中,记载了3例晕针案例,其中两例晕针后疗效显著[6]。1981年笔者也报道了31例晕针患者中获得显著效果者10例(大约1/3)[7]。近40年来,不仅有关晕针后疗效显著的报道屡见不鲜[8-17],对晕针的发生率、安全性及其预防又有了更多的临床观察[18-21]。现代研究认为晕针属于血管迷走性晕厥,至今对血管迷走性晕厥的大量研究成果[22-29],包括针刺调控自主神经张力的各种研究[30],均适合于晕针机制的解读。
自20世纪50年代至今已经有晕针的大量个案报道、回顾性或前瞻性研究[31-33]、针灸从业者调查[34-35]与文献的系统评论[36-40]乃至映射评论(map review)[41],尽管其中许多晕针资讯来自对针灸不良反应或体检采血、献血晕针的研究。本文通过Medline与中国知网的检索,收集与回顾了迄今为止几乎全部可以收集到的上述主题的中、英文文献,以及有关血管迷走性晕厥的各种最新研究,归纳、总结了晕针的临床表现、性质、发生率及影响因素,详细分析了晕针“不伤人”的病理生理学基础,以及晕针可能“获大效”的原理,并根据其神经机制把其分型,提出改良晕针处置法供临床参考,在保证“不伤人”与期待“获大效”的目标之间作出权衡。
临床上观察到,不论手动针刺、电针还是热灸,都会发生晕针或晕灸。体检静脉采血或献血时也会发生晕针。无论是哪类刺激导致的晕针,其临床表现大同小异,除短暂的意识丧失外,主要是与自主神经兴奋性变化有关的表现,以及一些躯体症状。一般来说,晕针的典型临床表现可以分为三期[7]。
(1)先兆期:头部的各种不适感,上腹部或全身不适,眼花、耳鸣、心慌、面色苍白、出冷汗、打呵欠等。
(2)发作期:头晕、恶心进一步加剧,大汗,肢体发软发凉,身体摇晃、站立不稳,瞬间意识恍惚,嗜睡等。严重者可以突然意识丧失、摔倒,小便失禁,短暂惊厥发作等。血压和/或心率明显降低。
(3)恢复期:以上症状逐渐消失,血压与心率也恢复正常,但有不同程度的疲乏。
先兆期的时间可长可短,与患者的晕厥易感性、体位及相对刺激强度有关。发作期短暂的,如果是直坐位晕针者,只要躺平,不超过几分钟就会自然消失,进入恢复期(一般数小时)。在献血晕针的研究中,有人根据晕针表现发生的快慢,分为“早期反应(early reactions)”与“延迟反应(delayed reactions)”。前者在刺破手指进行血型鉴定时立即出现晕厥;后者是在放血结束后5~10 min乃至半小时以上发生晕厥。大多数献血晕针者在几个小时内就感觉正常并恢复了正常活动,少数献血晕针者在1~2 d内仍然感到不适和虚弱[42],但这种虚弱很可能是献血导致的,而非晕针所致。
根据2018年欧洲心脏病学会(ESC)指南[24],临床上的晕厥存在3种类型:反射性晕厥或神经介导性晕厥(与特定触发因素相关),体位性低血压(因直立性低血压引起的晕厥,定义为站立3 min后收缩压下降>20 mmHg或舒张压下降>10 mmHg)以及心源性晕厥(由心脏和大血管的结构性疾病引起)。晕针,显然属于其中最常见的反射性晕厥-血管迷走性晕厥(vasovagal syncope)[25]。
晕针发生时,心率和/或血压的下降是最明显的表现。根据晕厥时患者血压与心率变化,有研究者把血管迷走性晕厥分为三型:①血管抑制型(血压下降明显、心率可以稍减慢而不显著);②心脏抑制型(心率明显减慢,血压降低不明显);③混合型(血压、心率均明显降低)[22]。这样分类是基于晕厥时心迷走神经抑制性驱动是优于心交感神经(心脏抑制型)还是血管运动交感神经驱动(血管抑制型),或优于两者(混合型)[23]。针灸临床上的晕针,也同样可以观察到血压、心率的这三种类型的变化。但特别要指出,由于晕针过程的短暂,血压、心率的测定一定要迅速与及时[42],否则一旦触发因素排除和/或在动脉压力感受性反射作用下,它们的异常会迅速恢复正常。
笔者于1981年报道的31例晕针患者多有明显的先兆症状,但因及时处理无突然摔倒的。除1例患者脉搏细而稍增快(89次/min)外,其余均伴有脉搏弱而缓慢(45~55次/min),到恢复期脉搏先由弱变强,后由缓变快,逐渐恢复正常。出汗也是多数病例共有的症状,约半数有全身大汗,个别仅有针刺局部出汗。多数晕针患者有轻度血压下降。1例针合谷穴发生晕针时有耳鸣。1例除满头大汗外,还立即要解小便,不能熬。1例有明显嗜睡感。3例有短暂意识丧失,并且伴两手抽搐,其中1例发出类似鼾睡时的“呼噜”声,但卧平后均迅速恢复[7]。
据1990年台北的一项报道,52名患者出现55次晕针时所有患者均处于直坐位。他们通常的表现是面色苍白、出冷汗、恶心和心动过缓,但躺下后不久,他们就都恢复正常。没有人完全失去意识。没有注意到死亡率[18]。一项研究报道了非洲莱索托王国的两家医院理疗科接受针灸治疗的2050名患者中有2例晕针。他们的临床表现各异,主要症状是头晕、全身无力、额头出汗、心悸、呼吸困难和恶心。他们以前从未经历过这样的情况,在治疗前都抱怨饥饿。该研究小组认为这两个患者的晕针是继发于饥饿状态的。饥饿可能是与针灸有关的昏厥的最重要原因之一[19]。晕针时的表现也有肌肉不规则阵挛性运动-惊厥性晕厥(convulsive syncope),在针灸临床并不常见[21],但在献血中心采血的晕针似乎多见[42]。
韩国2017年报道了一位20岁女性学生被针刺右侧合谷晕针时脑电图的变化[20]。由于该学生是一项旨在观察针刺合谷与健康成人脑电图之间关系的临床试验参与者,故及时捕捉到了她晕针时的脑电图变化:其脑电图模式发生了两次变化。第一个变化是对毫针插入的反应,第二个变化是在针插入后4 min发生晕厥期间。这两种变化都包括脑电图振幅的爆发,但细节的模式不同。针插入时,仅感觉皮层被激活,γ波比例增加;而晕厥期间皮质多个区域被激活,但未观察到γ波比例增加。该研究尽管缺乏统计数据和可重复性,但这个案例有助于提高对晕针事件的理解,并提示针灸治病的机制。该学生晕针时以仰卧姿势放在床上,1 min后就恢复了,并且喝了一杯温水,躺在床上休息30 min。在晕针后7 d和30 d观察其身体状况,她没有报告任何不舒服的感觉或状况不佳,她也没有表现出任何创伤反应或对针灸治疗的负面看法,并愿意再次接受针灸治疗。
晕针,是几乎每一位针灸师在临床上都会或多或少遇到的,至于其发生率,至今已经有不少报道。多数是小样本,也有较大样本。来自体检采血或献血晕针的样本更大些,但用的不是毫针。1981年,笔者曾统计自己在以往5年间3万多人次的针刺治疗中积累了有完整记录的31例晕针病例,晕针发生率约为0.1%。其中男20例,女11例,年龄21~49岁(23例),50岁以上5例,年龄最高60岁,年龄最小17岁[7]。从1988年8月—1989年4月,台北CHEN F P等在传统中医中心对2855名患者进行了28 285次针刺治疗,观察到52名患者出现55次晕针,晕针发生率为0.19%。他们观察到的这些晕厥患者中,男35例,女17例,平均年龄45岁(11~72岁);发生晕针时,所有患者均处于直坐位。躺下后不久就都恢复正常;没有人完全失去意识;其中首次就诊时的晕针发生率(0.94%)几乎是后续治时的晕针率(0.11%)的9倍[18],提示患者首次接受针刺治疗时的精神紧张很可能是主要因素,当然也不排除患者对从未经历过的针感的不适应性。来自非洲莱索托王国两家医院的数据,自2017年10月—2018年4月的2050名接受针灸治疗的患者中有2例晕针[19],发生率略低于0.1%,与笔者的观察(0.1%)及来自台北的报道(0.19%)基本一致。
针灸临床的晕针发生率也可以参考体检静脉采血或献血晕针的数据。因为后两者的情景与针灸临床的晕针极为相似,尽管它用的是注射针,主要是在肘部内侧血管部穿刺,但把它们看作是一种针刺干预并无不妥。血管穿刺采血的过程,也相当于古典针灸的“刺脉”或现代流行的“刺络放血”。一项研究比较了连续两年对同一家大型船务公司员工体检采血时的晕针发生率[43]:2011年6157名员工体检时共发生采血晕针23例,晕针率为0.37%。2012年在相同的厂区环境内,也是对该厂的员工体检采血,其主体显然还是2011年同一批员工,但该年数目增加到了6519名。由于对体检者实施一系列有针对性、人性化的护理干预措施后,体检者中只有3例晕针,晕针率为0.05%,比2011年有了明显下降。该晕针率甚至低于前述针灸晕针的0.1%或0.19%,这显然要归功于采血前受检者精神紧张的消除及对晕针高危人群体位性低血压的防备。献血晕针的发生率如美国LIN JT等[42]所报道的:在回顾性研究中大约0.31%(262 935次献血者中824例晕针),而在前瞻性研究中因为加入了操作者对晕针现象的关注与采取心理疏导等预防措施,观察到晕针发生率明显减少,只有0.12%(约70000名献血者中84例晕针)。该研究的回顾性统计结果与上述船务公司2011年的采血体检晕针发生率(0.37%)几乎完全一致,而前瞻性统计结果仍是上述船务公司2012年的晕针发生率(0.05%)的一倍余,这或许与献血者的血量流失远大于体检采血量有关。
哪些人容易晕针?因为晕针属于血管迷走性晕厥,后者易感性的有关研究为晕针提供了大量可借鉴的数据。血管迷走性晕厥影响所有年龄段的人,更有可能发生在年轻时,但也存在与衰老或心血管、神经或代谢疾病(例如糖尿病)相关的复发形式。老年人发生晕厥可能是因为与年龄相关的自主神经功能障碍和压力感受性反射无法适应生理挑战。血管迷走性晕厥发生率和临床表现存在性别差异:女性出现晕厥先兆体征和症状的可能性比男性高50%。影响晕针发生率的因素,除遗传因素之外,精神紧张、体位与针刺强度、针刺部位的特异性等都可以是。精神紧张通常是首位,其中惧针的影响最明显[44]。笔者自1990年后在美国大约3万人次的针灸门诊中只遇到2例典型的晕针,其原因多与大多数患者取平卧位、少用强刺激以及西方人的体质不同于国人有关[45]。
须特别指出的,晕针不是休克。常见的休克有出血性休克与感染性休克,其主要病理生理基础为微循环障碍、有效血容量不足以及重要脏器(脑、心、肾)和组织血流灌注不足。换言之,休克是全身对血压突然下降的反应,身体通过收缩四肢(手和脚)的血管来应对,企图保存流向重要器官的血液。它是一种危及生命的疾病,需要及时抢救。而属于血管迷走性晕厥的晕针通常是无害的,不需要治疗[46]。2012年天津郭义团队的一项有关针灸不良反应个案的中文文献研究,包含了自1956—2010年的28篇文献报告的468个与针灸相关的晕厥案例,其中包括晕针(453例)、晕灸(1例)、晕拔罐(14例)。98%发生在治疗过程中,只有10例在治疗后晕倒。晕厥是主要由以下原因引起:首次接受针灸治疗、精神紧张、疲劳、饥饿或姿势不当。其中除74例没有提到结局,其他患者在正确处置后全部康复,无后遗症[39]。兰州YANG C Q团队[41]从各种数据库收集了至2022年6月为止的535篇有关针灸不良反应的系统回顾文献,其中86项文献系统回顾报告了与针灸相关的晕厥,认同它属于迷走神经兴奋引起的反射,是针灸期间常见的不良事件[47],而且大多数晕针事件都是由针灸强度引起的;但大多数研究表明,晕针可以通过休息和对症治疗得到改善,只有少数严重病例。
表1罗列了自1956年至今世界各地(主要在中国)报道的晕针发生率与结局,这些数据主要来自那些大样本、有统计数据的回顾性、前瞻性研究或文献的系统评论,从中可见晕针发生率在前瞻性研究中明显低于回顾性研究(提示晕针的发生经常是可以预防或避免的),但均未见晕针导致死亡的任何报道。显然,晕针“不伤人”,应该是经过无数临床实践验证的事实。据最新的认知,晕厥还可能是一种保护大脑和心脏的防御机制:晕厥时的短暂性意识丧失和肌张力下降可以对抗由于重力引起的脑、心血流量减少的影响[48],或是身体的一种“放大”的适应性反应,旨在身体受到创伤时本能地降低血压和心率,以减少出血量[29]。还有一种心脏防御理论(heart defense theory)认为:血管迷走神经反射似乎是一种针对交感神经过度活跃的保护机制,因为心脏是交感过度兴奋时最脆弱的器官[49]。
晕针是在针灸临床的情景下,患者发生以动脉低血压和意识短暂丧失(晕厥)为标志的临床现象。尽管其机制细节扑朔迷离,至今尚未完全清楚,但以下几点是肯定的。
首先,晕针由于发生突然与恢复快捷,是反射性晕厥或神经介导的晕厥的一种常见形式——血管迷走性晕厥,后者被定义为一种复杂的血流动力学反应,其特征是心动过缓、明显低血压和意识丧失。动脉血压突然下降导致脑灌注压下降即大脑短暂性供血不足,是其发生晕针先兆乃至意识短暂丧失等症状的根本原因。血压下降是交感神经活动减少与迷走神经活动突然增强的结果,主要机制涉及血管张力的降低与心输出量的抑制。
其次,由于晕针是在针灸临床(包括静脉穿刺)的情景下发生,也是一种情景性晕厥(situational syncope),但它与一般性情境性晕厥的原因还是有区别的。因为晕针发生时经常有体表的针刺刺激存在(如果是晕灸,则有灸刺激),而一般性情境性晕厥可以在完全没有体表刺激的情况下发生,如看见流血或一进入治疗室均可以发生。对于反复晕针者,第2次或以后的晕针或许也可以是条件反射型,可以在针灸刺激前就开始晕厥。但对于首次晕针者,针灸刺激本身是明显的诱因。这些患者经常是由于针感较强(刺激部位较敏感或刺激强度较大)又处于非卧位而发生晕针,但也有处于卧位或针感不强甚至无针感时发生。简言之,晕针的情境刺激可以是心理性的(如精神紧张或条件反射),但更多是躯体感觉性的(穿刺疼痛或针灸感觉)。
第三,晕针现象在坐位要比卧位多见,直坐体位对晕针的影响显而易见。至今有关直立性晕厥或血管迷走性晕厥机制的研究成果,大多适合晕针机制的解读。
简单说来,晕针发生机制的病理生理学基础大致有以下两方面。
(1)血压稳态快速调控的失效:正常情况下,动脉血压的稳态是由压力感受性反射的负反馈快速维持的。动脉压力感受器位于颈动脉窦和主动脉弓中。它们的传入分别通过舌咽神经与迷走神经到达孤束核(nucleus tractus solitarius,NTS)。如插页Ⅷ图1所示,孤束核是动脉压力感受性反射中枢传递的关键核团[50]。它与尾侧腹外侧延髓(caudal ventrolateral medulla,CVLM)、头端腹外侧延髓(rostral ventrolateral medulla,RVLM)以及迷走神经背侧运动核(dorsal motor nucleus of the vagus,DMNX)、疑核(nucleus ambiguus,NM)等组成了延髓血管运动中枢(其实称“网络”最合适)。该反射弧的传出臂分迷走和交感控制反射两个方面[51]。当全身脉压或平均动脉压升高时,颈动脉窦和主动脉弓中的动脉压力感受器的刺激增加,迷走神经传出增加而心交感神经兴奋性抑制,导致心率减慢、心输出量的降低与外周血管扩张使原来升高的血压降低,恢复正常。当全身脉压或平均动脉压降低时,该反射的效应正好与上述相反(心率增加,阻力血管收缩)。这是正常动脉血压之所以能够快速维持稳定的机制。脑血流量也具有自动调节,通常可以在较宽的平均动脉压范围内恒定脑血流量,只有当平均动脉压低于其自动调节能力时,脑血流量迅速下降,脑功能恶化,患者才会失去意识(晕厥)[25]。然而,一旦患者跌倒或仰卧,下肢回心血量增加,加上将血液输送到大脑所需做功减少(即心脏不必抵抗重力“上坡”泵血),患者就会迅速恢复意识[29]。
机体维持血压稳态的神经机制,除动脉压力感受性反射外,还有静脉压力感受性反射(也称低压压力反射、心肺感受性反射),参与血容量的调节。血容量决定整个系统的平均压力,尤其是容纳大部分血液的静脉侧。其感受器主要是存在于心房、心室和肺循环大血管壁的心肺感受器(cardiopulmonary receptors),但也可能存在于外周静脉壁[52]。它们的适宜刺激是血管壁的机械牵张,故主要对心、肺腔与静脉腔的容积信息作出反应,其传入信号也经非髓鞘迷走神经向孤束核发送,其反射中枢和传出臂均与动脉压力感受性反射相同[28]。研究还发现,来自心脏或大静脉的传入刺激,只是一种“迷走神经反射”[53],即其效应只是使心迷走紧张加强,交感紧张降低,导致心率减慢,心输出量减少,外周血管阻力降低,故血压下降[54]。
显然,动脉压力感受性反射功能的健全,是大多数人不易发生晕针的基础。目前已有证据证明,血管迷走性晕厥的患者大多有动脉压力感受性反射的不稳定性或障碍(敏感性降低)[22,55]。希腊FLEVARI等2002年研究了39名有典型的血管迷走性晕厥史(过去6个月内至少发生过两次晕厥)且倾斜试验阳性的患者,并且和26名倾斜试验呈阴性的正常受试者相比较,观察到所有晕厥患者的动脉压力感受性反射介导的反应,表现出明显的不稳定或受损。反射障碍(不敏感)似乎在①血管抑制型占主导地位,而压力感受不稳定是②心脏抑制型的特征。③混合型患者则可能普遍存在压力感受反射障碍或不稳定[22]。因为晕针属于血管迷走性晕厥,可以推测一些患者之所以容易晕针,多半与他们的动脉压力感受性反射障碍或不稳定有关(常见那些针刚进皮甚至还未进针就晕针的)。
但是,产生血管抑制性晕厥的交感血管收缩肌张力的撤退,并不一定是动脉压力感受反射功能受损的结果。因为经倾斜桌试验发现,一些直立性晕厥患者在晕厥发生前阶段,其动脉压力感受反射调节仍然存在,表现为伴随血压下降的心率增快,直到晕厥前1 min才被以相对心动过缓和阻力血管松弛为特点(即血压与心率均同时降低)的另一反向的反射所抵消[27]。该反向反射即前述的“迷走神经反射”,其起源尚不确定,一种观点是来自位于左心室壁的机械感受器的激发。该机械感受器通常对扩张刺激敏感,但也可能对低血容量作出反应[56]。如果同时存在心肌刺激和充盈不足,心壁的变形会以与拉伸相同的方式触发该机械感受器,经无髓鞘迷走神经传入中枢。心脏充盈不足的原因,有可能是回心血量减少所致。有报道,强烈的情绪刺激交感神经,会增加循环肾上腺素的浓度[53]。而肾上腺素可以扩张肌肉内血管,减少回心血量。所以,原先动脉压力感受性反射正常的,也可能会因为回心血量的减少导致“迷走神经反射”的抵消而失效,发生晕厥(插页Ⅷ图2)。
(2)心理应激、体位应激合并针灸(躯体神经)刺激:针灸临床上常见的晕针多与精神紧张(心理应激)、直坐位(体位应激)以及较强烈的针灸感觉(感觉性或微创性躯体刺激)有关。研究发现,原先动脉压力感受性反射正常的,也可以因为这些应激刺激单独或合并影响(调制)而改变自主神经张力,导致血压下降乃至晕厥。
同时有迷走神经激活和交感神经抑制,是晕针或血管迷走性晕厥的自主神经活动特征。它可以沿着至少两个不同的神经通路激活[27]。前文分析的由动脉压力感受性反射短暂失效或被静脉压力性“迷走神经反射”所抵消,是其“外周传入通路”。其第二条通道是从大脑皮层-下丘脑中心下降到延髓血管运动中枢的通路。临床上常见精神紧张或视、嗅觉(如见血)或剧烈疼痛(内脏或躯体深层)触发晕针,或者说情绪事件诱发血管迷走性昏厥走的就是这条通路[26]。这种类型的血管迷走神经反应被称为“中枢型”,在心动过缓和低血压发生前通常先出现中度心动过速。尽管人类所涉及的该神经中枢尚未完全确定,在动物实验中,两个高级中枢已被确定:边缘叶的“防御反应区”与边缘交感抑制中枢。刺激前者会增加心率和血压,并引发类似于人类对焦虑和肌肉锻炼预期的反应(“斗或逃”反应)。后者的刺激会导致低血压和心动过缓[27]。
插页Ⅷ图2显示了导致晕针的各种应激刺激以及神经介导的心血管反应。以孤束核为中心的动脉压力感受性反射受大脑皮层、边缘系统、下丘脑等高位中枢的调制。情绪、视嗅觉等心理应激刺激可直接作用于大脑皮层及包括下丘脑的边缘系统[26],而针灸的神经刺激输入可以直接作用于大脑皮层、边缘系统、下丘脑室旁核与孤束核等[51,57-58]。针灸临床情景的设置下,不仅心理应激经常存在,而且还要加上针刺穿皮时的疼痛,尤其是针灸操作期间的得气(酸麻胀痛、触电感等)感觉,都会进一步强化机体的应激反应。
然而,必须指出的是,平时大多数情况下,人类情绪或心理应激对血压的影响,主要是升高,而不是下降。例如,平时血压正常者因为进入诊室后的精神紧张经常导致交感神经兴奋性或血压的短暂升高,即所谓“白大衣高血压”。长期的精神紧张已被怀疑与高血压病的发生有关[54]。2021年美国的一项通过数值平台进行的大样本心理应激对血压影响的研究观察到,当人们处于强烈的高唤醒负面情绪(例如愤怒和恐惧)时,表现出明显更高的血压和心率反应性[59]。那么一个突如其来的“噩耗”或恐惧,反而使有些人晕厥[60]或那些见血或刚进入治疗室尚未接受针灸就发生晕针,又如何解释呢?这是因为来自大脑皮层、下丘脑的刺激可以对位于延髓的血管运动中枢产生强大的兴奋或抑制作用,具体取决于它们作用的精确部位及刺激强度;下丘脑后外侧部主要引起兴奋,而前部可以引起轻度兴奋或抑制[61]。如前所述,以孤束核为枢纽的延髓血管运动中枢相当于稳压器,通过压力感受性反射的负反馈来快速维持血压稳态,但它同时受来自下丘脑传出的调制[62]。所以,心理应激无论是导致血压短暂升高或晕厥,均离不开大脑皮层经下丘脑对压力感受性反射的调制。
体位应激,主要发生在直立或直坐位时,是与直立位置相关的血容量位移激发的神经性心血管调节。一些易感人群发生直立性晕厥就是通过该应激反应:直坐位时,血液因为重力滞留下肢而减少了回心血量,它可触发前述低压感受性反射的传入,旨在抵抗血液在身体下部的重力汇集,维持静脉回流,避免或恢复中枢血容量的不足[27]。临床上观察到,所有体位均可发生晕针,但以站立位较易发生,坐位次之,卧位较少发生[10]。换言之,晕针的发生率在卧位要明显低于直坐位。这提示体位应激也必定参与晕针机制。体位应激可以单独或强化同时存在的心理应激或躯体神经刺激,导致晕针。有研究在20名健康受试者证明在右前臂的手三里穴短暂针刺1 min,坐位受试者的心率会仰卧位受试者更大程度地降低[63]。
晕针的触发因素除心理应激与体位应激外,更可以是由躯体体表的神经刺激诱发的针灸应激(它也有心理应激的成分)[64-65]:进针穿皮或在穴位内其他层次组织伴有或不伴有感觉的刺激(得气或不得气),都可能促发晕针。带有针感(疼痛或酸麻胀)的刺激,主要通过躯体感觉神经传入;不带有针感的刺激可以通过直接刺激迷走感觉神经(如耳甲区穴位)或微创刺激(如刺破血管壁出血时)传入。这可以解释为什么临床上经常观察到,针感越强,越容易晕针,或刺激虽强但有时并无明显针感(如浮针在皮下组织内扫散时),也常见晕针。尽管健康人接受感觉刺激(针灸)时的交感、副交感神经活动变化取决于刺激部位和观察时间[66],大多数时候针刺首先或最容易先激发交感兴奋性[67]。这是因为针刺作为躯体体表的神经(感觉性或微创)刺激,是一种应激源,必然会一定程度上激发下丘脑-脑垂体-肾上腺(HPA)轴;而针刺或电针导致的降压效应,可以通过调制动脉压力感受性反射实现[58],已经证明,以不同模式(例如电针、手针或艾灸)进行穴位刺激时,感觉神经元的激活最终可能通过相似的中枢过程降低交感神经兴奋反应[68]。
综上所述,患者对于晕厥的易感性,压力感受性反射障碍或不稳定性,心理应激、体位应激尤其合并躯体神经刺激(针灸)激发的血管迷走性反应,是晕针的病理生理学基础。平时压力感受性反射不稳定或障碍的患者,在心理应激(尤其是极端的情绪事件)下合并直立(坐)位时,或合并较强的躯体神经刺激如针灸,更容易诱发晕针。
至今临床上主要根据患者血压、心率变化的不同组合而把血管迷走性晕厥分为①血管抑制型、②心脏抑制型与③混合型。虽这样的分型也适合晕针,但笔者认为,只有分析晕厥前后自主神经功能的变化,才可以深入地理解不同类型晕厥背后的神经机制,因为血压、心率的变化都是自主神经张力变化的结果。目前这方面的研究经常借助心率变异性(heart rate variability,HRV)的指标:其高频(high frequency,HF)功率与低频(low frequency,LF)功率或LF/HF比值分别反映迷走神经与心交感神经活性。
1999年意大利的一项研究以心率变异性为指标,详细观察了健康人偶发血管迷走性晕厥发生前的自主神经功能变化。该研究观察到22名健康人由倾斜试验诱发晕厥发生前,都有交感神经兴奋性的增高,而且有两种不同的模式:一是渐进性交感神经激活型,13名晕厥受试者在倾斜的早期阶段心交感神经张力逐渐增加直至晕厥发生前的最后一分钟才有心率下降,显示迷走神经兴奋性增加;二是进行性交感神经抑制型,其余9名昏厥患者的交感神经活性,在倾斜试验最初明显占优势,达到最大值后缓慢下降,然后心动过缓开始,显示交感-迷走神经平衡缓慢、渐进的反转以及随后的心交感神经抑制为特征[69]。为什么会有这两类不同模式,笔者认为可能与他们的压力感受性反射功能的健全程度有关,虽然该研究没有作这方面的实验。前者很可能没有明显的压力感受性反射障碍,而后者则有。虽然这两类模式都是发生在由倾斜试验诱发的晕厥受试者,但可以推测它们同样存在于针灸临床上的晕针患者,笔者把晕针按照其神经机制分为以下3个类型。
一是心理应激型(Ⅰ型)(快速交感抑制型):这类晕针患者针刺前就有压力感受性反射障碍或不稳定。针灸临床情景下,他们一进入治疗室尚未接受针灸或针刺刚刚穿皮,由于精神紧张或视觉影响(类似晕血)就发生晕针。精神紧张或心理应激可经大脑边缘系统、下丘脑直接抑制交感缩血管神经活动,导致动脉血压下降,短暂性脑供血不足。该型晕针,一般在进针前后立即发生,多处在非卧位时,晕厥程度稍轻,多表现为先兆反应,针刺前的躺平经常可以预防。其临床表现大致符合前述①血管抑制型。
二是交感触发型(Ⅱ型)[交感过度反应型(sympathetic overactivity)]。该型晕针患者可以有或无针灸干预前的精神紧张,有或无压力感受性反射的障碍或不稳定。它进一步分为两个亚型:渐进性交感神经激活型(Ⅱa型)与进行性交感神经抑制型(Ⅱb型)。
渐进性交感神经激活型(Ⅱa型),该型患者针刺前也常有精神紧张或疼痛,致使交感兴奋性较高[70],它在针刺作用下进一步提高,虽然动脉压力感受性反射的活动起初可以正常,但它受随着回心血容量减少而激发的低压感受性迷走反射的抵消,交感神经突然反转,发生明显的抑制与迷走兴奋,使血压急剧下降,导致晕针。反转的机制常与血容量不足(包括直位姿势或脱水)有关[25]。该亚型患者晕针前可无迷走性活动增高的先兆症状,心率不减慢,甚至短暂增快,直至晕厥发生时才突然减慢,这支持该型是由于最初的交感神经过度活跃促进了后续发生的血管迷走性晕厥的解释。其临床表现大致符合前述②心脏抑制型。
渐进性交感神经抑制型(Ⅱb型),是在压力感受性反射功能原先有障碍或同时受针灸调制而暂时失效的患者:此时的降压效应本来就是同时逐渐抑制交感神经与兴奋迷走神经的结果,直至晕针发生。该亚型患者晕针前经常有明显的先兆症状,其临床表现大致符合前述①血管抑制型。该型晕针的部分患者,原先就存在压力感受性反射的障碍或不稳定,即使针灸刺激的强度不大,或刺激的是非敏感性高的穴位,也会发生晕针。但如果原先的压力感受性反射正常,其失效是受针灸刺激调制所致,则通常需要在一些特殊的穴位(如四肢末梢敏感性高的部位)施予较强的刺激才会发生晕针。
三是迷走触发型(Ⅲ型)(迷走过度反应型)。针刺一些特殊部位(如耳甲区)极大地激发了迷走神经传入,心率与血压下降,导致以迷走神经极度兴奋为主的晕针。该型晕针患者,可以预先没有明显的精神紧张或交感神经兴奋性增高,随着针刺刺激,迷走神经兴奋性增加,交感兴奋性降低,留针一段时间后出现晕针。该型晕针患者,心率减慢明显,同时有血压的降低。其晕针发生时的临床表现属于前述③混合型。
该型晕针最容易发生在直接针刺迷走传入神经的场合,如针刺耳甲区分布的耳迷走神经分支,此时发生的晕针可以是因为直接的迷走神经兴奋性提高,导致明显的心率减慢、血压降低。这类晕厥已经可以由静脉注射苯双胍(PBG)来模拟,它刺激迷走神经传入末梢引起心动过缓和血管抑制,可模拟神经介导的晕厥[71]。该型晕针也可以发生在针刺四肢深部穴位(如足三里、曲池等)时,因为激发躯体感觉传入的同时可以刺激到带有PROKR2-Cre标记的迷走传入纤维[70],此时经常既有交感抑制又有迷走兴奋,故其临床表现也属于前述③混合型晕针。但是,由于耳廓皮肤及四肢深部(靠近骨膜处)均十分敏感,耳甲区或四肢的深部针刺经常刺激较强,在刺激到迷走传入纤维的同时又作为一种应激刺激兴奋交感神经,故此时也可以没有血压的明显变化,不发生晕针(类似足三里电针抗晕厥)。如果发生晕针,因为迷走与交感同时兴奋,前者使心率减慢,后者使血压变化不大,其临床表现也可以是前述②心脏抑制型。
插页Ⅷ图3显示了晕针的临床分型与上述机制分型的关系。在以上三型晕针中,因为Ⅰ型晕针通常在针刺前发生,而Ⅱ、Ⅲ型晕针则在针刺期间发生,故其发生多于Ⅰ型,而且与刺激部位、强度的关系密切,也可以发生在卧位时,晕针程度较Ⅰ型明显,患者的动脉压力感受性反射原先可以正常,但可受针灸刺激调制。
尽管历来晕针被认为是针灸的不良反应而应被提防,但晕针后疗效显著的报道屡见不鲜。北京针灸研究所首任所长朱琏在其《新针灸学》书中,记载了3例晕针案例,其中两例晕针后疗效显著:一例是左肩疼痛、不能上举10余年,首次针刺治疗,取患侧肩颙,针感强烈,不到5 min发生晕针(脉搏与针前无异)。未拔针,等待其几分钟后醒来,伸出左臂穿衣时当即活动自如,10多年的肩痛顷刻消失了。另一例是严重流涎症,也是首次接受针刺。坐位取一侧合谷,针刚刺入皮肤(0.5 cm深)就发生晕针,不到2 min,还未拔针就醒了,自己笑着说是精神紧张惧怕针刺的缘故。第二天早上打来电话,以惊奇的声调说前一夜不流涎了[6]。
20世纪80年代初笔者报道了31例晕针患者中获得显著效果者10例(大约1/3),多数以疼痛为主症的患者,仅一次而愈[7]。以下是一则典型案例:女,57岁,中国人。患更年期高血压病6年。一直服用降压西药、草药等均未能持久控制在正常水平,曾体针治疗多次也无效。后接受耳针期间尚有一定的降压效果,但停针后又恢复高压(170~190/100 mm Hg)水平。1972年9月6日笔者给她再次耳针,取双侧心、交感、降压点,留针15 min后她感到头晕、眼花、胸闷、恶心,出现晕针先兆,笔者立即起针,并令其卧平。她片刻恢复,但一身大汗,其时心率56次/min,血压降到110/80 mm Hg。其后未再作针灸或服用任何降压西药,连续每周随访测压约半年,她的血压始终维持在120~136/70~80 mm Hg左右,显示出极佳的近期疗效。该例晕针的发生机制显然属于前述Ⅲ型(迷走触发型)。
近20多年来,国内类似报道越来越多,陈斟[8]总结了36例晕针患者,其中11例晕针后疾病痊愈(也占大约1/3),并且观察到风池穴晕针后痊愈的几率最高。吴新贵等[9]报道3例(2例为痛症、1例为呃逆)既往均无晕针或晕厥史的患者晕针后疗效显著,其中2例取的是坐位,1例为站立位。冯罡[11]报道了晕针后反收奇效的4例颈椎病、上颌窦炎、头痛、膈肌痉挛患者,晕针后患者的疼痛、嗅觉减退、呃逆等症状均豁然而愈。有研究者提出这些报道让人不得不重新思考“十针不如一晕”之说是有临床依据的[72]。
至于哪些疾病晕针后多见疗效较好,贺君等[10]对晕针后疗效提高的32例患者的分析发现晕针后患者症状明显改善或治愈的疾病,多为慢性疼痛性疾病,且多伴有不同程度的局部炎性病变,如肩周炎、颈椎病、腰椎病等居多。迄今观察到晕针后疗效提高的多为痛症及植物神经功能失调患者[73-77]。2023年詹影等总结了1981—2016年关于晕针起效的12篇临床报道,也持同样观点,他们还归纳出晕针起效好发的群体是女性患者,以再次针灸者为多,涉及的腧穴多位于神经血管丰富的部位,并且认为刺激量是针刺获效的关键,针刺晕针起效现象与患者个体形质、心理、生理特征、病理情况存在密切联系[78]。上述无论是“既往均无晕针或晕厥史的患者晕针后疗效显著”或“晕针起效好发的群体以再次针灸者为多”的观察结果,均提示晕针后疗效较好的患者应该多为Ⅱ、Ⅲ型晕针。
至于为什么晕针会在一些患者“获大效”,已有不少作者的初步推测[9]。笔者认为可以包括以下三方面:一是晕针总是伴随下丘脑-垂体-肾上腺轴(HPA)的极大激发。针灸作为一种体表刺激,具备应激源的特征,较大强度的针灸刺激可以导致应激反应[64]。应激反应是双刃剑,它是机体内稳态“平衡-失衡-重构平衡”的过程,只要持续时间不过久,对身体健康其实是有益的。针灸已被证实在调节HPA轴方面发挥着重要作用[65]。晕针是一种过于强烈的应激反应,其导致HPA激发的程度,一方面与患者是否容易或经常发生晕厥有关:容易发生晕厥的,应激刺激的程度低,自然HPA的激发也少;另方面与体表刺激的强度相关:刺激或针感越强,应激反应越明显,故针感强烈的晕针可能疗效越好。一般说来,晕针后能提高疗效的病人,大多是平时植物神经系统功能比较稳定,一旦晕针改变了他们的植物神经系统功能状态,也就可能对改变病态起较大的影响,产生所谓的“大效”。相反,对于那些平日植物神经系统功能就不稳定的人,如常有晕厥史者,因为只要轻微的针刺刺激便会晕针,晕针时的应激反应不会明显,故对疗效影响不会明显。换言之,他们的机体早就适应了这种极易发生的晕厥,也就不易因晕针受益了。
二是晕针时胆碱能迷走抗炎途径的极度激发。胆碱能迷走抗炎通路的深入研究已经揭示针灸治疗炎症性疼痛、炎症性疾病以及炎症相关性疾病的广泛前景与明显疗效[79],晕针过程中明显的迷走神经兴奋性增高,可能是晕针后“获大效”的另一原因。晕针时胆碱能迷走抗炎途径激发的程度,很可能与患者心率减慢与血压降低的程度相关。
三是晕针时短暂性脑缺血的冲击,可能对某些疾病稳定态的设定点发生再设置,促进疾病的自愈。疾病稳定态是生理稳态设定点的持续偏离所致,是许多慢性病,如顽固性疼痛、高血压病、糖尿病等之所以难愈的主要原因[80]。
但仍必须强调,要得出晕针可以“获大效”的结论,必须通过与先前治疗无晕针的疗效对比。如果没有比较,就不能下这个结论,因为许多患者首次接受针灸治疗就有较佳疗效,如果同时发生了晕针,就不能把疗效归功于晕针。此外,临床观察到首次接受针灸导致晕针的比例远高于后续治疗,提示首次治疗就发生晕针的患者多有较高的晕针易感性,即使刺激不强或还未刺激,也都可能晕针,故首次治疗发生晕针的患者,其疗效且不说难以归功于晕针,甚至很难说源自针灸(可能只是晕厥的效应)。
无论是为了避免晕针保安全,还是期待晕针后可以“获大效”,都必须搞清晕针的发生与所刺激的穴位或身体部位是否有关联,或者说晕针的发生是否具有刺激穴位的特异性。
从至今有关晕针的大量临床报道来看,似乎全身的穴位都可能发生晕针,但因为临床针灸大多应用多个穴位,很少使用单穴,故晕针的发生很难与某一个单穴挂钩;人体的晕针实验因为伦理也很难实施;故目前最多只能根据临床观察比较晕针的发生是否具有刺激身体部位的特异性。如笔者观察到头面、四肢部的穴位诱发晕针最为多见,而躯干部穴位发生晕针的几率较低[7],或头面部穴位发生晕针最多,四肢次之,躯干最少[8]。在一份包含82个案例的报道中,60%的患者在第1次治疗期间晕倒。其中49人晕倒,其83%发生在针刺头部或颈部时[33]。
其实,除临床观察之外,还可以从针灸影响自主神经活动的部位特异性来寻觅线索。据2014年对14项有关针刺对心率变异性影响的随机对照试验系统评价和荟萃分析[30],针刺足三里或内关等一般四肢穴位主要通过降低交感神经活动来增高副交感神经系统的优势,如可以降低心率变异性的LF(交感神经张力)及LF/HF比值,但不影响HF(副交感神经张力)。这正好可以解释为什么大多数针灸场合或大多数针灸患者并不容易发生晕针,或者说临床上发生晕针的几率毕竟很低,因为据前述的晕针机制,大多数晕针患者是Ⅱ型,他们接受针灸刺激之初会先提高交感兴奋性。临床上有针刺下肢穴位(如丘墟透照海)减慢心动过速的报道[81]或许也可以用降低心交感神经活动来解释。
但是,马秋富团队近年在电针抗炎研究中发现,电针刺激四肢的一些部位可以经PROKR2-Cre(prokineticin receptor 2,促动力素受体2;Cre,cyclization recombinase,环化重组酶)标记的感觉神经纤维诱发迷走神经抗炎效应。这类神经纤维在下肢的分布有明显的区域特异性,如胫骨附近筋膜组织(足三里深部)中有密集投射的PROKR2-Cre标记神经纤维,而下肢后部腓肠肌、半腱肌中该纤维的神经支配少,故在低强度电针刺激时,前者(如足三里)具有抑制脂多糖(lipopolysaccharide,LPS)诱导炎症的作用,而后者(如承筋穴)则缺乏。上肢也有类似情况,其深筋膜组织,如手三里区域因为也有PROKR2-Cre标记的感觉神经纤维的密集支配,受针刺时也能显著抑制LPS诱导的炎症反应。该研究证明,即使在上下肢,只要有该神经元的支配,都会具有类似的抗炎效应;但即使在同一下肢,由不同神经元支配的穴位则并非都有相同的抗炎效应[70]。尽管至今尚未研究PROKR2-Cre标记的感觉神经纤维与降压效应的关系,但可以推论刺激四肢某些穴位(如足三里、曲池)具有明显降压作用[54]也与迷走神经传入的激发有关。因为晕针时的血压降低,可以看作是针灸减压效应的“放大”,针灸降压的刺激部(穴)位特异性也可以提示晕针的刺激部(穴)位特异性。
至于刺激头面部尤其耳廓上的一些穴位,则完全可能经三叉-迷走反射直接刺激耳迷走神经来提高迷走神经兴奋性,使晕针的几率增加。布有迷走神经耳支的耳甲区刺激有明显的降压、抗炎与调节内脏功能的作用[7,82]。刺激颈部的颈神经,则可以通过与三叉神经或面神经的连接兴奋迷走神经,至今已经有许多证据显示三叉神经与枕神经传入的会聚[83]。刺激位于颈动脉窦之上的人迎穴也可以激发迷走神经。在高血压病患者针灸降压的临床研究发现,针刺人迎有比四肢穴位(足三里、曲池等)较显著的降压效应[84-85]。当然,头面部或耳穴刺激并不总是只能激发迷走神经兴奋性的,只要刺激强到一定程度,依然可以激发交感神经兴奋性,类似于四肢末梢那些敏感性较高的表浅穴位。颈上神经节作为交感神经系统的一部分(交感神经节),通常与“战或逃”反应有关[83]。至于刺激脊神经发布的胸腹部穴位对自主神经活动的影响,有证据以胃肠道活动为指标,腹部刺激可以激发交感,与下肢刺激激发副交感不同[86];以抗炎效应为指标,也证明腹部穴位(如天枢)的感觉性传入,可能经交感神经干的交通支联系,受刺激时容易激发交感神经活性[79]。
关于头面、耳廓及四肢末梢穴位刺激容易诱发晕针的机理,也离不开这些部位密集分布的肥大细胞的激发。李永明的研究揭示人体皮肤肥大细胞分布具有“行于端,聚于窍”的特征[87],指的就是这些部位。已经有证据,肥大细胞是穴位敏化局部反应机制的核心细胞之一[88],它的激发参与了针刺反应的启动过程[89]。所以,肥大细胞的密集分布不仅是导致这些部位敏感性高而且也是针刺时容易晕针的原因之一。
有研究者[90]最近指出:针灸通过在体表施加适宜的物理刺激,实现了对自主神经功能的有效、有限和规律性的调控。这种调控的规律性一定程度上表现为体表“纵横”位域的效应差异:从体表水平节段来看,胸腹部穴位主要引起节段性交感传出效应,而头面和四肢部穴位既可以引起迷走神经传出,也可以引起交感传出效应;从躯体纵向层次的角度,在特定的干预强度下,躯体浅表刺激常常引发交感反射[91-92],深层刺激可以引起迷走传出活动增加[70]。
综上所述,诱发晕针的刺激部位特异性很可能存在。刺激部位与晕针神经机制类型的关系,可以简述如下:一些部位的刺激可以经迷走神经传入神经(耳甲区)或通过三叉神经-迷走反射(头面部)或经四肢的躯体感觉神经中的迷走传入(如足三里、手三里深部),直接导致迷走神经兴奋性增高,所发生的晕针多为Ⅲ型。其他部位刺激诱发的晕针多为Ⅱ型,如刺激四肢末梢或躯体表浅敏感部位的感觉神经时,交感兴奋性先短暂提高,再逐渐或突然抑制,转变为迷走神经兴奋,导致晕针。
其实,除刺激部位以外,晕针与刺激强度或不同刺激手段的关系或许更为紧密。因为体表的强刺激都是伤害性刺激,诱发下丘脑-垂体-肾上腺轴应激反应是必然的,故任何部(穴)位、任何组织层次的重度刺激都可能提高交感神经兴奋性。有报道,较易引起晕针的穴位,一般为针感较强的穴位,如风池、合谷、内关、十二井、十宣等[10]。当采用轻刺激或者患者的针感不明显时,显然可以大大降低晕针的发生率。这可以解释为什么多用浅刺或轻刺激的海外针灸临床遇到晕针的几率要比国内应用强刺激的明显减少(当然,海外晕针少见也与多采用平卧位有关)。但是,针感与刺激强度有时可以发生分离。如在同一身体部位,寻找敏感点或反映点的针刺方法,即使刺激轻也会有较强的针感或神经传入,也容易诱发强烈的自主神经反应,诱发晕针[7];或者,即使没有明显的针感,只要刺激强也会导致晕针,浮针就是一个例子。浮针,是一种应用类似注射针头的粗针在“患肌”部位的皮下疏松结缔组织作左右“扫散”的疗法,对局部肌肉疼痛效果甚佳[93]。由于皮下很少神经纤维分布,多数患者在接受浮针治疗时没有明显针刺感觉,但其临床上晕针的几率明显高于传统针刺(有临床医生估计高出5倍),通常是在进针后做扫散动作时发生,尤其是年轻男性取坐位首次接受浮针刺激时,故浮针培训时特别强调预防晕针。更有意思的是,有报道浮针可以改善直立性晕厥的症状[94]。如何解释浮针的这个“双向作用”,笔者认为,浮针的扫散刺激最有可能是大幅度拨动了皮下组织中分布的皮穿支血管(perforator)[肌皮穿支、肌间隔(隙)穿支或轴型血管直接皮穿支的总称][95-96](插页Ⅷ图4),由此触发其(尤其是肌皮穿支)连接的“患肌”血管的反射性疏缩活动:原先肌肉血管收缩的可以扩张,导致局部血流量改善,有利于立即改善患肌的痉挛与疼痛,这应该是浮针治疗局部患肌病痛疗效快捷的主要机制;尽管至今尚不清楚浮针机械刺激下的这种反射活动影响的范围有多大,或许可以触发全身性的交感缩血管张力下降。一旦较大范围的肌肉、皮肤血管扩张,显然可使外周阻力下降,导致血压下降,这或许就是浮针治疗多发晕针的原因。如果治疗前躯体局部血管张力低,浮针则可能提高其张力,尤其是较长时期的重复刺激皮穿支血管,很可能有助于提高其对交感神经的敏感性,这或许是上述报道浮针可以对抗直立性晕厥的机制之一。总之,浮针治疗局部肌肉病痛及多发晕针的主要机制,很大可能离不开它对患肌局部皮穿支血管的强力“扫散”(机械)刺激。当然,这一推测尚有待验证,并且值得深入研究。
晕针来得突然,又经常似乎来势凶险,针灸临床上既要保证晕针“不伤人”,又要期待有机会“获大效”。为了晕针的两个目标,临床处置措施之间难免经常需要权衡(tradeoff)。
因为晕针属于血管迷走性晕厥,现代医学对血管迷走性晕厥的临床处置均适用于晕针。晕厥的发作通常会被特征性的先兆症状,例如恶心、出汗(或感觉热)、头痛、腹痛和面色苍白所排除[97]。即使晕厥发生,绝大多数患者几分钟或半小时内即可完全恢复,其后也无须随访或医疗干预。晕厥时的紧急处置,首先让患者在凉爽、安静的地方躺平,确保呼吸畅通,严密观察是否仍有呼吸与监测心率、血压。如果无法躺平,亦可坐着,将头放在膝盖之间至少10~15 min,以增加流向心脏并进而流向大脑的血液。如果患者感到恶心,可侧身以防止窒息,饮用冷水[46]。有研究证明,直立性晕厥前期饮用200 mL冷水或冷碳酸水比温水更会升高血压并改善压力感受性反射功能[98]。
因为晕针是在针灸情景下的晕厥,又有自己的特点。患者出现晕针先兆时,是否要拔针?是否要再在其他穴位施针急救?一般来说,此时只要把患者置于平卧位,停止针灸刺激(拔除毫针或保持留针但不再运针或加电刺激),往往瞬间就会恢复,可以避免晕厥的发生。因为晕针不是休克,对生命没有危害,没有必要再作针灸干预。但是,如果患者晕针后神志不清,未能及时苏醒,或下降的血压、心率迟迟没有恢复正常,则可以对症施针或按压一些急救穴位。如对于上述Ⅲ型迷走神经高度兴奋导致的晕针患者,可应用针刺四肢末梢或躯体正中线那些能提高交感或中枢兴奋性的穴位(如十宣、十二井、合谷、水沟等)来促醒[45];而对于Ⅱ型因为交感神经兴奋性受抑制的晕针患者,则可以针刺耳迷走神经分布区——耳甲区来对抗。
现代的针灸学教材中,晕针被列为针刺异常情况的首位而防范,但对临床上有时出现病人晕针后反而疗效增加的事实从未涉及,这显然是片面的。应该认识到,晕针虽然来势汹汹,会增加患者对针灸的恐惧,有时甚至会导致患者跌倒致伤,但至今未见晕针导致死亡的报道,而且其生物学目的还是保护患者,有利于疾病状态的自愈。因此,除对易感人群特别关注外无须刻意预防,出现晕针先兆时防范跌倒损伤为首位,对晕厥者可拔针并且取平卧位等待自然恢复,严密监视心率、血压与呼吸;除非晕厥持续,无须再施针。但对无晕厥或晕厥迅速苏醒者,也可不拔针,继续留针但不再增加刺激,期待增效。
何为晕针的易感(即高危)人群,如何特别关注,晕针的易感性,首先是曾经有晕针或晕厥史的患者,因为晕针一旦首次发生,经常后续再次发生,故初诊时要首先了解患者晕针或晕厥史,包括以往晕厥时的体位、触发因素、临床表现及家属晕厥史。再者是动脉压力感受性反射不稳定或交感神经兴奋性较高(心率或血压偏高)的人群。前者多为体质虚弱或老人(即古人所云“神气虚”者),后者多见青年男性(如前述浮针晕针者)。为此,有条件时可测定心率变异性与动脉压力感受性反射的稳定性。测定心率变异性经常以HF/LF的比值大小来评估交感/副交感神经的联合工作状态。动脉压力感受性反射的状态经常以脉压差的大小来粗略估计。其三,平时精神紧张或情绪不稳定者,面对针灸临床情景可以导致交感神经兴奋性的进一步提高,导致晕针的易感性增加。以上这些易感人群在直立(坐)位更容易晕针;当然,如果再加上强烈针感的应激刺激,晕针的几率更高。所以,对这些易感人群的特别关注措施包括:疏解紧张情绪,选择平躺体位,以及控制适宜的刺激强度包括避免刺激敏感部位的穴位。已经有许多已经观察到采取这些措施对晕针的预防作用十分明显[99]。
关于与晕针相关的体位,临床上最常见的是坐位,卧位较少发生[10]。其实坐位也有一种特别的姿势-坐位头偏一侧伏在桌面上,有助于避免晕针。有报道,坐位头偏一侧伏在采血台上采血发生晕针的几率与平卧位采血无明显差别[100];该体位采血时配合深呼吸,转移其注意力和消除顾虑,可以明显减少晕针的发生[43]。临床上如果晕针发生在平卧位,则可以让患者进一步以头低足高的姿势克服之。以上简述了如何避免或减少晕针发生以及在晕厥发生前后的临床处置,适合于那些晕针易感性高或即使发生晕针对疗效也无明显影响的患者。
综上所述,晕针是针灸临床情景下的血管迷走性晕厥-由神经反射导致的短暂性的脑缺血。因为至今为止的大量临床实践已经证明,晕针通常不会威胁生命,而且可以迅速恢复,晕针时的应激反应与迷走神经活动增加,有时还可能提高针灸抗炎、镇痛、改善自主神经功能紊乱的疗效,故临床上偶然发生晕针这类不良反应不再只是坏事,其处置方法也要相应变化。笔者以为,李守先有关晕针“不伤人”与“获大效”的表述,恰当地反映了晕针现象的这两个特点。搞清这六个字背后的神经机制,无疑有利于改良目前的晕针处置措施,而且可以从放大针灸效应的角度,去理解针灸治病的一般机制及启示提高疗效的对策。
在保证“不伤人”与期待“获大效”的目标之间,经常需要权衡,这对于提高针灸临床的安全性与有效性均有重要意义。简单说来,一方面不可一味追求疗效,而故意促发晕针,须因人、因病、因刺激部位制宜,实施合适的针刺刺激,实现安全而有效的针刺治疗[78];另一方面对于晕针易感性低,常规针灸疗效不显著的患者,也大可不必担忧晕针的发生,甚至可以刻意取坐位、选用敏感性高的刺激部(穴)位、强刺激手段,通过增大刺激量来打破疾病稳定态。

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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
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