Pelvic muscle electromyography of levator ani and external anal sphincter in nulliparous women and women with pelvic floor dysfunction.

Published

Journal Article

The purpose of this study was to compare results of electromyographic assessment of muscular recruitment between nulliparous control subjects without pelvic floor dysfunction and parous subjects with genuine stress urinary incontinence and with pelvic organ prolapse. Interference pattern analysis is an electromyographic technique that reproducibly measures muscular recruitment by detecting both "turns" in the electromyographic signal produced by positive and negative peaks of the motor unit potentials and motor unit potential amplitude. Fewer turns can indicate loss of motor units or failure of central activation of contraction, whereas greater amplitude can indicate reinnervation after nerve damage.We performed concentric needle electrode electromyographic examinations of the levator ani and external anal sphincter in 15 nulliparous control subjects and 20 parous subjects with abnormalities (n = 9 with genuine stress urinary incontinence, n = 11 with stage III or IV pelvic organ prolapse). We made digital recordings at multiple sites at rest and with moderate and maximal contraction. Interference pattern analysis yielded the number of turns per second and the mean signal amplitude (in microvolts) for each site at each contraction level. We compared individual patient data with data from the healthy population by means of cloud analysis. Mean values of number of turns per second and mean amplitude in each group were then compared with nonparametric methods and regression models.Mean ages were 28.7 years (range, 20-49 years) for the control group, 54.3 years (range, 35-75 years) for subjects with genuine stress urinary incontinence, and 65 years (range, 41-77 years) for subjects with pelvic organ prolapse. Median clinical levator ani strengths were 9 (range, 5-9) in the control group, 5 (range, 2-7) in the genuine stress urinary incontinence group, and 5 (range, 2-8) in the pelvic organ prolapse group. Median external anal sphincter strengths were 9 (range, 7-9) in the control group, 5 (range, 3-9) in the genuine stress urinary incontinence group, and 8 (range, 4-9) in the pelvic organ prolapse group. The external anal sphincters of subjects with pelvic organ prolapse had the highest percentage of abnormal study results according to cloud analysis. Mean number of turns per second in levators was greater in control subjects than in subjects with abnormalities (P =.034). We found similar differences in number of turns per second for the external anal sphincter (P =.004). In contrast, we did not find differences between groups in mean amplitude in either the levator ani or the external anal sphincter. Comparison of patients with genuine stress urinary incontinence versus subjects with pelvic organ prolapse showed no significant difference in the number of turns per second in either muscle. Mean amplitude was greater in the pelvic organ prolapse group than in the genuine stress urinary incontinence group for both muscles (levator ani, P =.028; external anal sphincter, P =.048). Neither mean amplitude nor the number of turns per second could be predicted by clinically estimated levator ani strength, age, or fecal incontinence.Compared with nulliparous control subjects, patients with genuine stress urinary incontinence and pelvic organ prolapse had changes in the levator ani and external anal sphincter consistent with either motor unit loss or failure of central activation, or both. Subjects with pelvic organ prolapse had findings consistent with greater recovery than was found in those with genuine stress urinary incontinence. Measures of recruitment by interference pattern analysis correlated better with clinical external anal sphincter strength than with levator ani strength and were independent of age.

Full Text

Duke Authors

Cited Authors

  • Weidner, AC; Barber, MD; Visco, AG; Bump, RC; Sanders, DB

Published Date

  • December 2000

Published In

Volume / Issue

  • 183 / 6

Start / End Page

  • 1390 - 1399

PubMed ID

  • 11120502

Pubmed Central ID

  • 11120502

Electronic International Standard Serial Number (EISSN)

  • 1097-6868

International Standard Serial Number (ISSN)

  • 0002-9378

Digital Object Identifier (DOI)

  • 10.1067/mob.2000.111073

Language

  • eng