Acupuncture Side Effects

Non-acupuncture points

Non-acupuncture points
Non-acupuncture points were differentiated by their connection to different pathways in the central nervous system. We have found that the pathway connected to the acupuncture point is different from the pathway connected to the non-acupuncture point. In addition, pathway connected to the non-acupuncture point is restrained or prevented within the lateral periaqueductal gray when the analgesia inhibitory system (AIS) is activated. We have explored these pathways by means of selective damage or injury of discrete brain regions, selective stimulation of brain regions, as well as by recording inspiring potentials arising from stimulation of non-acupuncture points. It was found that the lateral centromedian nucleus of the thalamus and the posterior hypothalamus are parts of the AIS. The non-acupuncture (abdominal muscle) points are both connected to the AIS. Analgesia caused by stimulation of the acupuncture point is naloxone reversible, while that caused by stimulation of the non-acupuncture point after injury of AIS is dexamethasone reversible. Stress-induced analgesia caused by low frequency electrical shock is naloxone as well as dexamethasone reversible. All three kinds of analgesia were abolished by hypophysectomy. The features and the degree of analgesia caused by intraperitoneal(within) 0.5 mg/kg morphine were similar to analgesia caused by acupuncture point stimulation. D-phenylalanine acts like a lesion of AIS in analgesia caused by stimulation of non-acupuncture points, and enhances naloxone reversible analgesia. The descending pain inhibitory system plays a role as the common pathway to produce these three kinds of analgesia. This pathway is found in the arcuate nucleus (dopaminergic), ventromedian nucleus of the hypothalamus, raphe nucleus (serotonergic), reticular gigantocellular nucleus (noradrenergic) and reticular paragigantocellular nucleus.
Acupuncture analgesia (AA), caused by low-frequency stimulation of an acupuncture point (AP)–in this case the tibial muscle–was augmented. Nonacupuncture analgesia (NAA), caused under certain circumstances by stimulation of a nonacupuncture point (NAP)–in this case the abdominal muscle–was unmasked by danger in the lateral centromedian nucleus of the thalamus (L-CM) or part of the posterior hypothalamus (I-PH). Stimulation in these regions suppressed the augmented part of the AA and blocked the NAA. These regions were, collectively, given the name analgesia inhibitory system. NAA was abolished, the same as AA, by hypophysectomy. The pathways from the AP and NAP to the pituitary gland were different. AA was naloxone reversible, and NAA was dexamethasone reversible. The analgesia inhibitory system is activated nonspecifically by stimulation of either an AP or NAP. It ascends to the I-PH, literary from the place to the L-CM, and ultimately inhibits the pathway nonspecifically connected to the NAP and AP in the lateral part of the periaqueductal central gray (PAG), without affecting the pathway specifically connected to the AP. Thus, only stimulation of an AP will produce analgesia, whereas stimulation of an NAP will not normally produce analgesia. Stress-induced analgesia (SIA) is produced in a different way than AA or NAA.
In this study, we used the 3 phases of SC-RNV to evaluate the absorption of Tc-99m pertechnetate injected subcutaneously in the acupuncture point SP-10 (Xuehai) and in a non-acupuncture point near SP-10. The results revealed that the absorption of Tc-99m pertechnetate via SP-10 was significantly greater than that of non-acupuncture point, evidenced by shorter phase 1, higher peak activity and greater accelerating rate of phase 2. This suggests that the absorption of radioisotopes from acupuncture point is faster and greater than that of non-acupuncture point.