Anal-Rectal Tone at S4-S5: Neurophysiology and Clinical Significance
Neuroanatomical Foundation
The S4-S5 spinal segments provide critical motor innervation to the anal sphincter complex through direct sacral nerve branches, distinct from the pudendal nerve pathway, making these nerve roots essential for maintaining resting anal tone and continence. 1, 2
Primary Neural Pathways
The external anal sphincter (EAS) receives motor innervation primarily from the inferior rectal branches of the pudendal nerve (S2-S4), with approximately 31% of individuals having additional direct supply from the S4 sacral nerve root 1
The levator ani muscle (including puborectalis) is innervated by direct branches from S3-S5 nerve roots that split proximal to the sacral plexus and travel on the superior surface of the pelvic floor, completely independent of the pudendal nerve 3, 2
In 89.2% of individuals, the inferior rectal nerve emerges as a direct branch of S3 and S4 (distinct from the pudendal nerve) and innervates only the subcutaneous portion of the external anal sphincter 4
Functional Segregation
The three subdivisions of the external anal sphincter (subcutaneous, superficial, and deep) are anatomically discontinuous and have independent innervation patterns, suggesting potential for functional independence 4
Stimulation of the S3 nerve root produces minimal increase in anal pressure but causes impressive decrease in the rectoanal angle through levator ani contraction, whereas pudendal nerve stimulation primarily increases anal pressure through external sphincter contraction 2
The internal anal sphincter (IAS) is responsible for the majority of resting anal tone and sensation, while the EAS primarily provides voluntary squeeze pressure 5
Clinical Significance in Disease States
Neurogenic Dysfunction
Debridement of lower sacral segments (below S3/S4) during pelvic osteomyelitis treatment can damage the S2-S4 nerve roots innervating the EAS, resulting in permanent fecal incontinence in non-paraplegic patients 1
Patients with diabetes mellitus, Parkinson's disease, and other generalized neurological disorders commonly develop secondary visceral neuropathy affecting both parasympathetic and sympathetic nerves that innervate the anal sphincters 1
Diabetes is the most common cause of autonomic neuropathy affecting anal sphincter function 1
Surgical Implications
Intersphincteric dissections for low rectal cancer will most likely damage the inferior rectal branches because of their intersphincteric course, leading to loss of innervation to the major part of the internal anal sphincter 1
Fistula surgery involving the intersphincteric space places the inferior rectal branches at risk of injury 1
The levator ani muscle attaches directly to the longitudinal muscle of the rectum, and the spatial relationship between smooth and skeletal muscles differs in different portions of the anal canal, requiring careful selection of surgical planes during intersphincteric resection 6
Diagnostic Assessment Algorithm
Initial Physical Examination
During digital rectal examination, evaluate resting tone (reflecting IAS function) and squeeze augmentation (reflecting EAS and puborectalis function), with observation of perineal descent during simulated defecation 7, 1
The puborectalis muscle sits immediately above the internal sphincter at approximately 3-5 cm from the anal verge and should contract during squeeze maneuvers, creating a distinct sensation separate from the sphincter complex below 8
Acute localized tenderness to palpation along the puborectalis indicates levator ani syndrome, not normal anatomy 7, 8
Observe for patulous opening during simulated defecation, which suggests neurogenic constipation with or without incontinence 7
Objective Testing Sequence
Begin with anorectal manometry to quantify sphincter pressures and rectal sensation, which serves as both a diagnostic tool and therapeutic component for biofeedback therapy 7, 1
Follow with 3D anal ultrasonography or MRI to identify structural defects, atrophy, or sphincter tears 1
High-resolution MRI can assess anatomical layers including the internal anal sphincter, intersphincteric space between internal and external sphincters, external anal sphincter, puborectalis muscle, and levator ani muscle 7, 8
A normal digital rectal examination does not exclude pelvic floor dysfunction, necessitating objective testing when clinical suspicion remains 7, 8
Management Strategy for S4-S5 Nerve-Related Dysfunction
Conservative Therapy (Mandatory First-Line)
All patients must receive an optimal trial of conservative therapy before considering surgical intervention 1
Fiber supplementation (25-30g daily) with adequate fluid intake to optimize stool consistency 1
Pelvic floor biofeedback therapy is essential for patients with concurrent dyssynergic defecation or evacuation disorders, with success rates exceeding 70% 7, 1
Interventional Options After Conservative Failure
Dextranomer microspheres in hyaluronic acid (NASHA Dx) is the only FDA-approved bulking agent for fecal incontinence, with 52% of patients achieving ≥50% reduction in incontinence episodes at 6 months 1
Sacral nerve stimulation (SNS) should be considered for patients who fail conservative therapy and bulking agents, with initial test stimulation for 2-3 weeks targeting the S2-S4 nerve roots that supply the EAS 1
Overlapping sphincteroplasty is indicated for patients with documented structural sphincter defects on imaging who have failed conservative measures 1
Critical Contraindication
- Never perform manual anal dilatation, as it causes permanent incontinence in 10-30% of patients and is absolutely contraindicated 1
Common Clinical Pitfalls
Do not confuse normal puborectalis contraction during digital examination with pathology—this is an expected finding 8
Post-surgical sensory changes are typically neuropathic/myofascial rather than mechanical sphincter failure, requiring physical therapy (2-3 times weekly with internal and external myofascial release) rather than surgical revision 5
Failure to assess puborectalis function during simulated defecation can miss pelvic floor dysfunction 7, 8
Stimulation frequencies of 10-20 Hz can produce sustained changes in anal pressure without muscle fatigue, which is relevant for sacral nerve stimulation programming 2