Abstract

The aim of this study was to test the hypothesis that a delay in pudendal nerve conduction as measured by pudendal nerve terminal motor latency should be associated with atrophy of the external anal sphincter as measured using endoanal ultrasound. Sixty-two adult females (median age, 58.9 (range, 22-88) years) presenting for evaluation of fecal incontinence with no evidence of an external anal sphincter tear on ultrasound were recruited. Ultrasound was performed with a 7.5-MHz radial rotating axial endoprobe in the left lateral position. Four measurements were made in the transverse plane--the external anal sphincter thickness in the midanal canal at the 6 o'clock and 9 o'clock positions, the internal sphincter at the 9 o'clock position, and the external anal sphincter in the low canal at the 9 o'clock position. Pudendal nerve terminal motor latency was measured using a transrectal nerve stimulation technique with measurement of the evoked muscle response. Although there was a trend toward thinner external sphincter muscles in those with bilateral prolonged pudendal nerve terminal motor latency, independent sample t-tests and Pearson correlation coefficients showed no statistically significant relationship (right pudendal nerve terminal motor latency: P = 0.083, 0.184, 0.128, 0.910; r = 0.228, 0.175, -0.201, -0.015; left pudendal nerve terminal motor latency: P = 0.946, 0.276, 0.510, 0.123; r = -0.009, -0.143, -0.087, -0.201). No statistically significant relationship between ultrasound-measured anal sphincter muscle thickness and pudendal nerve terminal motor latency was identified. Although a trend was suggested that could be further evaluated by a study with a larger sample size and a control group with asymptomatic patients, the small differences in muscle thickness involved and the difficulties in measurement suggest that the establishment of clinically useful ultrasound criteria for the detection of the neuropathic anal sphincter complex is unlikely.

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