mandala medicine
Although the existence of topographic maps is well accepted and highly developed with respect to the primary sensory systems and somatomotor pathways. the establishment and acceptance of a sensory and motor viscerotopy for parasympathetic innervation of visceral structures are relatively recent. Earlier work was either contrary to the idea or ambivalent in its conclusions. With the arrival of better neural tracers and strategies for controlling spread at injection sites, data emerged supporting a viscerotopy for particular viscera innervated by the glossopharyngeal and vagal nerves. We found a dramatic representation of the stomach in the nucleus of the solitary tract (NTS) which spurred us on to further study. Viscerotopy was also reported in the pigeon. to Columns were identified in the dorsal motor nucleus of the vagus (DMV) and correlated to vagal branches which were potentially organ specific. nucleus ambiguus in the rat was shown to be viscerotopic in its motor innervation of the upper alimentary canal. Our work was aided by the use of a very sensitive tracer which transports retrogradely to motoneurons, fills out their dendritic arborizations beautifully and passes transganglionically to anterogradely fill out central terminal fields of sensory neurons. The tracer is cholera toxin conjugated to horseradish peroxidase which we prepare ourselves.' In our experience it is more sensitive than HRP alone, wheatgerm agglutinin alone or conjugated to HRP. or any fluorescent tracer. Much Of its sensitivity is attributable to its receptor binding affinity for GMI ganglioside which occurs in neural membranes. This feature also aids in reducing the spread of the tracer from the injection sites and permits the use of concentrations of tracer which are nearly an order of magnitude below those used for other tracers.
for GMI ganglioside which occurs in neural membranes. This feature also aids in reducing the spread of the tracer from the injection sites and permits the use of concentrations of tracer which are nearly an order of magnitude below those used for other tracers. The main focus of our own research has been on the vagal and glossopharyngeal in- nervation Of the structures of the alimentary canal. This chapter describes our current knowl- edge of the topographic representation of several of these viscera (including the soft palate, pharynx. esophagus, stomach, pancreas. cecum, and intestines) in the dorsal and ventral vagal complexes in rats. The majority Of these observations were made following injection of the neural tracer cholera toxin-horseradish peroxidase conjugate (CT-HRP) into various viscera and histological examination of subsequent anterograde and retrograde neural labeling in the medulla oblongata. For detailed descriptions of nrthodology and control procedures, the reader is referred to our prior published reports: Shapiro and Rinaman and Rinaman et al.;lS Altschuler et and Ferenci et al. We will review the highlights of these reports and refer you to the original papers for greater detail. 11. VAGAL SENSORY VISCEROTOPIC ORGANIZATION The vagus nerve is a truly mixed nerve; its afferent component contains general somatic, special visceral (taste), and general visceral sensory fibers while its efferent component contains general visceral efferent axons that are yna ic to autonomic motoneurons
sensory changes have also been seen in the corresponding "viscerotome" [28]. Such changes in localization and sensi- tivity of the referred pain areas may be a hallmark of dis- eased organs and if the experimental methods are improved they may serve as a biomarker of the disease. Viscero-visceral hyperalgesia is a complex form Of hypersensitivity probably explained by more than one mechanism. Since this phenomenon takes place between visceral organs which share their central afferent termina- tion, it is plausible that central sensitization plays an impor- tant role [29]. Recently, human experimental studies support the role of viscero-visceral hyperalgesia in GI diseases. Acidification of the distal esophagus resulted in hyperalge- sia in the proximal esophagus, and duodenal acidification was shown to induce esophageal hypersensitivity [30]. Recently, we showed that acidification of the esophagus in healthy volunteers involve widespread changes in the per- ception of experimental pain from remote organs such as the rectum [31]. The widespread visceral hypersensitivity in functional GI disorders (IBS, functional dyspepsia, etc.) may be due to this mechanism. As an example a marked reduction in colonic perception thresholds and alternation in the viscero-somatic referral pattern were seen in patients with IBS after lipid administration in the duodenum [32]. Vlscerovisceral hyperalgesia may also explain the epidemiological findings in several clinical conditions with organic diseases such as an increased number of anginal attacks in Patients with gallbladder calcinosis. and increased diseases, e.g., in patients with gastroesophageal reflux dis- ease (GERD) where increased sensitivity to gastric distenSion was shown. Therefore, the frequent airway symptoms in GERD (often refractory to treatment with proton pump inhibitors) may not only be related to direct aspiration of the gastric refluxate, but vasovagal reflex mechanisms evoked by acid-related hyperalgesia may also be important [34]. Repeated stimulations: Sensitization of the spinal neurons is known to occur with prolonged or repeated stimulation ("wind-up" or temporal summation) of the peripheral afferents. Thus, temporal summation results in a short-lasting spinal cord sensitization that persists after discontinuing the peripheral stimulation. In the laboratory, this is perceived as increased pain to a series of stimuli with the same intensity. Repeated electrical or mechanical stimuli to the small and large intestine in volunteers may cause increased sensation to subsequent stimuli, and this may be used as a model for enhanced central gain [1—3]. In functional pain Munakata et al. showed the importance of central mechanisms. In their study, patients with IBS developed rectal hyperalgesia following repetitive sigmoid distensions [35]. Paterson et al. [36] as well as studies from our group [4] also showed that repeated distensions conditioned the esophagus in functional chest pain patients resulted in higher pain scores. In organic diseases, repeated stimuli were also used to show the central amplification of pain in patients with chronic pancreatitis [371.
Although the existence of topographic maps is well accepted and highly developed with respect to the primary sensory systems and somatomotor pathways. the establishment and acceptance of a sensory and motor viscerotopy for parasympathetic innervation of visceral structures are relatively recent. Earlier work was either contrary to the idea or ambivalent in its conclusions. With the arrival of better neural tracers and strategies for controlling spread at injection sites, data emerged supporting a viscerotopy for particular viscera innervated by the glossopharyngeal and vagal nerves. We found a dramatic representation of the stomach in the nucleus of the solitary tract (NTS) which spurred us on to further study. Viscerotopy was also reported in the pigeon. to Columns were identified in the dorsal motor nucleus of the vagus (DMV) and correlated to vagal branches which were potentially organ specific. nucleus ambiguus in the rat was shown to be viscerotopic in its motor innervation of the upper alimentary canal. Our work was aided by the use of a very sensitive tracer which transports retrogradely to motoneurons, fills out their dendritic arborizations beautifully and passes transganglionically to anterogradely fill out central terminal fields of sensory neurons. The tracer is cholera toxin conjugated to horseradish peroxidase which we prepare ourselves.' In our experience it is more sensitive than HRP alone, wheatgerm agglutinin alone or conjugated to HRP. or any fluorescent tracer. Much Of its sensitivity is attributable to its receptor binding affinity for GMI ganglioside which occurs in neural membranes. This feature also aids in reducing the spread of the tracer from the injection sites and permits the use of concentrations of tracer which are nearly an order of magnitude below those used for other tracers.
for GMI ganglioside which occurs in neural membranes. This feature also aids in reducing the spread of the tracer from the injection sites and permits the use of concentrations of tracer which are nearly an order of magnitude below those used for other tracers. The main focus of our own research has been on the vagal and glossopharyngeal in- nervation Of the structures of the alimentary canal. This chapter describes our current knowl- edge of the topographic representation of several of these viscera (including the soft palate, pharynx. esophagus, stomach, pancreas. cecum, and intestines) in the dorsal and ventral vagal complexes in rats. The majority Of these observations were made following injection of the neural tracer cholera toxin-horseradish peroxidase conjugate (CT-HRP) into various viscera and histological examination of subsequent anterograde and retrograde neural labeling in the medulla oblongata. For detailed descriptions of nrthodology and control procedures, the reader is referred to our prior published reports: Shapiro and Rinaman and Rinaman et al.;lS Altschuler et and Ferenci et al. We will review the highlights of these reports and refer you to the original papers for greater detail. 11. VAGAL SENSORY VISCEROTOPIC ORGANIZATION The vagus nerve is a truly mixed nerve; its afferent component contains general somatic, special visceral (taste), and general visceral sensory fibers while its efferent component contains general visceral efferent axons that are yna ic to autonomic motoneurons
sensory changes have also been seen in the corresponding "viscerotome" [28]. Such changes in localization and sensi- tivity of the referred pain areas may be a hallmark of dis- eased organs and if the experimental methods are improved they may serve as a biomarker of the disease. Viscero-visceral hyperalgesia is a complex form Of hypersensitivity probably explained by more than one mechanism. Since this phenomenon takes place between visceral organs which share their central afferent termina- tion, it is plausible that central sensitization plays an impor- tant role [29]. Recently, human experimental studies support the role of viscero-visceral hyperalgesia in GI diseases. Acidification of the distal esophagus resulted in hyperalge- sia in the proximal esophagus, and duodenal acidification was shown to induce esophageal hypersensitivity [30]. Recently, we showed that acidification of the esophagus in healthy volunteers involve widespread changes in the per- ception of experimental pain from remote organs such as the rectum [31]. The widespread visceral hypersensitivity in functional GI disorders (IBS, functional dyspepsia, etc.) may be due to this mechanism. As an example a marked reduction in colonic perception thresholds and alternation in the viscero-somatic referral pattern were seen in patients with IBS after lipid administration in the duodenum [32]. Vlscerovisceral hyperalgesia may also explain the epidemiological findings in several clinical conditions with organic diseases such as an increased number of anginal attacks in Patients with gallbladder calcinosis. and increased diseases, e.g., in patients with gastroesophageal reflux dis- ease (GERD) where increased sensitivity to gastric distenSion was shown. Therefore, the frequent airway symptoms in GERD (often refractory to treatment with proton pump inhibitors) may not only be related to direct aspiration of the gastric refluxate, but vasovagal reflex mechanisms evoked by acid-related hyperalgesia may also be important [34]. Repeated stimulations: Sensitization of the spinal neurons is known to occur with prolonged or repeated stimulation ("wind-up" or temporal summation) of the peripheral afferents. Thus, temporal summation results in a short-lasting spinal cord sensitization that persists after discontinuing the peripheral stimulation. In the laboratory, this is perceived as increased pain to a series of stimuli with the same intensity. Repeated electrical or mechanical stimuli to the small and large intestine in volunteers may cause increased sensation to subsequent stimuli, and this may be used as a model for enhanced central gain [1—3]. In functional pain Munakata et al. showed the importance of central mechanisms. In their study, patients with IBS developed rectal hyperalgesia following repetitive sigmoid distensions [35]. Paterson et al. [36] as well as studies from our group [4] also showed that repeated distensions conditioned the esophagus in functional chest pain patients resulted in higher pain scores. In organic diseases, repeated stimuli were also used to show the central amplification of pain in patients with chronic pancreatitis [371.
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