Parity as a factor in incontinence in multiple sclerosis.

Twelve consecutively selected patients with multiple sclerosis and incontinence had electrophysiologic studies performed of the pudendal and perineal innervations of the anal and urinary sphincter. Single-fiber electromyogram density measurements were obtained in the external anal sphincter. Fecal incontinence was found to be unexpectedly frequent. The results suggest that incontinence in patients with multiple sclerosis is often due to the interaction of several factors, including central lesions, lesions of the conus medullaris and, also, coincidental pelvic nerve lesions associated with childbirth. Thus, incontinence is especially a problem in women with this disease.

Neurologic cause of idiopathic incontinence.

The relationship between the pudendal and perineal nerve terminal motor latencies and descent (weakness) of the perineum on straining was investigated in 31 patients with idiopathic fecal incontinence, and in 30 patients with double incontinence. Pelvic floor descent was correlated with increased pudendal nerve terminal motor latency in both groups of patients. In the patients with double incontinence, there was a less significant correlation between perineal descent and increased perineal nerve terminal motor latency. In the patients with fecal incontinence, but without urinary incontinence, there was no correlation between perineal descent and perineal nerve terminal motor latency. These data support the concept that pelvic floor weakness can result in damage to the pudendal and perineal nerves, leading to fecal and urinary incontinence. In patients with isolated fecal incontinence the perineal nerves are relatively spared. Thus these common types of incontinence probably have a neurologic cause, and neurophysiologic methods can be used in their assessment.

Adenocarcinoma of the small bowel.

Cancer of the small bowel is a rare entity but its incidence is rising. Historically, outcome is poor despite apparent curative resection. At present surgery remains the only treatment modality of proven benefit in the management of this disease. Recent data would suggest 5-year survival rates in the order of 40-50% at all sites of small bowel cancer. To improve upon this, earlier diagnosis with a high index of suspicion and multicentre adjuvant therapy trials are required.

The innervation of the muscles of continence.

Electrophysiological evidence is presented that suggests that the innervation of the human puborectalis muscle differs from that of the external anal sphincter muscle. The latter is innervated by branches of the pudendal nerves, and the former by direct branches of the sacral plexus that enter the muscle from its pelvic surface. The striated urinary sphincter musculature also receives a dual innervation. The periurethral component is innervated by perineal branches of the pudendal nerves and the intramural portion by a different pathway, probably consisting of supralevator branches derived from the pelvic nerves. These findings are relevant to understanding the embryological derivation of these muscles and have practical importance in the surgery of this region of the body, particularly in the treatment of incontinence.

Investigation of disorders of the anorectum and colon.

Previously, investigation of disorders of the anorectum and colon have been limited to manometric, external anal sphincter muscle electromyographic and contrast radiological techniques. In this paper we describe other investigative techniques recently developed at St. Mark's Hospital, London and their application in the investigation of certain disorders of the anorectum and colon.

Abnormalities in central and peripheral nerve conduction in patients with anorectal incontinence.

Thirty women with idiopathic anorectal incontinence were investigated by nerve conduction studies. Twenty-two (73%) patients had abnormal nerve conduction studies. In 7 (23%) of these patients there was conduction delay in the cauda equina between L1 and L4 vertebral levels but in the remainder the distal innervation of the pelvic sphincters was abnormal.

Unifying concept of pelvic floor disorders and incontinence.

Denervation of pelvic floor sphincter muscles is a feature of pelvic floor disorders. When severe, it may be accompanied by stress incontinence of faeces, or of urine. The extent of chronic partial denervation of these pelvic floor muscles can be quantified by electromyography (EMG), and its cause identified by electrophysiological studies of the motor innervation of these striated muscles. Damage to this innervation is often initiated by childbirth, but appears to progress during a period of many years so that the functional disorder usually presents in middle life. Incontinence develops in some patients, but not in others. This can be predicted by the severity of the abnormalities found in EMG studies of the pelvic sphincter musculature and motor latency studies of its innervation. The results of such investigations in the six common types of pelvic floor disorder are presented. Recognition of the causative factors leading to damage to the innervation of the pelvic sphincter muscles implies new approaches to treatment and to prevention of pelvic floor disorders and incontinence.

Slowed motor conduction in lumbosacral nerve roots in cauda equina lesions: a new diagnostic technique.

New techniques have been developed for the electrophysiological assessment of patients with suspected cauda equina lesions using transcutaneous spinal stimulation (500-1500 V: time constant 50 microseconds) to measure motor latencies to the external and sphincter and puborectalis muscles from L1 and L4 vertebral levels. These latencies represent motor conduction in the S3 and S4 motor roots of the cauda equina between these levels. Similarly motor latencies can be recorded from spinal stimulation to the anterior tibial muscles (L4 and L5 motor roots). Transrectal stimulation of the pudendal nerves is used to measure the pudendal nerve terminal motor latency. In 32 control subjects, matched for age and sex, mean motor latencies from L1 and L4 spinal stimulation were 5.5 +/- 0.4 ms and 4.4 +/- 0.4 ms (mean + SD). In the 10 patients with cauda equina disease including ependymoma, spinal stenosis, arachnoiditis and trauma, these latencies were 7.2 +/- 0.8 ms and 4.6 +/- 0.9 ms, a significant increase in the L1 latency. The L1/L4 latency ratios to the puborectalis muscle were 1.36 +/- 0.09 in control subjects and 1.72 +/- 0.13 in cauda equina patients. Pudendal nerve terminal motor latencies were normal in eight of the 10 patients with cauda equina disease. The single fibre EMG fibre density in the external and sphincter muscle (normal, 1.5 +/- 0.16) was increased in patients with cauda equina lesions (1.73 +/- 0.28), but was increased more than two standard deviations from the mean only in three patients. This increase in fibre density was not of diagnostic value since it was also found in two of the four patients with low back pain. Slowing of motor conduction in the cauda equina is thus a useful indication of damage to these intraspinal motor roots. These investigations can be used in the selection of patients for myelography, and to follow progress in patients managed conservatively.

Abnormalities of the innervation of the urethral striated sphincter musculature in incontinence.

Perineal nerve and transcutaneous spinal cord stimulation have been used to study 17 patients with idiopathic neurogenic faecal incontinence, 12 of whom also had urinary incontinence. Significant increases in spinal, perineal and pudendal nerve motor latencies were demonstrated in all 17 patients. These results suggest that there is damage to the nerves innervating both the urethral and perianal sphincter musculature in these patients, including those with isolated faecal incontinence. There was evidence of both a distal (perineal nerve) and a proximal (sacral root) component to the damage to the nerve supply of the urethral striated sphincter muscle in half of the patients.

Perineal nerve and transcutaneous spinal stimulation: new methods for investigation of the urethral striated sphincter musculature.

The distal motor latencies in the perineal and pudendal nerves were measured in 20 normal subjects using digitally directed pudendal nerve stimulation. The mean pudendal and perineal nerve latencies were 1.9 ms +/- 0.2 (SD) and 2.4 ms +/- 0.2 (SD) respectively. In a further eight normal subjects transcutaneous spinal stimulation was used to record the motor latency from L1 and L4 stimulation sites to the urethral striated sphincter musculature. The mean spinal nerve terminal latencies from L1 and L4 were 4.9 ms +/- 0.3 (SD) and 4.1 ms +/- 0.2 (SD) respectively. These techniques can be applied to the investigation of the nerve supply to the urethral striated musculature in stress urinary incontinence and other disorders affecting the innervation of the anterior pelvic floor musculature.

Motor conduction velocity in the human spinal cord: slowed conduction in multiple sclerosis and radiation myelopathy.

Transcutaneous electrical stimulation of the central nervous system was used to measure motor conduction velocity in the human spinal cord in 21 subjects aged 22 to 75 years (mean 55 years), none of whom had neurological disease. The motor conduction velocity between the sixth cervical (C6) and first lumbar (L1) vertebral levels was 67.4 +/- 9.1 m/s. This probably represents conduction velocity in the corticospinal tracts. In these subjects the motor conduction velocity in the cauda equina, between the first lumbar (L1) and fourth lumbar (L4) vertebral levels, was 57.9 +/- 10.3 m/s. In four of five patients with multiple sclerosis, all with corticospinal signs in the legs, motor conduction velocity between C6 and L1 was slowed (41.8 +/- 16.8 m/s), but cauda equina conduction was normal (55.8 +/- 7.8 m/s). Similar slowing of spinal cord motor conduction was found in a patient with radiation myelopathy. This method should provide a relevant, simple clinical test in patients with spinal cord disease.

How should we preclot knitted Dacron grafts?

We studied the change in water porosity over time of 10 Sauvage Bionit-II and 10 DeBakey Vasculour-II knitted velour Dacron grafts throughout the four stages of the Sauvage preclotting technique. Graft porosity decreased significantly (p less than 0.001) at the ends of stages 1 and 2 for both types of grafts, but stages 3 and 4 did not further reduce graft porosity. These results demonstrate that a two-stage preclotting technique is adequate for the preclotting of knitted velour Dacron grafts. A final rinse with heparinized blood is recommended as this may reduce graft thrombogenicity.

Damage to the innervation of the voluntary anal and periurethral sphincter musculature in incontinence: an electrophysiological study.

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 less than 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 less than 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.

Gastric cancer: a continuing diagnostic challenge--a district general hospital's experience.

We present the results of 87 consecutively referred patients with malignant gastric tumours who presented to the North Middlesex Hospital between 1980 and 1984, inclusively. The results of this prospective study showed a high incidence of adenocarcinoma situated in the cardia (16 per cent of patients), and antral carcinomas presented more commonly with chronic blood loss. Delay in diagnosis was still a serious problem and weight loss remained an underestimated symptom, especially when combined with other upper gastrointestinal symptomology. The majority of tumours were adenocarcinomas. Six patients had unusual tumours which had special therapeutic and prognostic implications. The results of the above study are compared with the European experience of the management of malignant gastric tumours.

Anorectal incontinence and rectal prolapse: differential assessment of the innervation to puborectalis and external anal sphincter muscles.

The innervation of the puborectalis and external anal sphincter muscles was studied in 32 patients with idiopathic (neurogenic) faecal incontinence, 12 of whom also had complete rectal prolapse, using transcutaneous spinal stimulation, transrectal pudendal nerve stimulation, single fibre EMG, anorectal manometry, and measurement of perineal descent. Fourteen normal subjects served as controls. Significant increases in the spinal motor latencies from L1 to the puborectalis and external anal sphincter muscles were shown in all 32 incontinent patients (p less than 0.01). The single fibre (EMG) fibre density was increased in the puborectalis muscle in 60% and in the external anal sphincter in 75% of patients. An increased pudendal nerve terminal motor latency was found in 68% of patients; 69% had an abnormal degree of perineal descent and all had reduced anal canal contraction pressures. These data show that the different innervations of the puborectalis and external anal sphincter muscles are both damaged in patients with anorectal incontinence.

Faecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology.

The commonest cause of external anal sphincter division is injury during childbirth. We have studied 20 patients with anterior external anal sphincter division using physical and electrophysiological techniques. There was evidence of pudendal nerve damage in 60% of these patients. This finding suggests that damage to the innervation of the external anal sphincter often co-exists with direct injury to the muscle; in these patients pelvic floor surgery may be required, in addition to sphincter repair itself.

Electrophysiologic and manometric assessment of failed postanal repair for anorectal incontinence.

The reason for failure to improve fecal incontinence after postanal repair in idiopathic (neurogenic) anorectal incontinence is unknown. The authors have studied 20 patients whose anorectal continence was not improved after Parks' postanal repair. Anorectal manometry, single fiber EMG of the external anal sphincter muscle, and measurements of the pudendal nerve terminal motor latency were studied before and nine months after postanal repair. All 20 patients had evidence of reinnervation within the external anal sphincter muscle before operation; 17 had a raised pudendal nerve terminal motor latency and all 20 had low resting voluntary contraction anal canal pressures. No significant differences were found between the resting, voluntary contraction anal canal pressures and single fiber EMG fiber density values before or after postanal repair. However, a significant increase in the pudendal nerve terminal motor latency was found after postanal repair (P less than 0.001) using a student's paired t test. These results suggest that, in patients who are not rendered continent by postanal repair, a continuing neuropathic process takes place.