SUMMARY In 40 women with idiopathic (neurogenic) faecal incontinence, 20 of whom also had stress urinary incontinence, single fibre EMG studies showed an increased fibre density in the external anal sphincter muscle. All these patients showed excessive descent of the pelvic floor on straining. The mean terminal motor latencies in the pudendal and perineal nerves, measured by a digitally-directed intrarectal stimulating technique, were increased when compared with 20 control subjects (p < 0.01). The perineal nerve terminal motor latency was more markedly increased in the 20 patients with double incontinence than in those with faecal incontinence alone (p < 0.01). These results provide direct electrophysiological evidence of damage to the innervation of the pelvic floor musculature in idiopathic faecal and double incontinence, and imply that idiopathic stress urinary incontinence may have a similar cause.Histological and electrophysiological studies have revealed denervation of the pelvic floor musculature in 75% of patients with idiopathic (neurogenic) faecal incontinence.'-3 Kiff and Swash have provided direct evidence of damage to the innervation of the perianal musculature, consisting of an increase in the terminal motor latency in the pudendal nerves measured by recording the compound muscle action potential in the external anal sphincter muscle after stimulating the pudendal nerves at the level of the ischial spines.4 In addition to supplying the external anal sphincter muscle, the pudendal nerves via their perineal branches also innervate the periurethral striated sphincter musculature.5 About 12% of our patients with neurogenic faecal incontinence also suffer from urinary incontinence of stress type.' These observations have therefore suggested to us that denervation of the periurethral striated musculature may be a factor in some patients with urinary incontinence, perhaps particularly in women in whom urinary incontinence of gradual onset in middle life is associated with perineal descent, and in those who have experienced a difficult labour. This suggestion is consistent with the clinical finding

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SUMMARY In 17 women with chronic constipation, and abnormal perineal descent on straining at stool, there was more severe neurogenic damage to the external anal sphincter muscle and to its pudendal innervation in those patients with a long history than in those with a short history. These results suggest that recurrent trauma to the pudendal nerves can occur during perineal descent, and that this can lead to denervation and weakness of the external anal sphincter muscle.Between 30% and 66% of patients with faecal incontinence give a long history of excessive straining at stool.' 2 It has been suggested that prolonged straininf during defaecation may cause perineal descent; this in turn may result in recurrent injury to the pudendal nerves and so to progressive denervation atrophy of the external anal sphincter muscle supplied by these nerves. The activity of this muscle is reduced in incontinent patients as has been shown by anorectal manometry and electromyography (EMG).2 4Using single fibre EMG, Neill and Swash5 found an increased motor unit fibre density in the external anal sphincter muscle of incontinent patients. This increased fibre density was consistent with the histological evidence of reinnervation in biopsies of this muscle taken from similar patients.3 6 7 Henry, Parks, and Swash7 found muscle fibre hypertrophy in the external anal sphincter muscle of both continent and incontinent patients with abnormal degrees of perineal descent. They suggested that this hypertrophy represents compensation for the loss of muscle fibres caused by pudendal nerve damage induced by the perineal descent.We have reported an increased terminal motor latency in the pudendal nerves after stimulation of these nerves at the level of the ischial spine in patients with neurogenic faecal incontinence.' This work supports our suggestion that the site of damage to this nerve may be at the point where it passes beneath the sacrospinous ligament.3 We have now tested this hypothesis that the pudendal nerves may be damaged in patients with perineal descent and Address for correspondence: Dr M Swash, Neurological Department, The London Hospital, London El 1BB. Received for publication 29 January 1984 1279 chronic constipation by direct measurement of pudendal nerve conduction. Methods PATIENTSSeventeen women with a history of chronic constipation were studied. All had perineal descent on straining. Eleven patients, aged 34-70 years (mean 48-1±9.7 years) had been intermittently straining at stool for between 20 and 50 years (mean 26 years), whereas in the other six patients aged 22-25 years (mean 23*8±1-5 years) the history of straining was of 10 years or less (mean 6-8 years). The mean frequency of straining per week was similar in both groups; 6-0 and 6-3 respectively. None of the six young patients was parous and none had had pelvic surgery, whereas nine of the group with a long history of straining were parous and two of these women gave a history of difficult labour. In addition three patients in this group had had a hysterect...

SUMMARYThe defaecatory mechanism using a balloon model with simultaneous measurement of intrarectal pressure has been studied in 15 control subjects with normal bowel habit and in 39 patients with chronic constipation; 31 with a normal barium enema and eight with idiopathic megarectum. Fourteen of those with a normal barium enema had prolonged whole gut transit times as measured by radio-opaque shapes. The ability of the patient to expel a rectal balloon containing 50, 100, and 150 ml of water, lying on their side in the left lateral position was tested and if unsuccessful, in the sitting position with the knees raised. All but one of the control subjects could expel balloons in the left lateral position. Only five of 17 constipated patients with normal barium enemas and transit times could expel balloons lying on their side although a further three could do so when sitting. None of 14 patients with slow transit and normal barium enemas could expel balloons in left lateral position although three could do so when sitting. Patients with megarectum could not expel balloons in either position. Levels of intrarectal pressure with straining were not significantly different between controls, who were able to expel balloons, and constipated patients with a normal barium enema, but were greater (p<0.01) in patients with megacolon than in control subjects. Using the balloon model a disorder of the defaecatory mechanism is present in patients with constipation of different types, but this is not because of an inability to raise intrarectal pressure.The term constipation lacks strict definition but most patients refer to infrequent bowel actions or the difficult passage of hard stool, usually associated with defaecation straining.' Patients described in this paper were those who failed to respond to fibre supplements and other simple measures and required treatment with laxatives, suppositories, or enemas. Many of the patients complained of severe abdominal discomfort, distension, and general malaise to the extent that their health was disrupted.It is possible to define constipation by the delayed transit of radio-opaque markers around the gastrointestinal tract.2 This definition provides a useful physiological classification for constipation. Patients with slow intestinal transit can be separated radiologically into those patients with a megacolon or megarectum and those patients with a normal sized colon.3 Other patients with complaints of constipation have normal transit times and normal barium enemas.

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