Is Deqi an Indicator of Clinical Efficacy of Acupuncture? A Systematic Review

Table 1

A summary of studies on Deqi mechanism in acupuncture.

Study ID	Acupoints	Instrument	Results
Lin 1991 [4]	Acupoints on the human thorax	Voll’s electroacupuncture devise and electric resistance tester	The electric resistance at acupoints on the human thorax was not correlated with the existence of Deqi sensations at the same point.
Ma 1998 [5]	NA	NA	It is hypothesized that activation of the stretch-activated ion channels is a mediator of the Deqi sensation and the transduction of stimulation signals.
Huang et al. 2012 [6]	LI3, LI4, LI5, LI11	Speckle laser blood flow scanner	AWD at LI11 increased microvascular perfusion at 3 meridian acupoints.
Watanabe et al. 1994 [7]	LI10	DP1100 system	The latency of the event-related potential triggered triggered by AWD was greater than that by electric stimulation. This showed that AWD may influence CNS functions.
Huang 1999 [8]	ST36	EGEG-2DZ	EGG amplitude and the waveform reaction area in two types of Deqi groups differed greatly from those in AOD control.
Sandberg et al. 2003 [9]	ST36	PPG	AWD markedly increased muscle and skin blood flow compared with AOD.
Zhang et al. 2009 [10]	ST36	CDU	AWD greatly changed hemodynamic parameters of the anterior tibial artery.
Yu et al. 2008 [11]	ST36, LI11	CDU	AWD at both points markedly increased the average displacement of the surrounding connective tissues.
Karst et al. 2003 [12]	LI11	Flow cytometry	AWD significantly increased the respiratory burst of neutrophils and slightly dropped beta-endorphin levels.
Streitberger et al. 2008 [13]	LI4	NA	AWD induced more frequent occurrence of vegetative effects and increased occipital EEG power compared with placebo.
Huang et al. 2009 [14]	PC6	PCS	AWD at PC6 markedly increased TCE values measured at a nonacupoint on the meridian.
Huang et al. 2010 [15]	PC6	PCS	AWD at PC6 markedly increased TCE values measured at two nonacupoints on the meridian and at PC3.
Takamoto et al. 2010[16]	#	Functional near-infrared spectroscopy	AWD decreased oxy-Hb concentration in SMA, pre-SMA, and the anterior dorsomedial prefrontal cortex for all stimulated points.
Zhang et al. 2011 [17]	SJ5	PET	AWD activated BA7, -13, -20, -22, -39, -42, and -45.
Lai et al. 2009 [18]	TE5	PET	AWD markedly activated BA13 and 42 and the left cerebellum compared with sham needling.
Chen et al. 2012 [19]	TE5	SPECT	AWD significantly activated BA6, -8, -19, -21, -28, -33, -35, -37, and -47, parahippocampal gyrus, lentiform nucleus, claustrum, and red nucleus, and it deactivated BA9 and -25 compared with sham needling.
Pan et al. 2008 [20]	SP6	fMRI	AWD activated the cortex, the subcortical limbic system, the cingulated gyrus, the lentiform nucleus, the corpus albicans, and the inferior semilunar lobule, and it deactivated the anterior central gyrus and the anterior cingulate.
Zeng 2009 [21]	SJ5	fMRI	AWD markedly activated BA13, -22, -37, -40, -44, -45, and -47, hippocampus, amygdale, and substantia nigra.
Chen et al. 2011 [22]	LI4	fMRI	AWD activated BA4, -6, -9, -13, -17, -18, -19, -21, -22, -23, -29, -30, -35, -36, -37, -39, -40, -41, -42, -43, -44, and -46, and it deactivated medial frontal gyrus, BA24, and the right superior frontal gyrus.
Fang et al. 2012 [23]	LI4	fMRI	AWD deactivated the right amygdale, the cingulated gyrus, the midbrain, the medial frontal gyrus, and the cuneus gyrus.
Fang et al. 2012 [24]	LR3	fMRI	AWD deactivated the limbic-paralimbic-neocortical network and strengthened the connection of these deactivated brain regions.
Tan et al. 2009 [25]	ST36	fMRI	AWD activated functional areas of the cerebral limbic system and dropped serum gastrin levels.
Zhang 2011 [26]	ST36	fMRI	AWD activated cerebral areas SI and SII, the left temporal cortex, the insular cortex, the motor, and supplementary motor cortices, the cingulated gyrus, the hypothalamus, and the amygdaloid body.
Hu et al. 2012 [27]	ST36	fMRI	AWD deactivated the cerebral limbic system and the functional regions associated with language, cognition, and motor control.
Wu et al. 1999 [28]	LI4, ST36	fMRI	AWD at both points activated the hypothalamus and the nucleus accumbens, and it deactivated the rostral part of the anterior cingulate cortex, the amygdala formation, and the hippocampal complex compared with no such effects from AOD.
Gong et al. 2003 [29]	ST36, ST37	fMRI	AWD at both points activated bilateral cingulated gyrus, insular lobe, superior wall of lateral sulcus, and precentral gyrus. AOD at both points activated the left posterior central gyrus. Different cerebral areas were activated during Deqi and non-Deqi at the same point.
Claunch et al. 2012 [30]	LI4, ST36, LR3	fMRI	AWD at all three points deactivated the right subgenual, the right subgenual cingulate, the right isthmus of the cingulum bundle, and the right BA31.
Asghar et al. 2010 [31]	LI4	fMRI	Marked deactivation of the brain area was observed during Deqi in contrast to the occurrence of a mixture of activations and deactivations in the acute pain group.
Hui et al. 2005 [32]	ST36	fMRI	Attenuation of signal intensity in the limbic and paralimbic structures of cortical and subcortical regions in telencephalon, the diencephalon, the brainstem, and the cerebellum was observed during AWD compared with signal increase with the acute pain and the AOD group.

#: acupoints and nonacupoints within the right extensor muscle in the forearm; AOD: acupuncture without Deqi; AWD: acupuncture with Deqi; BA: brodmann area; CDU: color Doppler ultrasound; CNS: central nervous system; EGG: electrogastroenterogram; fMRI: functional magnetic resonance imaging; NA: not available; PCS: percutaneous carbon dioxide sensor; PET: positron emission tomography; PPG: photoplethysmography; SI: secondary somatosensory cortex; SII: primal somatosensory cortex; SMA: supplementary motor area; SPECT: single-photon emission computed tomography; TCE: transcutaneous CO₂ emission.