Innervation of the Colon
The colon receives dual innervation from both the parasympathetic and sympathetic nervous systems, with the parasympathetic system promoting motility through the vagus nerve (proximal colon) and pelvic nerves (distal colon), while the sympathetic system via hypogastric nerves inhibits colonic motility. 1
Extrinsic Innervation
The colon receives extrinsic innervation from three main sources:
Vagal Innervation (Parasympathetic)
- Extends from the proximal colon to the distal colon 2
- Stimulation causes significant contractions in the mid and distal colon
- Acts via muscarinic receptors (blocked by atropine)
- Promotes motility and secretion
Pelvic Nerve Innervation (Parasympathetic)
- Innervates primarily the rectum through mid colon 2
- Creates a pattern of dual parasympathetic innervation in the left colon
- Stimulation elicits significant contractions in the rectum, mid colon, and distal colon
- Also acts via muscarinic receptors
Hypogastric Nerve Innervation (Sympathetic)
- Causes relaxation in the rectum, mid colon, and distal colon 2
- Acts via beta-adrenoceptors (blocked by propranolol)
- Inhibits colonic motility
Functional Significance
The balance between these systems is critical for normal colonic function:
Parasympathetic dominance: Increases motility, as seen in studies where electrical stimulation of vagus and pelvic nerves significantly increases the motility index 3
Sympathetic dominance: Decreases motility, as demonstrated by hypogastric nerve stimulation causing relaxation 2
Pathological implications: In slow transit constipation, studies show decreased cholinergic (parasympathetic) activity and increased non-adrenergic non-cholinergic inhibitory nerve activity 4
Clinical Relevance
Disruptions in autonomic innervation can lead to various gastrointestinal disorders:
Irritable Bowel Syndrome (IBS): Often features reduced parasympathetic activity and increased sympathetic nervous system activity 5
- IBS-D (diarrhea predominant): Associated with increased motility, more high amplitude propagating contractions, and accelerated colonic transit
- IBS-C (constipation predominant): Shows reduced motility, fewer high amplitude propagating contractions, and delayed transit
Visceral Hypersensitivity: Autonomic dysfunction contributes to enhanced visceral perception in 20-60% of IBS patients 5
Therapeutic Applications: Understanding autonomic innervation is crucial for treatments like sacral nerve stimulation for fecal incontinence 6
Neurotransmitters and Signaling
The primary neurotransmitters involved in colonic innervation include:
- Acetylcholine: Primary parasympathetic neurotransmitter promoting contraction
- Norepinephrine/Epinephrine: Sympathetic neurotransmitters causing relaxation
- Serotonin (5-HT): Important modulator of gastrointestinal motility, with altered levels reported in IBS patients (high levels in IBS-D, low levels in IBS-C) 5
Pathological Considerations
Autonomic neuropathies affecting the colon can arise from:
- Diabetes mellitus: Most common cause of extrinsic neuropathy affecting gut motility 5
- Paraneoplastic syndromes: Associated with small cell lung cancer, carcinoid tumors, neuroblastoma, and thymoma 5
- Autoimmune conditions: Including antibodies directed at enteric neurons 5
- Infections: Chagas' disease, Lyme disease, and viral infections (herpes, cytomegalovirus) 5
- Medications: Vincristine, anticholinergics, clozapine, and other drugs can cause visceral neuropathy 5
Clinical Pearls
- The colon has a unique pattern of dual parasympathetic innervation in the left colon, with both vagal and pelvic nerve contributions 2
- Autonomic testing may be valuable in patients with unexplained motility disorders
- Medications affecting autonomic function should be considered when evaluating patients with new-onset bowel dysfunction
- Sacral nerve stimulation likely works by modulating these autonomic pathways to improve fecal continence 6