Journal of Neurogastroenterology and Motility 2019; 25(3): 340-342
Evaluation of Anorectal Afferent Pathway: Does It Help Overcome Unmet Diagnostic Needs in the Management of Fecal Incontinence?
Tae Hee Lee
Institute for Digestive Research, Soonchunhyang University Seoul Hospital, Seoul, Korea
Correspondence to: Tae Hee Lee, MD, PhD
Institute for Digestive Research, Digestive Disease Center, Soonchunhyang University Seoul Hospital, 59 Daesagwan-ro, HannamDong, Yongsan-Gu, Seoul 04401, Korea
Tel: +82-2-710-3084, Fax: +82-2-709-9696, E-mail:
Received: June 20, 2019; Accepted: July 8, 2019; Published online: July 1, 2019.
© The Korean Society of Neurogastroenterology and Motility. All rights reserved.

cc This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Fecal incontinence (FI) is a complex disease resulting from overflow, reduced storage capacity, weakness of internal anal sphincter, disruption of external anal sphincter or puborectalis muscle and decreased perception of rectal sensation.1 The clinical assessment including a detailed history, physical examination, and digital rectal examination should be taken to arrive at an accurate diagnosis, establish rapport with the patient, and making a proper management strategy for diagnostic testing and treatment. Diagnostic testing currently available includes endoscopy, anorectal manometry with sensory testing, anal endosonography/magnetic resonance image, defecography, pudendal nerve motor latency, balloon expulsion test, and saline infusion test (Table). The extent of diagnostic testing is influenced by the availability of tests and the clinical features such as symptom severity and response of conservative management.2

Although the contribution of anal weakness to FI is well recognized, the role of altered rectal sensation in FI is under-recognized. Rectal sensation is evaluated by progressively distending a latex balloon manually or by distending a polyethylene balloon with a barostat.3 Rectal hyposensitivity is clinically defined as elevated perception thresholds to rectal balloon distension.3 When rectal sensation is reduced, this condition allows stool to enter the anal canal and possibly leak before the external anal sphincter contracts. It means that rectal hyposensitivity causes impaired sensory-aware mechanism to properly trigger continence action. However, the pathophysiology of rectal hyposensitivity remains unknown. It is plausible that RH is secondary to afferent nerve dysfunction. However, rectal sensation assessed by distending a latex balloon during anorectal manometry examination reflects rectal mechanoreceptor’s distension sensitivity and is affected by rectal compliance. This technique cannot clarify whether afferent neural pathway is intact (ie, primary rectal hyposensitivity).

A sensory evoked potential (SEP) is an electrical potential recorded from the nervous system following presentation of an electrical stimulus.4 The measurement of SEP to anal/rectal electrical stimulation (ASEP/RSEP) is an objective neurophysiological technique for assessing the integrity of afferent pathways from anorectal structures.5 This technique has been assessed in healthy volunteers,68 irritable bowel syndrome,9,10 and constipation.11 At the present time, little is known about the role of altered sensory pathways as a pathophysiological mechanism of patients with FI. In this issue of Journal of Neurogastroenterology and Motility, Mundet et al12 assessed ASEP/RESP with neurophysiologic technique in 19 healthy volunteers (HVs) and 175 women with FI. The main finding is that abnormal conduction of anorectal afferents as well as mechanical anal sphincter dysfunctions contributes to pathophysiology of FI (Figure). ASEP latencies were significantly longer in patients with in HVs and approximately half of patients had ASEP latency outside the reference values. RESP latencies were significantly longer in patients than in HVs and approximately 50% of patients had abnormal RESP parameters (including latencies and amplitude). Patients had significantly reduced activated cortical area compared than HVs. This difference in activation of cortical area between HVs and patients do not suggests that brain cortex plays a role in the pathogenesis of FI among the patients enrolled in this study. Impaired sensory perception and integration processing may cause reduced activated cortical area in the patients.

This study is the first to indicate that application of ASEP/RESP neurophysiology technology provides novel insights regarding the pathogenesis of FI. The presence of impaired conduction in anorectal afferent pathways may be important in explaining the reason why sacral neuromodulation improves symptoms of FI in some patients with any mechanical effect on anal sphincter function. This evolution also offers great promise in understanding of the contribution of impaired rectal afferents and developing more specific treatments for patients with FI. However, this study does not involve the data of ASEP/RESP neurophysiology test regarding rectal hypersensitivity which may contribute to the symptom of urgency in FI and is often observed in patients with FI.13 In addition, it challenges to perform the measurement of ASEP/RESP through this neurophysiological technique in every practice environment. Now, this technique is not in routine clinical use but seems to provide useful insights into the mechanism of anorectal sensory dysfunction. Further studies with SEP analysis in response to electrical stimuli are also necessary to understand functional consequences and clinical utility of delayed anorectal afferent pathways for stratifying patients with FI to medical, behavioral and surgical therapies.

Fig. 1. Visual representation of the key findings. IAS, internal anal sphincter; EAS, external anal sphincter; HV, healthy volunteers; FI, fecal incontinence; ASEP, anal sensory evoked potential; RESP, rectal sensory evoked potential. Reproduced from Mundet et al.


Clinical Assessment and Diagnostic Testing Currently Available

Detailed historyOnset and precipitating events
Duration, severity, and timing
Stool consistency and urgency
Co-existing problems/surgery/urinary incontinence/back injury
Obstetric history
Drugs, caffeine, and diet
Clinical subtypes-passive, urge incontinence, or fecal seepage
Clinical grading of severity
History of fecal impaction
Physical examinationBack and the lower limbs
Perianal inspection
Prolapsed hemorrhoid
Anal deformity
Dermatitis resulting from frequent soiling
Digital rectal examinationAnal sphincter tone and strength
Perineal descent
Rectal prolapse
EndoscopyMucosal disease
Anorectal manometry with sensory testingFunctional weakness of the IAS/EAS
Abnormal rectal sensation
Rectal compliance
Anal endosonography/MRIStructural defects of the anal sphincter
ElectromyographyStructural defects of the anal sphincter
Rectal barostatRectal compliance
Abnormal rectal sensation
DefecographySuspected rectal prolapse
Poor rectal evacuation
Pudendal nerve terminal latencyMotor efferent pathways
Balloon expulsion testImpaired evacuation in patients with fecal seepage or fecal impaction
Saline infusion testClinical improvement after treatment

IAS, internal anal sphincter; EAS, external anal sphincter; MRI, magnetic resonance image.


Financial support: This work was supported by the Soonchunhyang University Research Fund.

Conflicts of interest: None.

Author contributions: Tae Hee Lee designed, wrote, and critically reviewed the study.

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