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Updated: Jul 12, 2026

Quantification of Levator Ani Hiatus Enlargement by Magnetic Resonance Imaging in Males and Females with Pelvic Organ Prolapse
Published on: April 17, 2019
Abnormal pelvic response to cough in women with stress urinary incontinence
Xavier Deffieux1, Katelyne Hubeaux, Raphael Porcher
1Université Pierre et Marie Curie-Paris 6, Faculté de Médecine, Paris, France. x.deffieux@free.fr
Aims:
To assess how muscular fatigue deteriorates the modulation of pelvic contraction during increasing cough efforts. Furthermore, we investigated the correlation between the temporal course of pelvic floor activation during cough.
Methods:
Informed consent was obtained from 20 women presenting with SUI and 6 continent women (overactive bladder syndrome [OAB]). Bladder pressure (BP) and external anal sphincter electromyographic activity (EAS EMGi) were recorded concomitantly during increasing cough efforts. Modulation of pelvic contraction was assessed before and after two types of intense pelvic exercise (Exercise #1: 10 successive strong cough efforts; Exercise #2: 10 pelvic contractions followed by a maximal pelvic contraction) at 0, 200, and 400 ml of bladder filling. We have also recorded electromyographic activity of external intercostal (EIC) muscles.
Results:
Whereas the Exercise 1 had no effect on modulation, the Exercise 2 altered significantly the modulation of pelvic contraction during increasing cough efforts (P = 0.043) only in women presenting with SUI. The bladder filling volume seems to not significantly modify this modulation (P = 0.12). Median latency between the onset of the EAS EMGi and the onset of the EIC EMGi was -470 and -60 msec in OAB group and in SUI group, respectively (P = 0.012). There was a good correlation between mean latency (default of EAS EMGi pre-activation) and an altered modulation of pelvic contraction during increasing cough efforts (P = 0.040).
Conclusions:
Some women with SUI exhibit an altered pattern of the PFM response during increasing coughing efforts. The lack of this modulation of PFM response to stress may be one of the pathophysiologic factors of SUI.
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