Medical School · Year 1 · Anatomy Thorax Abdomen · includes a quiz and discussion video

Lecture 13: Autonomic Nervous System of the Abdomen

Unit 1.4: Human Gross Anatomy II - Thorax and Abdomen


Learning Objectives

By the end of this lecture, students will be able to:

  1. Describe the organization of the autonomic nervous system in the abdomen
  2. Identify the sympathetic trunk, splanchnic nerves, and prevertebral ganglia
  3. Describe the course and distribution of the vagus nerve in the abdomen
  4. Explain the innervation patterns of abdominal viscera
  5. Describe the enteric nervous system
  6. Correlate anatomical features with referred pain and clinical conditions

Overview of Autonomic Innervation

The autonomic nervous system provides involuntary control of the abdominal viscera, regulating functions such as gastrointestinal motility, secretion, and blood flow. Three components of the autonomic system are present in the abdomen: the sympathetic division originating from the thoracolumbar spinal cord, the parasympathetic division arriving via the vagus nerve and pelvic splanchnic nerves, and the enteric nervous system, which is intrinsic to the gastrointestinal tract wall.

The sympathetic and parasympathetic divisions generally have opposing effects on abdominal organs. Sympathetic activation, originating from spinal cord segments T5-L2, typically decreases gastrointestinal motility, causes vasoconstriction in the splanchnic circulation, and contracts sphincters—the "fight or flight" responses that divert blood away from digestion. Parasympathetic activation, from the vagus nerve (cranial nerve X) for the foregut and midgut, and from the pelvic splanchnic nerves (S2-S4) for the hindgut, generally increases motility, increases secretion, and relaxes sphincters to promote digestion.

<image>Panel A: The spinal cord with sympathetic outflow from T5-L2 lateral horn neurons indicated. Panel B: Sympathetic fibers as green lines traveling through the sympathetic trunk and splanchnic nerves to prevertebral ganglia at the celiac, aorticorenal, superior mesenteric, and inferior mesenteric positions with postganglionic fibers following arteries to organs. Panel C: Parasympathetic fibers as yellow lines from the vagus nerve descending along the esophagus to reach foregut and midgut structures to the splenic flexure. Panel D: Pelvic splanchnic nerves from S2-S4 ascending to reach hindgut structures from the splenic flexure distally with the transition zone marked.</image>


Sympathetic Innervation

The sympathetic supply to the abdomen originates from preganglionic neurons in the lateral horn of the spinal cord at levels T5 through L2. These preganglionic fibers have a distinctive pathway that differs from the sympathetic supply to the body wall and limbs.

The lumbar sympathetic trunk is a continuation of the thoracic trunk, descending along the anterior surface of the lumbar vertebral bodies. It typically contains 4-5 lumbar ganglia, which are connected by interganglionicfibers. Gray rami communicantes carry postganglionic fibers from these ganglia to the lumbar spinal nerves for distribution to the body wall, blood vessels, and lower limbs. Importantly, there are no white rami communicantes below L2, since preganglionic sympathetic neurons exist only in spinal segments T1-L2.

The splanchnic nerves are the critical pathways for sympathetic innervation of the abdominal viscera. These nerves carry preganglionic sympathetic fibers that pass through the sympathetic trunk without synapsing. Instead, they synapse in the prevertebral ganglia located around the abdominal aorta. The greater splanchnic nerve arises from sympathetic ganglia T5-T9 and descends through the diaphragm to synapse in the celiac ganglion. The lesser splanchnic nerve arises from T10-T11 and reaches the aorticorenal ganglion. The least splanchnic nerve arises from T12 and joins the renal plexus. The lumbar splanchnic nerves arise from L1-L2 and reach the superior and inferior mesenteric ganglia and the superior hypogastric plexus.

<image>Panel A: A preganglionic neuron in the lateral horn of the spinal cord at T5-L2 with the axon exiting via the ventral root and entering the sympathetic trunk via a white ramus communicans. Panel B: The preganglionic fiber passing through the sympathetic trunk without synapsing and descending in a splanchnic nerve labeled with spinal levels of origin. Panel C: The synapse occurring in a prevertebral ganglion (celiac, aorticorenal, superior mesenteric, or inferior mesenteric) shown as a connection between the green preganglionic and orange postganglionic neuron. Panel D: The postganglionic fiber following an artery in red to reach the target organ with labels indicating each step of the pathway.</image>


Prevertebral Ganglia and Plexuses

The prevertebral (or preaortic) ganglia are clusters of sympathetic neuron cell bodies located around the origins of the major abdominal arterial branches. Postganglionic sympathetic fibers from these ganglia travel along the arteries to reach their target organs.

The celiac ganglion is the largest of the prevertebral ganglia, located around the celiac trunk at approximately T12-L1. It receives preganglionic input from the greater splanchnic nerve. Postganglionic fibers distribute along the celiac trunk branches to supply the foregut derivatives: the stomach, liver, gallbladder, spleen, pancreas, and proximal duodenum (to the ampulla of Vater).

The aorticorenal ganglion is located around the origin of the renal arteries. It receives input from the lesser splanchnic nerve. Its fibers supply the kidney and contribute to suprarenal medulla innervation. The adrenal medulla is unique in that it receives preganglionic sympathetic fibers directly, without an intervening ganglion synapse, because the chromaffin cells of the adrenal medulla are themselves modified postganglionic neurons.

The superior mesenteric ganglion surrounds the origin of the superior mesenteric artery at approximately L1. It receives input from the lesser and lumbar splanchnic nerves. Postganglionic fibers travel along the SMA branches to supply the midgut derivatives: the distal duodenum, jejunum, ileum, cecum, appendix, ascending colon, and proximal two-thirds of the transverse colon.

The inferior mesenteric ganglion surrounds the origin of the inferior mesenteric artery at approximately L3. It receives lumbar splanchnic nerve input. Postganglionic fibers supply the hindgut derivatives: the distal one-third of the transverse colon, descending colon, sigmoid colon, and upper rectum.

<image>Panel A: The celiac ganglion as a large green cluster surrounding the celiac trunk receiving the greater splanchnic nerve from T5-T9 and distributing along the left gastric, common hepatic, and splenic arteries to foregut organs. Panel B: The aorticorenal ganglion as a green cluster near the renal artery origin receiving the lesser splanchnic nerve with fibers to the kidney and adrenal gland which also receives direct preganglionic fibers. Panel C: The superior mesenteric ganglion as a green cluster receiving lesser and lumbar splanchnics and distributing along SMA branches to midgut organs. Panel D: The inferior mesenteric ganglion as a green cluster receiving lumbar splanchnics and distributing along IMA branches to hindgut organs.</image>


Autonomic Plexuses

The autonomic plexuses are networks of nerve fibers and ganglia that surround the major abdominal vessels and distribute autonomic fibers to the viscera. These plexuses contain both sympathetic and parasympathetic components.

The celiac plexus, also called the solar plexus, is the largest autonomic plexus in the body. It surrounds the celiac trunk and the origin of the superior mesenteric artery. The celiac ganglia are embedded within this plexus. The plexus receives preganglionic sympathetic input from the greater splanchnic nerves and parasympathetic input from the posterior vagal trunk (celiac branches). Subsidiary plexuses extend along the branches of the celiac trunk: the hepatic plexus along the hepatic artery, the splenic plexus along the splenic artery, and the gastric plexuses along the gastric arteries.

The superior mesenteric plexus surrounds the superior mesenteric artery and contains the superior mesenteric ganglion. It receives sympathetic input from the lesser and lumbar splanchnic nerves and parasympathetic input from the vagus via the celiac plexus. It supplies the midgut.

The inferior mesenteric plexus surrounds the inferior mesenteric artery and contains the inferior mesenteric ganglion. It receives sympathetic input from the lumbar splanchnic nerves. Parasympathetic supply to this region comes not from the vagus but from the pelvic splanchnic nerves (S2-S4), which ascend retroperitoneally from the pelvis.

The renal plexus surrounds the renal arteries and receives input from the celiac plexus, least splanchnic nerve, and aorticorenal ganglion.

The superior hypogastric plexus lies anterior to the aortic bifurcation at L5-S1. It represents a continuation of the intermesenteric plexus and receives lumbar splanchnic input. It divides into the right and left hypogastric nerves, which descend into the pelvis.

The inferior hypogastric (pelvic) plexuses lie on either side of the rectum in the pelvis. They receive the hypogastric nerves (sympathetic) and the pelvic splanchnic nerves (parasympathetic), distributing to the pelvic viscera.

<image>Panel A: The celiac plexus as a large yellow network with embedded green ganglia surrounding the celiac trunk with extensions as hepatic, splenic, and gastric plexuses along the respective arteries receiving input from greater splanchnic nerves and vagal branches. Panel B: The superior mesenteric plexus as a yellow network with green ganglion surrounding the SMA and the renal plexus as a small yellow network surrounding each renal artery. Panel C: The inferior mesenteric plexus as a yellow network with green ganglion surrounding the IMA connected to the superior mesenteric plexus by the intermesenteric plexus. Panel D: The superior hypogastric plexus as a yellow network at L5-S1 giving rise to the hypogastric nerves descending into the pelvis.</image>


Parasympathetic Innervation

The parasympathetic supply to the abdomen comes from two sources depending on the embryological origin of the organ: the vagus nerve (CN X) for foregut and midgut derivatives, and the pelvic splanchnic nerves (S2-S4) for hindgut derivatives.

The vagus nerve provides parasympathetic innervation to the foregut and midgut. The right and left vagus nerves form the esophageal plexus around the lower esophagus and then reorganize into the anterior and posterior vagal trunks that enter the abdomen through the esophageal hiatus at T10.

The anterior vagal trunk, derived primarily from the left vagus nerve, lies on the anterior surface of the esophagus and stomach. It gives off anterior gastric branches to the anterior stomach wall, hepatic branches that travel in the lesser omentum to the liver and gallbladder, and pyloric branches to the pylorus and proximal duodenum.

The posterior vagal trunk, derived primarily from the right vagus nerve and larger than the anterior trunk, lies on the posterior esophageal and gastric surface. It gives off posterior gastric branches to the posterior stomach and celiac branches that travel with the left gastric artery to the celiac plexus. From the celiac plexus, vagal fibers distribute along the arterial branches to reach the intestines as far as the splenic flexure of the colon.

The pelvic splanchnic nerves arise from spinal segments S2-S4, the sacral parasympathetic outflow. These nerves are sometimes called the nervi erigentes. They enter the inferior hypogastric plexus in the pelvis and provide parasympathetic innervation to the hindgut (distal one-third of transverse colon, descending colon, sigmoid colon, and rectum), as well as to the pelvic organs. To reach the hindgut, fibers ascend retroperitoneally along the inferior mesenteric artery branches.

<image>Panel A: The anterior and posterior vagal trunks as yellow cords descending through the esophageal hiatus alongside the esophagus. Panel B: The anterior trunk giving off anterior gastric branches to the anterior stomach wall, hepatic branches through the lesser omentum to the liver and gallbladder, and pyloric branches to the pylorus. Panel C: The posterior trunk giving off posterior gastric branches to the posterior stomach and celiac branches descending along the left gastric artery to the celiac plexus with vagal fibers distributing to midgut organs. Panel D: The boundary of vagal territory at the splenic flexure with pelvic splanchnic nerve territory from S2-S4 ascending from below to supply the hindgut distally.</image>


Enteric Nervous System

The enteric nervous system is an intrinsic nervous system embedded within the wall of the gastrointestinal tract from the esophagus to the anus. It contains approximately 100 million neurons—more than in the spinal cord—and is capable of controlling gastrointestinal function independently of central nervous system input, earning it the designation of "the brain of the gut" or the "second brain."

The enteric nervous system consists of two main plexuses. The myenteric plexus, also called Auerbach's plexus, lies between the circular and longitudinal muscle layers of the muscularis externa. It primarily controls gastrointestinal motility, coordinating peristalsis and segmentation. The submucosal plexus, also called Meissner's plexus, lies within the submucosa. It primarily controls secretion from mucosal glands, absorption, and local blood flow.

The enteric nervous system uses numerous neurotransmitters. Excitatory transmitters include acetylcholine and substance P, which stimulate muscle contraction and secretion. Inhibitory transmitters include vasoactive intestinal peptide (VIP) and nitric oxide (NO), which cause smooth muscle relaxation.

Although the enteric nervous system can function autonomously, it receives modulating input from the sympathetic and parasympathetic divisions. Sympathetic input generally inhibits enteric activity, slowing motility and reducing secretion. Parasympathetic input generally enhances enteric activity, increasing motility and secretion. The enteric system integrates these inputs with local sensory information to produce coordinated responses.

<image>Panel A: Cross-sectional view of the intestinal wall layers: mucosa with villi, submucosa, circular muscle layer, longitudinal muscle layer, and serosa. Panel B: The myenteric plexus (Auerbach's plexus) as a network of neurons between the circular and longitudinal muscle layers controlling motility with arrows to both muscle layers. Panel C: The submucosal plexus (Meissner's plexus) as a network of neurons in the submucosa controlling secretion and blood flow with connections to mucosal glands and submucosal vessels. Panel D: External inputs from sympathetic fibers in green and parasympathetic fibers in yellow synapsing on enteric neurons with an inset showing a magnified ganglion with interconnected neurons.</image>


Innervation of Specific Organs

Understanding the autonomic innervation of individual organs helps predict the effects of nerve injury or pharmacological intervention.

The stomach receives parasympathetic innervation from the vagus nerve, which increases motility, stimulates gastric acid and pepsin secretion, and relaxes the pyloric sphincter to promote gastric emptying. Sympathetic innervation, from the celiac ganglion via the celiac plexus, decreases motility, causes vasoconstriction reducing blood flow and secretion, and contracts the pyloric sphincter to inhibit emptying.

The liver and gallbladder receive parasympathetic innervation from hepatic branches of the anterior vagal trunk, which increases bile secretion and promotes gallbladder contraction. Sympathetic input causes vasoconstriction and inhibits bile secretion.

The pancreas receives parasympathetic innervation from the vagus, which stimulates both exocrine secretion (digestive enzymes) and endocrine secretion (insulin release). Sympathetic input inhibits secretion and causes vasoconstriction.

The small intestine receives vagal parasympathetic input that increases motility and secretion. Sympathetic input from the celiac and superior mesenteric ganglia decreases motility and causes vasoconstriction.

The large intestine has a division of parasympathetic supply at the splenic flexure. The proximal colon (to the splenic flexure) receives vagal innervation via the superior mesenteric plexus. The distal colon (from the splenic flexure) receives parasympathetic innervation from the pelvic splanchnic nerves via the inferior hypogastric plexus. Sympathetic supply to the entire colon comes from the superior and inferior mesenteric ganglia.

<image>Panel A: Schematic showing the stomach, liver, gallbladder, and pancreas with their parasympathetic source from the vagus nerve and sympathetic source from the celiac ganglion. Panel B: The small intestine with parasympathetic supply from the vagus and sympathetic supply from the celiac and superior mesenteric ganglia. Panel C: The colon divided at the splenic flexure with the proximal colon receiving vagal parasympathetic supply and the distal colon receiving pelvic splanchnic nerve supply from S2-S4. Panel D: Summary of autonomic effects for each organ showing parasympathetic stimulation increasing motility and secretion and relaxing sphincters versus sympathetic stimulation decreasing motility causing vasoconstriction and contracting sphincters.</image>


Afferent (Sensory) Pathways

Visceral afferent fibers accompany the autonomic efferent fibers, carrying sensory information from the abdominal organs to the central nervous system. These sensory fibers are not technically part of the autonomic nervous system (which by definition is efferent only), but they travel with autonomic nerves and are clinically important for understanding visceral pain.

Afferents traveling with sympathetic nerves carry pain sensation from the viscera. These fibers have their cell bodies in the dorsal root ganglia of the spinal nerves T5-L2. Visceral pain transmitted by these pathways is typically dull, poorly localized, and perceived in the midline because visceral sensory fibers from paired organs converge on the same spinal cord segments.

Afferents traveling with parasympathetic nerves primarily carry physiological sensations such as fullness, distension, and nausea rather than pain. The cell bodies of vagal afferents are in the sensory ganglia of the vagus (nodose ganglion), while those of pelvic splanchnic afferents are in the sacral dorsal root ganglia.

Referred pain occurs when visceral afferents and somatic afferents from the skin and body wall converge on the same neurons in the spinal cord dorsal horn. The brain, more accustomed to receiving somatic input, misinterprets the visceral pain as originating from the somatic region sharing that spinal segment.

<image>Panel A: A visceral afferent fiber in blue carrying pain traveling with a splanchnic nerve through a prevertebral ganglion without synapsing and through the sympathetic trunk via the white ramus to the dorsal root ganglion. Panel B: The same afferent fiber entering the spinal cord dorsal horn for pain processing. Panel C: A visceral afferent fiber traveling with the vagus to the nodose ganglion and then to the brainstem carrying physiological sensations. Panel D: Inset illustrating convergence in the spinal cord where a visceral afferent and a somatic afferent from the skin synapse on the same dorsal horn neuron projecting to higher centers explaining referred pain.</image>


Referred Pain Patterns

Referred pain patterns follow predictable dermatomal distributions based on the embryological origin and segmental innervation of abdominal organs.

Diaphragmatic irritation, particularly of the central portion innervated by the phrenic nerve (C3-C5), causes referred pain to the shoulder, which shares the same cervical dermatomes. This explains why subphrenic abscess, ruptured spleen, or ruptured ectopic pregnancy with blood under the diaphragm can present with shoulder pain.

Stomach pain is typically referred to the epigastrium, corresponding to dermatomes T6-T9. Liver and gallbladder pain is referred to the right upper quadrant and may radiate to the right shoulder (via diaphragmatic irritation) or right scapula, corresponding to T7-T9.

Small intestine pain is referred to the periumbilical region, corresponding to dermatome T9-T10. This explains why early appendicitis, before parietal peritoneal involvement, causes periumbilical rather than right lower quadrant pain.

The appendix initially produces periumbilical pain (visceral, T10) because it is a midgut derivative. As inflammation progresses to involve the parietal peritoneum, pain localizes to the right lower quadrant because the parietal peritoneum has somatic innervation that is precisely localized.

Kidney and ureteral pain is referred to the flank and groin along the T10-L1 dermatomes. Colonic pain is typically referred to the lower abdomen, hypogastrium, corresponding to T11-L1.

<image>Panel A: Anterior view of the torso with the shoulder region shaded for diaphragmatic irritation at C3-C5 and the epigastrium shaded for stomach and gallbladder pain at T6-T9. Panel B: The periumbilical region shaded for small intestine and early appendicitis at T9-T10 and the right lower quadrant marked for late appendicitis with parietal peritoneal localization. Panel C: The flanks extending to the groin shaded for kidney and ureteral pain at T10-L1 and the hypogastrium shaded for colonic pain at T11-L1 with dermatomal levels indicated. Panel D: Inset showing appendicitis pain migration from initial periumbilical visceral pain at T10 to localized somatic pain in the right lower quadrant.</image>


Clinical Correlations

Vagotomy was historically performed as a treatment for peptic ulcer disease to reduce gastric acid secretion. Several types were performed: truncal vagotomy divided the main vagal trunks above the stomach, highly selective (parietal cell) vagotomy divided only the branches to the acid-secreting body of the stomach while preserving the antral innervation, and selective vagotomy divided the gastric branches while preserving the celiac branches. Complications of vagotomy include dumping syndrome (from rapid gastric emptying), diarrhea (from altered intestinal motility), and delayed gastric emptying (from loss of pyloric relaxation normally coordinated with gastric contractions).

Hirschsprung disease is a congenital condition in which the enteric ganglia fail to develop in a segment of the colon, most commonly the rectosigmoid region. The aganglionic segment cannot relax and remains in tonic contraction, causing functional obstruction. The proximal colon dilates with accumulated feces (megacolon). Treatment requires surgical resection of the aganglionic segment.

Celiac plexus block is a pain management procedure used for chronic abdominal pain, particularly from pancreatic cancer. Neurolytic agents or local anesthetics are injected into the celiac plexus under imaging guidance, interrupting the transmission of visceral pain from upper abdominal organs.

Diabetic autonomic neuropathy can affect the gastrointestinal tract, causing gastroparesis (delayed gastric emptying from impaired motility), constipation, or diarrhea. These symptoms result from damage to autonomic nerves supplying the gastrointestinal tract.

Splanchnic vasoconstriction in shock states diverts blood from the gastrointestinal tract to vital organs. This can cause ischemic colitis, particularly at watershed areas (the splenic flexure and rectosigmoid junction), where collateral blood supply is limited.

<image>Panel A: Vagotomy types showing a diagram of the stomach with truncal vagotomy cutting the main trunks above, selective vagotomy cutting gastric branches only, and highly selective vagotomy cutting only parietal cell branches while preserving antral branches. Panel B: Hirschsprung disease showing the colon with a dilated proximal segment (megacolon) and a narrow aganglionic distal segment at the rectosigmoid with a histology inset showing absent ganglion cells in the myenteric plexus. Panel C: Celiac plexus block showing a needle under CT guidance positioned at the celiac plexus near the aorta. Panel D: Ischemic colitis at watershed areas showing the colon with darkened segments at the splenic flexure and rectosigmoid junction.</image>


Summary

The sympathetic supply to abdominal viscera reaches organs via splanchnic nerves that synapse in prevertebral ganglia (celiac, aorticorenal, superior mesenteric, inferior mesenteric), with postganglionic fibers traveling along arteries to their targets. Sympathetic activation decreases motility, causes vasoconstriction, and contracts sphincters.

The vagus nerve supplies parasympathetic innervation to the foregut and midgut (to the splenic flexure) via the anterior and posterior vagal trunks and celiac plexus. The pelvic splanchnic nerves (S2-S4) supply the hindgut (from the splenic flexure). Parasympathetic activation increases motility, increases secretion, and relaxes sphincters.

The enteric nervous system (myenteric and submucosal plexuses) controls local gastrointestinal function and can operate independently, though it receives modulating input from sympathetic and parasympathetic divisions.

Visceral afferents traveling with sympathetic nerves carry pain, which is poorly localized and referred to dermatomal regions based on embryological origin. The classic migration of appendicitis pain from periumbilical (visceral, T10) to right lower quadrant (somatic, parietal peritoneal) illustrates these principles.


Key Terms

TermDefinition
Splanchnic nervesPreganglionic sympathetic nerves (greater, lesser, least, lumbar) that pass to the prevertebral ganglia
Celiac plexusLargest autonomic plexus surrounding the celiac trunk; contains celiac ganglia and receives vagal input
Vagal trunksAnterior and posterior continuations of the vagus nerve entering the abdomen at the esophageal hiatus
Enteric nervous systemIntrinsic nervous system of the gastrointestinal tract; includes myenteric and submucosal plexuses
Referred painVisceral pain perceived at a somatic location due to convergence of afferents in the spinal cord
Pelvic splanchnic nervesParasympathetic nerves from S2-S4 supplying the hindgut and pelvic organs

This content is subject to the MIT License. © 2024–2026 Hibbert School of Medicine.

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