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ELECTROMYOGRAPHIC
STUDY OF THE STRIATED URETHRAL SPHINCTER IN TYPE 3 STRESS INCONTINENCE:
EVIDENCE OF MYOGENIC-DOMINANT DAMAGES
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Authors:
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S.Takahashi, Y.Homma,
Y.Hosaka, T.Kitamura, and K.Kawabe
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Institution:
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Department of Urology,
The University of Tokyo, Tokyo, Japan
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Aims of
Study:
Recently, several studies have reported evidences of partial denervation in
the pelvic floor muscles in Stress incontinence(SI) patients, using electrophysiological
and histomorphological methods. These results suggested that the denervation
in the pelvic floor muscles possibly caused by childbirth vaginally is one of
the etiological factors of type 2 SI accompanied with urethral hypermobility.
Whereas, an etiology of another type of SI, that is type 3 SI considered due
to intrinsic sphincteric deficiency remains unclear. We determined electromyographic
features of the striated urethral sphincter in type 3 SI patients and evaluated
the correlation of electromyographic changes with the clinical findings.
Methods:
We performed electromyography(EMG) of the striated urethral sphincter muscle
and urodynamic studies including Valsalva leak point pressure measurement in
a total of 51 women, 41 female patients with type 3 SI due to intrinsic sphincteric
deficiency(ISD) and 10 women with normal urinary control(NUC). EMG parameters
evaluated were duration, amplitude, and number of phases in individual motor
unit potentials(MUP) of the striated urethral sphincter at rest, and also an
interference pattern at maximal voluntary contraction.
Results:
In patients with SI, mean values of MUP parametersü}SD were duration 4.2ü}0.9
msec., amplitude 299.9ü}112.0 mV. and number of phases 4.1ü}0.7. The values
in women with NUC were 5.2ü}0.3 msec., 428.2ü}25.6 mV., and 3.4ü}0.4, respectively.
The MUP of SI patients showed significantly shorter duration (p=0.0014) , lower
amplitude (p=0.0008) and larger number of phases (p=0.0022). 30 (73%) of the
SI patients showed an obvious low amplitude (<350 mV)/short duration(<4.5 msec.)/polyphasic
pattern and early recruitment of interference activity with low amplitude at
voluntary contraction of the striated sphincter, both indicating existence of
myogenic damages. These patients showing myogenic damages had significantly
lower Valsalva leakpoint pressure (p<0.0001) and more leakage in pad weigh test
(p=0.0101), compared with the SI patients without myogenic damage findings.
Conclusions:
These results suggested that myogenic-dominant damages of the striated urethral
sphincter may contribute to the etiology of ISD in the majority of type 3 SI.