Mechanical Pull of Anal Sphincters on Pudendal Nerves
Direct Answer
The external and internal anal sphincters do not exert meaningful mechanical "pull" on the pudendal nerve in a way that would be perceived or cause symptoms. The pudendal nerve and its inferior rectal branches traverse through the intersphincteric space but are not mechanically tethered to or pulled by sphincter contractions 1.
Anatomical Relationship Between Sphincters and Pudendal Nerve
Nerve Course and Sphincter Anatomy
The inferior rectal branches of the pudendal nerve (S2-S4) run along the conjoint longitudinal muscle coat in the intersphincteric space, positioned between the internal and external anal sphincters rather than being attached to them 1.
The internal anal sphincter (IAS) is composed of flat rings of smooth muscle bundles stacked like slats of a Venetian blind, each covered by its own fascia, and generates continuous myogenic tone independent of nerve input 2, 3.
The external anal sphincter (EAS) consists of three ellipsoid rings (subcutaneous, superficial, and deep) of skeletal muscle that encircle the anal canal 2.
The longitudinal anal muscle (LAM) between the IAS and EAS consists of helical striated and smooth muscle fibers that create a functional connection but do not mechanically tether nerves 4.
Why Sphincters Don't "Pull" on Nerves
The pudendal nerve branches supply motor innervation to the EAS and sensory innervation to the anal canal, but the nerves are not structurally anchored to the sphincter muscles in a way that would transmit mechanical tension 1, 5.
Sphincter contraction (either IAS smooth muscle tone or EAS voluntary squeeze) compresses and narrows the anal canal through muscle shortening, but this does not create traction on the nerve trunks 4, 3.
The inferior rectal branches traverse the intersphincteric space in a relatively protected anatomical plane, making them vulnerable to surgical injury during intersphincteric dissection but not to physiologic mechanical stress from normal sphincter function 1.
Clinical Context: Post-Surgical Sensory Loss
Mechanism of Injury After Colorectal Surgery
Loss of anal sensation, bladder control, and sexual function after major colorectal surgery reflects direct iatrogenic nerve injury during intersphincteric dissection, not mechanical traction from sphincter activity 6, 1.
Intersphincteric dissection places the inferior rectal branches at high risk because they traverse this surgical plane; transection or crush injury during dissection causes neuropathic dysfunction 6, 1.
The major autonomic nerve input to the IAS originates from the inferior rectal branches of the pelvic plexus (IRB-PX), and injury to these nerves results in loss of innervation to the major part of the IAS 1.
In 89.2% of individuals, the inferior rectal nerve emerges as a branch of S3 and S4 distinct from the main pudendal trunk, making it particularly vulnerable during low pelvic dissections 5.
Secondary Compensatory Dysfunction
Low internal sphincter resting pressure after nerve injury triggers compensatory hypertonicity of the puborectalis and external anal sphincter, creating persistent pelvic floor tension 6, 7.
This protective guarding pattern persists after anatomical healing and interferes with normal pelvic floor relaxation during sexual arousal and bladder function 6.
The resulting dysfunction is neuropathic and myofascial rather than mechanical sphincter failure, requiring physical therapy rather than surgical revision 6, 8.
Management of Post-Surgical Neuropathic Dysfunction
First-Line Conservative Therapy
Initiate intensive pelvic-floor physical therapy 2–3 times per week, emphasizing internal and external myofascial release to reduce compensatory hypertonicity 6, 8, 7.
Techniques include manual release of puborectalis and external sphincter tension, gradual desensitization exercises, and muscle-coordination retraining to break protective guarding patterns 6.
Pelvic-floor biofeedback therapy achieves success rates exceeding 70% in patients with dyssynergic pelvic-floor patterns 7.
Topical lidocaine 5% ointment applied to the perianal and anal canal areas provides temporary relief of neuropathic dysesthesia 6.
Diagnostic Evaluation
Anorectal manometry quantifies resting pressure and detects paradoxical contraction (anismus) during simulated defecation 6, 7.
High-resolution pelvic MRI visualizes the sphincter complex and identifies any unrecognized structural complications 6, 7.
Digital rectal examination may reveal localized tenderness over the puborectalis if levator ani syndrome (chronic hypertonicity) has developed 6, 7.
What to Avoid
Additional surgical revision for sensory loss is absolutely contraindicated because the underlying problem is neuropathic and myofascial, not mechanical sphincter failure 6, 8.
Revision surgery carries a high risk of further pudendal-nerve injury 6.
Manual anal dilatation is absolutely contraindicated; it causes permanent incontinence in 10–30% of patients 9, 6, 7.
Prognosis
Significant axonal injury may render the neuropathic component partially irreversible 6.
Conservative physical-therapy-based treatment can restore some pelvic-floor relaxation capacity during sexual activity 6.
Sensory adaptation and neuroplasticity may gradually improve perception over 12–24 months, although full restoration is unlikely if nerve branches were transected 6.
Continue conservative therapy for 6–12 months before assessing maximal recovery 6, 8.
Key Clinical Pitfall
The common misconception that sphincter muscle activity mechanically "pulls" on pudendal nerves leads to inappropriate surgical interventions. The pudendal nerve branches are injured by surgical dissection, not by physiologic sphincter contraction. Post-surgical sensory dysfunction requires neuromuscular rehabilitation, not additional surgery 6, 8, 1.