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[Neurogenic myopathy of pelvic floor and sphincter musculature in idiopathic incontinence].

F. Beersiek

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Abstract

The underlying cause of so-called idiopathic incontinence is probably neurogenic myopathy. As compared with a control group, 16 patients with anorectal incontinence were found to have a type I fibre predominance in the external and sphincter, the puborectal and levator ani muscles. The mean diameter of type II fibres was greater in external sphincter and puborectal muscles of the control group. In contrast, the mean diameters of type I fibres in female subjects of the control group were significantly greater than that of type II fibres. In patients with incontinence, marked fibre hypertrophy of both histochemical fibre types was observed. This finding was most evident in puborectal and external anal sphincter muscles. In 12 of the 16 incontinent patients under study, histological and statistical findings indeed appeared to be due to neurogenic damage of the sphincter muscles. Birth trauma or stretch injury due to excessive straining on defecation represent causes of damage to the pudendal nerve which innervates the anal sphincters. Tensioning of the external sphincters to restore the anorectal angle as in the Parks' technique of post-anal repair appears to be a promising form of treatment of idiopathic incontinence.

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The underlying cause of so-called idiopathic incontinence is probably neurogenic myopathy. As compared with a control group, 16 patients with anorectal incontinence were found to have a type I fibre predominance in the external and sphincter, the puborectal and levator ani muscles. The mean diameter of type II fibres was greater in external sphincter and puborectal muscles of the control group. In contrast, the mean diameters of type I fibres in female subjects of the control group were significantly greater than that of type II fibres. In patients with incontinence, marked fibre hypertrophy of both histochemical fibre types was observed. This finding was most evident in puborectal and external anal sphincter muscles. In 12 of the 16 incontinent patients under study, histological and statistical findings indeed appeared to be due to neurogenic damage of the sphincter muscles. Birth trauma or stretch injury due to excessive straining on defecation represent causes of damage to the pudendal nerve which innervates the anal sphincters. Tensioning of the external sphincters to restore the anorectal angle as in the Parks' technique of post-anal repair appears to be a promising form of treatment of idiopathic incontinence.

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Available abstract

The underlying cause of so-called idiopathic incontinence is probably neurogenic myopathy. As compared with a control group, 16 patients with anorectal incontinence were found to have a type I fibre predominance in the external and sphincter, the puborectal and levator ani muscles. The mean diameter of type II fibres was greater in external sphincter and puborectal muscles of the control group. In contrast, the mean diameters of type I fibres in female subjects of the control group were significantly greater than that of type II fibres. In patients with incontinence, marked fibre hypertrophy of both histochemical fibre types was observed. This finding was most evident in puborectal and external anal sphincter muscles. In 12 of the 16 incontinent patients under study, histological and statistical findings indeed appeared to be due to neurogenic damage of the sphincter muscles. Birth trauma or stretch injury due to excessive straining on defecation represent causes of damage to the pudendal nerve which innervates the anal sphincters. Tensioning of the external sphincters to restore the anorectal angle as in the Parks' technique of post-anal repair appears to be a promising form of treatment of idiopathic incontinence.

Key concepts: External anal sphincter, Medicine, Sphincter, Pudendal nerve, Levator ani, Urethral sphincter, Pelvic floor, Fecal incontinence

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[Neurogenic myopathy of pelvic floor and sphincter musculature in idiopathic incontinence]. — Research Paper | ScholarLens