Visceral versus somatic pain: an educational review of anatomy and clinical implications

2021 ◽  
Vol 46 (7) ◽  
pp. 629-636
Author(s):  
Andre P Boezaart ◽  
Cameron R Smith ◽  
Svetlana Chembrovich ◽  
Yury Zasimovich ◽  
Anna Server ◽  
...  

Somatic and visceral nociceptive signals travel via different pathways to reach the spinal cord. Additionally, signals regulating visceral blood flow and gastrointestinal tract (GIT) motility travel via efferent sympathetic nerves. To offer optimal pain relief and increase GIT motility and blood flow, we should interfere with all these pathways. These include the afferent nerves that travel with the sympathetic trunks, the somatic fibers that innervate the abdominal wall and part of the parietal peritoneum, and the sympathetic efferent fibers. All somatic and visceral afferent neural and sympathetic efferent pathways are effectively blocked by appropriately placed segmental thoracic epidural blocks (TEBs), whereas well-placed truncal fascial plane blocks evidently do not consistently block the afferent visceral neural pathways nor the sympathetic efferent nerves. It is generally accepted that it would be beneficial to counter the effects of the stress response on the GIT, therefore most enhanced recovery after surgery protocols involve TEB. The TEB failure rate, however, can be high, enticing practitioners to resort to truncal fascial plane blocks. In this educational article, we discuss the differences between visceral and somatic pain, their management and the clinical implications of these differences.

2008 ◽  
Vol 5 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Sae Uchida ◽  
Harumi Hotta

In this review, our recent studies using anesthetized animals concerning the neural mechanisms of vasodilative effect of acupuncture-like stimulation in various organs are briefly summarized. Responses of cortical cerebral blood flow and uterine blood flow are characterized as non-segmental and segmental reflexes. Among acupuncture-like stimuli delivered to five different segmental areas of the body; afferent inputs to the brain stem (face) and to the spinal cord at the cervical (forepaw), thoracic (chest or abdomen), lumbar (hindpaw) and sacral (perineum) levels, cortical cerebral blood flow was increased by stimuli to face, forepaw and hindpaw. The afferent pathway of the responses is composed of somatic groups III and IV afferent nerves and whose efferent nerve pathway includes intrinsic cholinergic vasodilators originating in the basal forebrain. Uterine blood flow was increased by cutaneous stimulation of the hindpaw and perineal area, with perineal predominance. The afferent pathway of the response is composed of somatic group II, III and IV afferent nerves and the efferent nerve pathway includes the pelvic parasympathetic cholinergic vasodilator nerves. Furthermore, we briefly summarize vasodilative regulation of skeletal muscle blood flow via a calcitonin gene-related peptide (CGRP) induced by antidromic activation of group IV somatic afferent nerves. These findings in healthy but anesthetized animals may be applicable to understanding the neural mechanisms improving blood flow in various organs following clinical acupuncture.


1989 ◽  
Vol 257 (1) ◽  
pp. H157-H161 ◽  
Author(s):  
F. M. Faraci ◽  
K. A. Kadel ◽  
D. D. Heistad

The goal of this study was to examine vascular responses of the dura mater. Microspheres were used to measure blood flow to the dura and brain in anesthetized dogs. Under control conditions, blood flow to the dura was 38 +/- 3 (SE) ml.min-1.100 g-1. Values for blood flow to the dura obtained with simultaneous injection of 15- and 50-microns microspheres were similar, which suggests that shunting of 15-microns spheres was minimal. Left atrial infusion of substance P (100 ng.kg-1.min-1) and serotonin (40 micrograms.kg-1.min-1), two agonists that have been reported to increase vascular permeability in the dura, increased blood flow to the dura two- to threefold. Adenosine (iv) produced vasodilatation in the dura. Adenosine and serotonin did not affect cerebral blood flow, but substance P increased blood flow to the brain by approximately 40%. Seizures, which produce pronounced dilatation of cerebral vessels despite activation of sympathetic nerves, produced vasoconstriction in the dura. Thus 1) the dura is perfused at a relatively high level of blood flow under normal conditions and is very responsive to vasoactive stimuli, and 2) substance P and serotonin, which have been implicated in the pathogenesis of vascular headache, produce pronounced vasodilator responses in the dura mater.


1992 ◽  
Vol 263 (4) ◽  
pp. H1078-H1083 ◽  
Author(s):  
M. J. Joyner ◽  
L. A. Nauss ◽  
M. A. Warner ◽  
D. O. Warner

This study tested the effects of sympathetically mediated changes in blood flow to active muscles on muscle O2 uptake (VO2) in humans. Four minutes of graded (15-80% of maximum voluntary contraction, MVC) rhythmic handgrip exercise were performed. Forearm blood flow (FBF) (plethysmography) and deep vein O2 saturation were measured each minute. Forearm O2 uptake was calculated using the Fick principle. In protocol 1, exercise was performed while supine and again while upright to augment sympathetic outflow to the active muscles. Standing reduced FBF at rest from 3.6 to 2.2 ml.100 ml-1.min-1 (P < 0.05). During light exercise (15-40% MVC) FBF was unaffected by body position. Standing reduced FBF (P < 0.05) from 36.0 to 25.2 ml.100 ml-1.min-1 and forearm VO2 from 38.2 to 28.1 ml.kg-1.min-1 during the final work load. In protocol 2, exercise was performed while supine before and after local anesthetic block of the sympathetic nerves to the forearm. Sympathetic block increased FBF at rest from 3.1 to 8.9 ml.100 ml-1.min-1 (P < 0.05), and FBF was higher during all work loads At 70-80% of MVC sympathetic block increased FBF from 35.4 to 50.7 ml.100 ml-1.min-1 (P < 0.05), and forearm VO2 from 45.5 to 54.2 ml.kg-1.min-1 (P < 0.05). These results suggest that in humans sympathetic nerves modulate blood flow to active muscles during light and heavy rhythmic exercise and that this restraint of flow can limit O2 uptake in muscles performing heavy rhythmic exercise.


1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Wei Zhou ◽  
Kentaro Yamakawa ◽  
Olujimi Ajijola ◽  
Daigo Yagishita ◽  
Mariko Takemoto ◽  
...  

Background: Enhanced cardiac sympathetic tone has been associated with ventricular arrhythmias and sudden cardiac death. The spinal cord is an important integrative region of afferent and efferent pathways that participate in cardiovascular regulation. The purpose of this study is to investigate the role of spinal processing of cardiac afferent information on ventricular electrophysiology during cardiac sympathoexcitation. Methods: Female Yorkshire pigs (n=5) underwent surgical exposure of the heart and left stellate ganglion (LSG) through thoractomy as well as the dorsal and ventral roots of the spinal cord through laminectomy. A 56-electrode sock was placed over the ventricles to record epicardial electrograms. Animals underwent LSG stimulation in intact, after dorsal root transaction (DRTx), and followed by ventral root transaction (DVRTx). Activation recovery intervals (ARIs) were measured at each electrode before and during LSG stimulation. Results: With intact roots LSG stimulation resulted in significant global ARI shortening by 12.9% (p<0.05). After DRTx, mean global ARI shortened by 7.2%. LSG stimulation after DRTx and DVRTx resulted in greater ARI shortening compared to LSG stimulation with intact roots (21.5 and 18.4 vs 12.9%, p<0.05, see figure 1 below). ARI shortened more during LSG stimulation after DRTx than that after DVRTx (21.5 vs. 18.4%, p<0.05). Conclusion: Spinal afferent pathways play an inhibitory role in sympathoexcitation of ventricle induced by LSG stimulation. This finding provides insight into the mechanism underlying the beneficial effects of thoracic epidural anesthesia in reducing ventricular arrhythmias.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Qi Han ◽  
Josue D. Ordaz ◽  
Nai-Kui Liu ◽  
Zoe Richardson ◽  
Wei Wu ◽  
...  

AbstractLocomotor function, mediated by lumbar neural circuitry, is modulated by descending spinal pathways. Spinal cord injury (SCI) interrupts descending projections and denervates lumbar motor neurons (MNs). We previously reported that retrogradely transported neurotrophin-3 (NT-3) to lumbar MNs attenuated SCI-induced lumbar MN dendritic atrophy and enabled functional recovery after a rostral thoracic contusion. Here we functionally dissected the role of descending neural pathways in response to NT-3-mediated recovery after a T9 contusive SCI in mice. We find that residual projections to lumbar MNs are required to produce leg movements after SCI. Next, we show that the spared descending propriospinal pathway, rather than other pathways (including the corticospinal, rubrospinal, serotonergic, and dopaminergic pathways), accounts for NT-3-enhanced recovery. Lastly, we show that NT-3 induced propriospino-MN circuit reorganization after the T9 contusion via promotion of dendritic regrowth rather than prevention of dendritic atrophy.


1958 ◽  
Vol 194 (1) ◽  
pp. 155-159 ◽  
Author(s):  
Thomas M. Gilfoil ◽  
Robert T. Schopp ◽  
Gail R. Norris ◽  
W. B. Youmans

External constriction of the descending aorta elicits immediate inhibition of breathing in dogs under Pentothal-chloralose anesthesia both before and after sino-aortic denervation. Impulses initiated by traction of a ligature on the aorta are conducted into the thoracic part of the cord. There is no indication that this mechanism is activated in experiments involving internal occlusion in the innervated animals. Internal occlusion of the descending aorta elicits inhibition of breathing in dogs under morphine sulfate-chloralose anesthesia having all neural pathways intact. The inhibition is related in large part to reflexes from the sino-aortic zones. In the majority of dogs studied the delayed inhibition of breathing following internal occlusion of the descending aorta was greatly reduced but usually not entirely eliminated by sino-aortic denervation. Therefore, some other respiration-inhibiting mechanism is involved. That the respiratory center may be relatively insensitive to changes in blood flow under the conditions of these experiments is indicated by the fact that in individual cases sudden severe changes in blood pressure in sino-aortic denervated animals were not accompanied by changes in respiration.


1988 ◽  
Vol 255 (3) ◽  
pp. H563-H568
Author(s):  
C. D. Kurth ◽  
L. C. Wagerle ◽  
M. Delivoria-Papadopoulos

We examined cerebral blood flow (CBF) regulation by the sympathetic nerves in 12 newborn lambs (3–11 days old) during seizures, a potent reflex stimulator of the sympathetic nervous system. CBF was measured with microspheres, and seizures were induced with bicuculline. In six of these lambs, one hemibrain was denervated (D) chronically by interrupting the ipsilateral cervical sympathetic trunk; the other hemibrain remained innervated (I). Before and after 10, 35, and 70 min of seizures, cerebral gray matter blood flow (mean +/- SE ml.min-1.100 g-1) was, respectively, 12 +/- 3 (9%), 71 +/- 12 (21%), 120 +/- 15 (38%), and 54 +/- 5 (14%) greater (P less than 0.05) in the D than in the I hemibrain. In the cerebral white matter, hippocampus, caudate, and thalamus blood flows to the D and I hemibrains were similar before seizures but during seizures they were 10–39% greater (P less than 0.05) in the D than in the I hemibrain. Midbrain, brainstem, and cerebellum D and I blood flows were always similar. In the other six lambs, acute denervation during seizures increased ipsilateral cerebral gray and hippocampus blood flow by 10–31%, but unilateral electrical stimulation decreased ipsilateral cerebral gray, cerebral white, hippocampus, thalamus, and caudate blood flow by 17–27%. The data demonstrate that, during seizures, sympathetic nerve activity modifies regional CBF and the effect is sustained, suggesting a role for the sympathetic nervous system in newborn CBF regulation.


1980 ◽  
Vol 239 (3) ◽  
pp. H316-H325 ◽  
Author(s):  
K. A. Reimann ◽  
L. C. Weaver

Afferent neurons within cardiac sympathetic nerves can reflexly excite central sympathetic outflow. However, their contribution to cardiovascular control remains unclear because they are potentially opposed by inhibitory reflexes of cardiac vagal or arterial baroreceptor afferent origin. It was considered that sympathetically mediated, excitatory responses might be more prominent when initiated by chemical stimulation. In chloralose-anesthetized, vagotomized, sinoaortic-denervated cats, epicardial or intracoronary administration of bradykinin or potassium chloride evoked renal nerve excitation and pressor responses mediated by cardiac sympathetic afferent nerves. When upper thoracic sympathetic nerves were severed, and vagal afferent nerves remained intact, bradykinin and potassium chloride produced inhibition of renal nerve activity and depressor responses. When sympathetic and vagal components of cardiac innervation remained intact, these substances produced excitation, inhibition, or no change in sympathetic outflow. Excitation occurred as often as inhibition. A similar pattern was observed when arterial baroreceptor nerves remained intact. These data illustrate that cardiac sympathetic afferent neurons can have significant excitatory influences on the cardiovascular system in spite of opposition by inhibitory afferent groups.


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