Philip A.M. Rogers MRCVS

AP and Neurology


Abad-Alegría_F1; Bono Ariño J (1992) [Modulatory capability of the somatosensory afferents through AP reflexotherapy]. Arch Neurobiol (Madr) May-Jun 55(3):99-102. Clinical Neurophysiol Service, Univ Hospital, Zaragoza, Spain. This paper concerns the influence of the AP on the somatic afferent volley. As the main used points in experimental AP, we stimulated LI04 and HT07. AP modulated somaesthetic afference and different points had different modes of action.

Abad-Alegria_F2; Adelantado S; Martinez T (1995) The role of the cerebral cortex in AP modulation of the somaesthetic afferent. AJCM 23(1):11-14. Clinical Neurophysiol Service, Univ Hospital, Zaragoza, Spain. AP stimulation modifies the somaesthetic afferent to different degrees, depending on the AP point studied. In this study, SEPs of 21 healthy volunteers were recorded. AP at LI04 produced noticeable modifications, with a significant increase of latency and decrease of amplitude of the peaks which reflected the primary cortical afferent. These changes were minimal or absent when a non-AP point was stimulated. The effects on SEPs observed depended on the special quality of the AP point stimulated and not on the mere repetitive stimulation on the skin.

Abad-Alegria_F3; Galve JA; Martinez T (1995) Changes of cerebral endogenous evoked potentials by AP stimulation: a P300 study. AJCM 23(2):115-119. Clinical Neurophysiol Service, Univ Hospital, Zaragoza, Spain. The change of cerebral potential P300 in relation to superior cerebral functions by means of AP stimulation was studied immediately after, and within the next 15 min after, AP stimulation at HT07 and LI04, and at a non-AP control point. After stimulation at HT07, P300 amplitude changed significantly and increased with time. Changes were not detected after stimulation of LI04, or of a non-AP point. These findings support a real action of HT07 (Shen Men, Spirit Door) in different psychoneurological processes.

Andersson_S; Lundeberg T (1995) AP: from empiricism to science: functional background to AP effects in pain and disease. Med Hypotheses Sep 45(3):271-81. Dept of Physiol, Univ of Göteborg, Sweden. AP is part of TCM, a system with an empirical basis which has been used to treat and prevent disease for centuries. A lack of scientific studies to prove or disprove its claimed effects led to rejection by many of the western scientific community. Now that the mechanisms can be partly explained in terms of endogenous pain inhibitory systems, the integration of AP with conventional medicine may be possible. Its use for pain relief has been supported by clinical trials and this has facilitated its acceptance in pain clinics in most countries. AP effects must devolve from physiological and/or psychological mechanisms with biological foundations, and needle stimulation may represent the artificial activation of systems obtained by natural biological effects in functional situations. AP and some other forms of sensory stimulation elicit similar effects in man and other mammals, suggesting that they induce fundamental physiological changes. AP excites receptors or nerve fibres in the stimulated tissue which are also physiologically activated by strong muscle contractions and the effects on certain organ functions are similar to those obtained by protracted exercise. Both exercise and AP produce rhythmic discharges in nerve fibres, and cause the release of endogenous opioids and oxytocin essential to the induction of functional changes in different organ systems. Beta-End levels, important in pain control as well as in the regulation of blood pressure and body temperature, rise in the brain tissue of animals after both AP and strong exercise. Experimental and clinical evidence suggest that AP may affect the sympathetic system via mechanisms at the hypothalamic and brainstem levels, and that the hypothalamic beta-endorphinergic system has inhibitory effects on the vasomotor centre, VMC. Poststimulatory sympathetic inhibition, which reaches a maximum after a few hours and can be sustained for >12 h, occurs in both man and animals. Experimental and clinical studies suggest that afferent input in somatic nerve fibres has a significant effect on functions of the ANS. Hypothetically, the physiological counterpart lies in physical exercise, and the effect can be artificially reproduced via various types of electrical- or manual- stimulation of certain nerve fibres.

Anon_(1993) Western Physiological-Basis of AP: Editorial. J Equine Vet Sci Aug 13(8):442.

Bucinskaite_V1; Lundeberg T; Stenfors C; Ekblom A; Dahlin L; Theodorsson E (1994) Effects of EAP and physical exercise on regional levels of neuropeptides in rat brain. Brain Res 12 Dec 666(1):128-132. Dept of Physiology and Pharmacology, Karolinska Inst, Stockholm, Sweden. The effects of single or repeated treatments with manual AP, EAP or physical exercise on neuropeptide Y (NPY), neurokinin A (NKA), Substance-P (SP), galanin (GAL) and vasoactive intestinal peptide (VIP)-like immunoreactivity (-LI) in different regions of the rat brain were studied. Initially the effect of microwave irradiation (MWI) was compared to decapitation on the recovery of neuropeptides, and significantly higher levels of SP-LI, NKA-LI and NPY-LI were found in the hippocampus, occipital cortex, pituitary and striatum after MWI. Repeated EAP treatments significantly increased SP-LI, NKA-LI and NPY-LI in the hippocampus and NPY-LI in the occipital cortex. No changes were found in animals receiving AP or performing physical exercise.

Bucinskaite_V2; Theodorsson E; Crumpton K; Stenfors C; Ekblom A; Lundeberg T (1996) Effects of repeated sensory stimulation (EAP) and physical exercise (running) on open-field behaviour and levels of neuropeptides in the hippocampus in WKY and SHR rats. OUP European Journal of Neuroscience WWW service, 8(2):382-387. OUP Journals WWW Service. Copyright Oxford Univ Press. Dept of Physiol and Pharmacol, Karolinska Inst, Doktorsringen 6A, S-171 77 Stockholm, Sweden. The effects of repeated EAP and physical exercise (running) on open-field behaviour and on hippocampal levels of neuropeptide Y, neurokinin A, Substance-P, galanin and vasoactive intestinal peptide (VIP)-like immunoreactivities were studied in WKY (wistar-Kyoto) and SHR (spontaneously hypertensive) rats. Significantly higher levels of Substance-P-like immunoreactivity, neurokinin A-like immunoreactivity and neuropeptide Y-like immunoreactivity were found in the hippocampus immediately after 3 wk of treatment (EAP and running), but not 1 wk after the last (10th) changes in neuropeptide levels were similar in the 2 rat strains. Open-field behaviour was significantly less during the treatment period in both strains. Negative correlations between behaviour and neuropeptide levels in SHR rats were significant, suggesting interdependency with sympathetic activity. The effects of EAP and physical exercise in rats are related to increases in neuropeptide Y, neurokinin A and Substance-P in the hippocampus.

Cai_W (1992) AP and the nervous system. AJCM 20(3-4):331-337. Dept of Neurol, Stritch Sch of Med, Loyola Univ of Chicago, Maywood, IL 60153. AP is based on neuroanatomy and neurophysiology. At each AP point, there are peripheral nerves and terminals. AP will be useful for further understanding of the nervous system. A conceptual view of the physiology of AP is presented.

de_Carvalho LA (1994) Modelling the thalamocortical loop. Int J Biomed Comput May 35(4):267-296. COPPE, Universidade Federal do Rio de Janeiro, Brazil. This work proposes a mathematical model for the thalamic gateway to the cortex. In this model, the ionic currents considered and the structural details are in accordance with the bioMed experimental data. To validate the model, 3 series of simulations were performed in different levels of complexity. First, some experiments show that the model captures the electrophysiological properties of a single thalamic cell, that is, the relay and burst modes of operation. Second, a complete neural network representing the thalamic gateway to the cortex is assembled and the influences of the cortical projections over the thalamus are analyzed. Data on how the cortex opens and closes the thalamic gate, and the relation of this control with the phenomenon of attention, are shown. A third set of simulations establishes mechanisms of interaction between neighbouring thalamic regions, especially a form of somatosensory competition. The paper also hints at possible theoretical explanations for clinical facts like counterirritation, AP-analgesia (APA) and variations in the sensibility of somatosensory perception. The model may be a novel way to understand thalamocortical interactions.

de_Vernejoul_P; Albarede P; Darras JC (1992) Nuclear medicine and AP message transmission [editorial]. J Nucl Med Mar 33(3):409-412.

Dong_Q; Dong X; Li H; Chen D; Xian M (1993) [The relations between AP manipulations and responsive discharges of deep receptors]. Chen Tzu Yen Chiu 18(1):75-82. Dept of physiology, Inst of Clinical Medicine, Sichuan Acad of TCM, Chengdu. 29 rabbits were used. The spindle, tendon organ, light and heavy pressure receptors in medial gastrocnemius muscle were identified by recording discharges of single afferent fibre in medial gastrocnemius nerve from fine filaments by dissection. The discharge patterns of the receptors responding to the manipulations (lift and thrust, twist and twirl, rotate, scrape flick the needle and finger-pressure) were observed. Data at 85 units were collected totally. Every type of deep receptor can react to any manipulation. The discharge patterns of different receptors were alike when stimulated with same manipulation, but there were different patterns while varying manipulations acting on the same receptor. These are due to the movement forms, the force amount, the time duration of the manipulations. All these facts are nearly the same as in cutaneous receptors. AP effect on deep receptors was not limited to one point but within a certain area, namely distant effect existed. The area size varied from receptor to receptor and from manipulation to manipulation. Because of the distant effect on receptors by AP, and the lose of responsibility in units when receptor destroyed, we suggest that effective AP stimulation is induced mainly due to the receptor deformation, which is caused by the stress from pressure, stretch and vibration of AP. As the needling sensation is closely related to the curative effects, the receptors dealing with needling sensation are analyzed according to this series works and other facts, we further advance the opinion that the receptors of deep pain are the chief material foundation to induce the sensation of hand needling.

Dong_Q; Dong X; Chen D; Li H; Zhang S (1992) [The relation between AP manipulations and responsive discharges of cutaneous receptors]. Chen Tzu Yen Chiu 17(3):221-229. Dept of Physiology, Sichuan Acad of TCM, Chengu. Nine types of mechanoreceptors of hair skin in 46 rabbits were identified by recording discharges of single afferent fibres in posterior femoral cutaneous nerve from fine filaments by dissection. Responsive discharges were studied to 7 different types of stimuli by needle manipulation or pressure to each receptor: lift and thrust, twist and twirl, rotate, serape, flick the needle and finger-pressure. Data were collected for 165 units, of which 89 units were for the relation between manipulation and discharge patterns, and the other 76 units for discharges responding to manipulations at different distances from the receptive field. Nine types of receptors were observed as responsive to any type of AP manipulation. Thus, no special "AP receptor" exists. Different types of receptor had the same type of discharge pattern in response to the same type of AP manipulation, whereas different discharge patterns occurred at the same unit when the manipulation changed. This may be due to the movement form; force amount and time duration of the manipulations. Receptors responding to AP were not limited to one specific point, but involved a field surrounding the needle point. The size of this field varied with the types of receptors and of manipulation. We reported previously that the AP photograph leading from nerve and building on impulses induced by AP and the groups of afferent fibres conducting AP signals changed with different manipulations. This paper discusses the reasons for that by presenting the relationship between the responsive discharges of receptors and the manipulations.

Feely RA (1996) AP: The Basics Richard Feely DO, RHEMA Med Assoc Ltd. Adapted from WWW; email:

AP was a part of TCM >5,000 yr ago. TCM science had a very different paradigm/way of thinking than the Western world. It emphasized holistic patterns, relationships, cycles, and processes. In contrast the western paradigm emphasizes linear thinking, causality and reductionist explanations. AP was first introduced into Europe by the French Jesuits in the 17th Century. It was not widely accepted in the West because of the clash of paradigms that is Western linear thinking couldn't understand how a needle inserted into the hand could cure a toothache. APA did not fit into the existing physiological paradigms of WM and was thus dismissed.

Up until 1976, the evidence for APA was mainly anecdotal. There are few controlled scientific experiments. Since then, the situation has changed dramatically in the last few years there has been many scientifically controlled experiments in AP. At least 17 different lines of scientific evidence verify the AP effect upon humans and animals.

Does APA work?.
Research performed in animals and humans shows that specific AP relieved pain while sham AP (needles at non-AP points) had no pain relieving effect. Controlled clinical trials compared real AP to sham AP in chronic pain patients; AP worked better than placebo in many of the studies. More importantly, AP was as effective as conventional treatment in chronic pain, and had fewer side effects.

How does AP work?.
Needling simulates peripheral nerves in the muscles which send messages to the brain to release endorphins (morphine-like peptides in the brain). These neurochemicals then cause analgesia by blocking the transmission of painful messages. 3 main sites for endorphin APA are known:
1.        The pituitary gland releases endorphins into the blood stream. This hormone travels to the 3 parts of the brain and spinal cord to block the transmission of painful messages.
2.        The PAG neurons in the midbrain release endorphins that act as local transmitters to excite the rostral ventromedial medulla.
3.        The rostal ventromedial medulla in turn projects massively and selectively to pain transmitting neurons in the dorsal horn of the spinal cord and the trigeminal nucleus caudalis. Electrostimulation in the PAG and rostral ventromedial medulla (RVM) produces behavioral analgesia and inhibitions of spinal pain transmission. The spinal cord endorphin system, is where the spinal cord neurons release endorphins to block the release of neurotransmitters from afferent fibres carrying painful messages to the cord.

In 1977, research showed that APA inhibited the spinothalamic tract neurons from responding from painful inputs. This AP effect was then blocked by naloxone, an endorphin receptor blocker. Also, behaviour measurements in mice and humans showed that naloxone blocked APA. AP research has progressed since the 1970s to date to have 17 different lines of evidence convergent upon AP endorphin mechanisms verifying and supporting APA.

The 3 known sites of endorphin release (above), and other evidence (below) are convincing proof that APA is a physiological phenomenon that can occur and be manipulated through the use of AP needles and electrostimulation.

17 lines of convergent evidence of endorphin in APA.
1.        naloxone blocked APA.
2.        opiate antagonists block APA.
3.        dextro-naloxone doesn't block APA.
4.        antibodies to endorphins block APA.
5.        micro-injection of naloxone blocks APA.
6.        genetic defects in opiate receptors reduce or prevent APA.
7.        Depletion in endorphins reduce APA.
8.        endorphins rise in CSF and fall in the brain after APA.
9.        APA is enhanced by protecting from enzyme destruction.
10.        cross circulation of APA effects.
11.        reduced pituitary endorphins block APA.
12.        a rise in mRNA for proenkephalin with APA.
13.        C-fos gene protein rises in endorphin areas of brain.
14.        APA shows cross tolerance with morphine addiction.
15.        APA works best for emotional pain like endorphin.
16.        lesions of arcuate nucleus block APA.
17.        lesions of PAG block APA.

Testing the involvement of the pituitary, several experiments were carried out, both surgically removable pituitary and suppression of the pituitary endorphins by chemical manipulations all of the experiment suppressed APA in animals. Since morphine analgesia is mediated largely by this system, experiments to test the involvement of the midbrain in APA were done. Such experiments include direct lesions to the raphe by cutting the output fibres in the dorsal lateral tract, blockade of serotonin receptors in the spinal cord, blockade of serotonin synthesis and direct micro-injection of naloxone into the midbrain. All of these procedures reduced APA.

Enhancement of serotonin synthesis increased APA. An experiment measuring serotonin showed serotonin was released during APA along with noradrenaline.

Does AP work all the time?.
No, AP works in circa 70-80% of humans and animals. Meanwhile, placebo only works 30% of the time. AP does not work all the time in all people for various reasons. People with high levels of cholecystokinin (CCK) are poor responders to APA. Good responders have less CCK. CCK blocks AP tolerance, it acts in the PAG. In animal experiments, poor responders became better responders through the use of a CCK antagonist, and good responders became poor responders by the use of cDNA, CCK gene.

AP is not physiologically addictive. AP is however additive and cumulative in its effects. It is more powerful after 10-15 treatments. Neurologically we know AP works with a small myelinated fibres A delta-type III, and it does not work larger fibres, C-fibres.

Why does TENS not work as well as AP?.
TENS works by using the gate theory of pain and habituation occurs. TENS activates skin, neurons first and A-delta fibres, the key fibres which are in the muscle, are not activated. With the use of needle AP Deqi activates the small myelinated A-delta fibres. Dr Bruce Pomeranz reports that the A-delta fibres and the Deqi activate the stimulation of the endorphin mechanism.

In conclusion, AP has been used for over 5000 yr. A large body of empirical anecdotal evidence indicates its effectiveness. Scientific research indicates several causes and effects of AP. AP is effective for acute and chronic pain, the treatment of addiction and withdrawal from various drugs, gastrointestinal functions, environmental illnesses and cardiovascular illness, along with positively changing with learning/memory, conditioning and immunology.

More and more physicians outside China are using AP to treat many painful conditions. It is estimated that 5000 MDs in Germany, 30000 in France and 60000 in Japan use AP along with drugs, nerve blocks and other approaches to treat patients with chronic pain. Here in the USA >1000 physicians and surgeons are actively in the practice of AP. With increasing research and evidence, more and more physicians in the West will become AP practitioners.

Futaesaku_Y; Zhai N; Ono M; Watanabe M; Zhao J; Zhang C; Li L; Shi X (1995) Brain activity of a rat reflects apparently the stimulation of AP: radioautography using 2-deoxyglucose. Cell Mol Biol Noisy le grand Feb 41(1):161-170. Dept of Histol and Analytical Morphol, Sch of Allied Health Sci, Kitasato Univ, Kanagawa, Japan. To confirm a relationship between the CNS and AP, the response was examined in the rat brain using radioautography with tritiated 2-deoxyglucose, after stimulation of some AP points. 8 groups, of a total of 27 rats were submitted to AP at 6 different AP points (ST36, GV26, ST25, HT07, PC06, KI01) and control, with or without electric pulses or with anaesthesia respectively, before the injection with isotopic deoxyglucose. 120 cryosections were cut from a freshly frozen brain and exposed on single-coated X-ray films. Compared with the control group, AP at ST36, ST25, HT07 and PC06 enhanced neocortical-, limbic cortical- and thalamic nuclear- activity. AP at GV26 and KI01 depressed the activity on the thalamic nuclei and midbrain. Pentobarbital anaesthesia concealed most activity all over the brain, which hardly responded to any AP stimulus. Brain neuronal activity reflected the signals from AP stimuli and activity changed depending upon each AP point.

Gao_W; Peng G (1994) Surface anatomic observation of cerebral precentral and postcentral gyri for scalp AP. Chen Tzu Yen Chiu - AP Research 19(2):17-20. Ghongqing Univ of Med Sci, Sichuan, PRC. Heads of 10 adult corpses were used to investigate the motor and sensory area of scalp AP. AP textbook locations for the surface anatomy of the precentral and postcentral gyrus did not match exactly with the scalp motor- and sensory- area respectively. The locations of the respective gyri were more posterior than in the textbook. The upper precentral and postcentral gyrus points were 0.5 cm behind the motor area and 1 cm behind the sensory area; the lower precentral gyrus point was 1 cm behind the intersection of the eyebrow-occiput line and the anterior border of the natural temporal hairline; the lower postcentral gyrus point was 2.4 cm posterior to the intersecting point above described. In order to better coincide with the precentral and postcentral gyri, the motor and sensory areas of scalp AP should be placed further back than in the textbook. Best locations were: upper point of motor and sensory area: 1 cm and 3 cm posterior to the midpoint of anteroposterior midline, respectively; lower point of motor and sensory area: 1 cm and 2 cm posterior to the intersecting point described above, respectively.

Joseph_R (1992) Neurologic evaluation and its relation to AP: AP for neurologic disorders. Animal Med Centre, New York, New York 10021. Probl Vet Med Mar 4(1):98-106. AP provides companion animal Vets a valid therapeutic alternative to medicine and surgery in a variety of neurologic disorders. The Vet must arrive at a lesion localization in the nervous system and determine a presumptive diagnosis before instituting AP therapy. Signalment, type of neurologic disorder, efficacy of conventional treatments versus AP, financial constraints, and ethical issues are useful patient selection criteria. In general, animals with pain respond faster and more completely to AP than those with neurologic deficits consistent with loss of function. AP offers clients a noninvasive alternative when medications are contraindicated or surgery is not an option. This chapter serves as an introduction to AP for neurologic disorders in pets. It is hoped that the information here will inspire clinical investigations to evaluate more completely patient selection, patient response, and long-term outcome.

Kashiba_H; Nishigori A; Ueda Y (1992) Expression of galanin in rat primary sensory afferents after moxibustion to the skin. AJCM 20(2):103-114. Dept of Physiol, Kansai Coll of AP Med, Osaka, Japan. We examined the effects of moxibustion on primary sensory neurons in the skin of rats using immunocytochemistry combined with a fluorescent retrograde tracer dye, fluoro gold (FG). Galanin-like immunoreactive (IR) fibres were often observed in the dermis of treated skin at 18 h after moxibustion, while such fibres were rarely detected in untreated (control) skin. Moreover, most of galanin-IR fibres also displayed Substance-P (SP)-like immunoreactivity. Circa 20-30% of the dorsal root ganglion (DRG) neurons labelled when FG was injected intradermally into the moxibustion-treated skin showed galanin-like immunoreactivity, while the proportion of FG-labelled neurons with such immunoreactivity was <10% in control DRGs. Moxibustion induced galanin expression by primary sensory neurons containing SP. The possible functions of this peptide are discussed in relation to the effects of moxibustion.

Khramov_RN; Karpuk NI; Vorob'ev VV; Gal'chenko AA; Kosarskii LS (1993) The electrical activity of the hypothalamus in exposure to millimetre-wave radiation at biologically active points. Biull Eksp Biol Med Sep 116(9):263-265. Nonthermal local millimetre wave irradiation (55-76 GHz range) of Earpoint HT (after FG Portnov) of conscious rabbits significantly suppressed hypothalamic electrical activity at 5 and 16 Hz and enhanced at 7-8, 12 and 26 Hz. Radiation of TR20 (?? TH20, the "hypothalamus" point after R Voll) gave similar though less prominent results at 7-8 and 12 Hz. Radiation of ST36 (the "longevity" point) gave minimal EEG changes.

Lee_TN (1994) Thalamic neuron theory: theoretical basis for the role played by the CNS in the causes and cures of all diseases. Med Hypotheses Nov 43(5):285-302. Acad of Pain Research, San Francisco, CA 94132. The Thalamic Neuron Theory (TNT) postulates that the CNS is involved in all disease processes, as the CNS not only processes incoming physical and chemical information from the periphery, it also sends out physiological commands to the periphery in order to maintain homeostasis for the entire body. Inherent in its capacity to learn and adapt (e.g. to habituate) is the ability of the CNS to learn to be sick (pathological habituation) by looking in certain deranged CNS neural circuitries, leading to chronic disease states. Pathologically habituated states can be reversed by dehabituation. To mimic the habituation process, this can be done repetitively by modulation of abnormal neural circuits by physical neuromodulation (like AP), or by chemical neuromodulation (such as homeopathy, TCM, or WM techniques). Chemoneuromodulation can also be achieved by delivery of minute amounts of pharmacological agents to specific sites in the periphery such as the AP loci. It is hypothesized that humoral and neurotrophic factors and cytokines may be very effective neuromodulators. TNT assumes that the blue print for embryological development is embodied in the phylogenetically ancient part of the brain. This primordial Master Plan, organized in the form of a homunculus, possibly encased in a small nucleus, retains control over the subsequently evolved parts of the brain so that the entire CNS functions like a composite homunculus which controls the physiological functions of the entire body. TNT further postulates that the master homunculus takes the shape of a curled up embryo with its large head buried close to its pelvic region, with its large feet and hands crossed over to the contralateral sides. Neuronal clusters along a neuronal chain in the homunculus represent AP points in the periphery. The neuronal chain itself represents a Channel and Qi is nothing more than the phenomenon of neurotransmission. Certain new theoretical concepts such as the principles of Adynamic State and Bilaterality are also presented. TNT now can explain adequately many clinical findings which are difficult to explain in WM, CHM, AP and homeopathy. Based on this model, new therapeutic techniques can be launched to combat a whole host of intractable diseases.

Levashov_MI; Iaroshenko VT; Lytvynova AM; Gapon OI (1992) Hyperventilation Syndrome and reflexologic methods of its correction. Fiziol Zh Sep-Oct 38(5):42-45. AP was used to treat hyperventilation disorders, especially hyperventilation Syndrome (HVS). Diagnosis was based on clinical, Lab and functional methods. AP was carried out using the first (strong) variant of classical inhibitive procedure of AP. AP decreased EEG characters of dysrhythmia and exaltation and paroxysmal activity as well as inter-hemisphere asymmetry in patients with HVS. Parallel with a decrease in the degree of negative subjective sensations, minute respiratory volume, non-informity of regional ventilation decreased and partial oxygen pressure in alveolar air increased. Using no pharmacotherapy, it is possible to correct HVS by AP.

Liao_TJ; Nakanishi H; Nishikawa H (1993) The effect of AP stimulation of the middle latency auditory evoked potential. Tohoku J Exp Med Jun 170(2):103-112. Dept of Oriental Med, Meiji Coll of Oriental Med, Kyoto, Japan. The effects of AP stimulation on the middle latency auditory evoked potentials (MLAEPs) were studied in 19 normal male volunteers. Scalp recordings were made from 21 points (including Cz) and posterior auricular muscle (PAM) electrodes referenced to the linked mastoid. 4 components of MLAEPs (Po, Na, Pa and Nb) and 2 components of PAM reflex (N12 and P17) were statistically analyzed for changes in latency and amplitude. Wave phase of Po and Na reversed to N12 and P17, respectively, and the peak-to-peak amplitude of Po-Na, Na-Pa, Pa-Nb and N12-P17 showed a marked increase during AP to the ipsilateral side whereas no change in latency was detected. Each component's isovoltage topographic maps and dipole locations were calculated to be near both PAM (Po and Na) and temporal positions (Pa and Nb) during AP. AP promoted MLAEPs activity and these signals (Po and Na) may originate from increased activity in N12 and P17 of the PAM reflex, respectively. The auditory cortex of the temporal gyrus is the generator substrate of Pa and Nb.

Meng_Z; Lu GW (1993) The functional linkage among ST36 and the spinal dorsal horn-SN. Sci China B Oct 36(10):1198-1206. Dept of Neurobiology, Capital Inst of Med, Beijing, PRC. EAP of ST36 and the solitary tract nucleus (SN) as well as microelectrode recording from the laminae III-V of the lumbar spinal dorsal horn were used on pentobarbital-anaesthetized rats. We identified 57 spinal neurons responding to the stimulations of both ST36 and SN; 34 responded antidromically to SN; the others responded orthodromically to SN. Among them, low-threshold mechanoreceptive (LTM) neurons and wide-dynamic-range (WDR) neurons were 50% respectively. A single spinal dorsal horn neuron receives somatic afferent input and then conveys it to the visceral sensory nucleus-SN; some spinal dorsal horn neurons receive, in turn, innervation from the SN; convergence and integration between somatic and visceral sensory inputs might occur in the spinal dorsal horn neurons and/or SN.