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Biomedical subjects

S J Snooks

Publications and source records attributed to S J Snooks.

32 records · Page 2Linked to original sources
PubMed1985

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.

Adult↗
PubMed1985

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.

Adult↗
PubMed1985

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.

Adenocarcinoma↗
PubMed1985

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.

Adult↗
PubMed1985

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.

Anal Canal↗
PubMed1984

Injury to innervation of pelvic floor sphincter musculature in childbirth.

71 women delivered at St Bartholomew's Hospital, London, were studied by electrophysiological tests of the innervation of the external anal sphincter muscle and by manometry. The investigations were done 2-3 days after delivery and again, in 70% of these women, 2 months later. Faecal and urinary incontinence developing after vaginal delivery has been thought to be due to direct sphincter division, or muscle stretching, but the results of the study suggest that in most cases this incontinence results from damage to the innervation of the pelvic floor muscles.

Adolescent↗
PubMed1984

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.

Adult↗
PubMed1984

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.

Adult↗
PubMed1984

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.

Adult↗
PubMed1984

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.

Adult↗
PubMedDate not supplied

Faecal incontinence.

Explore the source record for details and available documents.

Fecal Incontinence↗