The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence

Citation
Cbo. Suilleabhain et al., The relationship of pudendal nerve terminal motor latency to squeeze pressure in patients with idiopathic fecal incontinence, DIS COL REC, 44(5), 2001, pp. 666-671
Citations number
18
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
DISEASES OF THE COLON & RECTUM
ISSN journal
00123706 → ACNP
Volume
44
Issue
5
Year of publication
2001
Pages
666 - 671
Database
ISI
SICI code
0012-3706(200105)44:5<666:TROPNT>2.0.ZU;2-G
Abstract
PURPOSE: With the advent of transanal ultrasonography it has been possible to identify those incontinent patients without sphincter defects. The major ity of these patients are now thought to have neurogenic fecal incontinence secondary to pudendal neuropathy. They hare been found to have reduced ana l sphincter pressures and increased pudendal nerve terminal motor latencies . The aim of this study was to determine whether in those incontinent patie nts who do not have a sphincter defect, prolonged pudendal nerve terminal m otor latency correlates with anal manometry in particular maximum squeeze p ressure. METHODS: Sixty-six incontinent patients were studied with transana l ultrasonography, anorectal manometry, and pudendal nerve terminal motor l atency. Twenty-seven continent controls had anorectal manometry and pudenda l nerve terminal motor latency measured. RESULTS: Maximum resting pressure and maximum squeeze pressure were significantly lower in the group of incon tinent patients with bilateral prolonged pudendal nerve terminal motor late ncy (median maximum resting pressure = 26.5 mmHg; median maximum squeeze pr essure = 60 mmHg) when compared with incontinent patients with normal bilat eral pudendal nerve terminal motor latencies (median maximum resting pressu re = 46 mmHg; median maximum squeeze pressure = 79 mmHg; maximum resting pr essure P = 0.004; and maximum squeeze pressure P = 0.04). In incontinent pa tients with no sphincter defects no correlation between pudendal nerve term inal motor latency and maximum squeeze pressure was found (r = -0.109, P = 0.48) and maximum squeeze pressure did not correlate with bilateral or unil ateral prolonged pudendal nerve terminal motor latency (r = -0.148, P = 0.5 6 and r = 0.355, P = 0.19 respectively). CONCLUSIONS: In patients with idio pathic fecal incontinence damage to the pelvic floor is more complex than d amage to the pudendal nerve alone. Although increased pudendal nerve termin al motor latency may indicate that neuropathy is present, in patients with neuropathic fecal incontinence, pudendal nerve terminal motor latency does not correlate with maximum squeeze pressure. Normal pudendal nerve terminal motor latency does not exclude weakness of the pelvic floor.