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| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 20 | The Relationship of Pudendal Nerve Terminal Motor Latency to Squeeze Pressure in Patients with Idiopathic Fecal Incontinence [2001년 5월 DCR] | 2011-11-17 | 3356 |
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C. B. 6 Sfiilleabhfiin, M.D., F.R.C.S.I., A. F. Horgan, M.D., F.R.C.S.I.,L. McEnroe, S.R.N., F. W. Poon, F.R.C.R., J. H. Anderson, M.D., F.R.C.S.(Gen.),I. G. Finlay, F.R.C.S.(Glasg.), R. F. McKee, M.D., F.R.C.S.(Glasg.)
From the Departments of Coloproctology and SRadiology, Glasgow Royal Infirmary, Glasgow,
United Kingdom PURPOSE: With the advent of transanal ultrasonography it has been possible to identifT those incontinent patients without sphincter defects. The majority of these patients are now thought to have neurogenic fecal incontinence secondary to pudendal neuropathy. They have been found to have reduced anal sphincter pressures and increased pudendal nerve terminal motor latencies. The aim of this study was to determine whether in those incontinent patients who do not have a sphincter defect, prolonged pudendal nerve terminal motor latency correlates with anal manometry, in particular maximum squeeze pressure.
METHODS: Sixty-six incontinent patients were studied with transanal ultrasonography, anorectal manometry, and pudendal nerve terminal motor latency. Twenty-seven continent controls had anorectal manometry and pudendal nerve terminal motor latency measured. RESULTS: Maximum resting pressure and maximum squeeze pressure were significantly lower in the group of incontinent patients with bilateral prolonged pudendal nerve terminal motor latency (median maximum resting pressure = 26.5 mmHg; median maximum squeeze pressure = 60 mmHg) when compared with incontinent patients with normal bilateral pudendal nerve terminal motor latencies (median maximum resting pressure = 46 mmltg; median maximum squeeze pressure = 79 mmHg; maximum resting pressure P = 0.004; and maximum squeeze pressure P = 0.04). In incontinent patients
with no sphincter defects no correlation between pudendal nerve terminal motor latency and maximum squeeze pressure was found @ = -0.109, P = 0.48) and maximum squeeze pressure did not correlate with bilateral or unilateral prolonged pudendal nerve terminal motor latency (r = -0.148, P = 0.56 and r = 0.355, P = 0.19 respectively). CONCLUSIONS: In patients with idiopathic fecal incontinence damage to the pelvic floor is more complex than damage to the pudendal nerve alone. Although increased pudendal nerve terminal motor latency may indicate that neuropathy is present, in patients with neuropathic fecal incontinence, pudendal nerve terminal motor latency does not correlate with maximum squeeze pressure. Normal pudendal nerve terminal motor latency does not exclude weakness of the peMc floor.
Fecal incontinence is a complex and challenging clinical condition that affects the lifestyle of a
significant number of patients. Although the pathophysiology of fecal incontinence may be multifactorial, the main surgical issue is whether a structural or neurogenic etiology prevails. Disruption of the external anal sphincter musculature is the most common surgically correctable cause of fecal incontinence with an initial postoperative success rate reported as high as 90 percent in some studies. Neuropathy of the pudendal nerve, which is caused mainly by vaginal delivery, has come to be recognized as the other principal cause of incontinence. The pudendal nerve (S2,S3), is tile main supply to the external anal sphincter (EAS) via its inferior rectal
and pudendal branches. Pudendal neuropathy is now thought to be the cause of many cases of incontinence formerly termed "idiopathic". It may coexist with an obvious defect in the EAS, and when this is the case, sphincter repair may be adversely affected. With the advent of transanal ultrasonography (TAUS) it is now possible to identify those incontinent patients who have a sphincter defect without recourse to anal electromyography. This enables improved categorisation of patients with fecal incontinence and improved selection of cases for surgery. It seems reasonable to assume that the majority of incontinent patients without sphincter defects on TAUS have neurogenic fecal incontinence secondary to pudendal neuropathy. Prolonged pudendal nerve terminal motor latency (PNTML) provides objective evidence of nerve injury and has been reported in up to 80 percent of incontinent patients with no sphincter defect identified on electromyography (EMG) mapping. Anorectal manometry correlates significantly with symptoms of incontinence and has been shown to
correlate well with anal sphincter defects visualized by TAUS. 6 Since prolonged PNTML represent~s a pudendal nem'opathy which frequently results in weakness to the EAS it would be expected that the maximum squeeze pressure (MSP) would correlate well with PNTML in incontinent patients with no sphincter defect. This however remains unclear, with differing reports in the literature. Thus, the aim of this study was to determine whether in those incontinent patients who do not have a sphincter defect, prolonged PNTML correlates with anal manometry, in particular MSP. DISCUSSION
In this study we found no direct correlation between MSP and PNTML in the patient group as a whole, in the incontinent patients, or in the incontinent patients without a sphincter defect. However, MSP was found to be significantly lower in incontinent patients with bilateral prolonged PNTML when compared with incontinent patients with normal bilateral PNTMLs.
Studies before the widespread availability of TAUS failed to demonstrate a relationship between prolonged PNTML or electromyographic evidence of pudendal neuropathy and anal sphincter pressures.
Felt-Bersma et al. found no correlation between MSP and electromyographic evidence of EAS denervation. Vernava et at. found that anorectat manometry was not useful in predicting the presence or absence of pudendal neuropathy in incontinent patients in general or in neurogenic incontinent patients in particular.
More recently, some studies have demonstrated a relationship between prolonged PNTML and anal
sphincter pressures. Rieger et al. have reported a significant negative correlation between PNTML and MSP in patients with disordered defecation and in particular with patients without an EAS defect. Roig et al studied 96 incontinent patients with anorectal manometry, electromyography and PNTML
and found that the voluntary component pressure (VCP = MSP - MRP) but not the MSP, was significantly less in incontinent patients with pudendal neuropathy when compared with those without. Furthermore they found a significant negative correlation between VCP and PNTML in all incontinent patients. These apparently contradictory results along with the present study require explanation. 1. It may be that the methodology used is unreliable. The methods of investigation used in this study are well established I and have been shown to be repeatable. Our results are consistent with previous observations, demonstrating lower pressures and increased PNTML in incontinent patients, increased PNTML and decreased pressures with age ~ and a prevalence of pudendal neuropathy at 65 percent of incontinent patients. 2. Case mix differs between studies. Some studies have included only incontinent patients while others have included patients with constipation and incontinence. 7-9 Before the advent of TAUS, patients with sphincter defects who had low pressures and normal PNTML may have been included in the studies, confusing the overall picture. In the study by Rieger et al. percent of patients had EAS defects and a further 20 percent did not have TAUS performed. Furthermore, this group were unable to show an increase in PNTML and a reduction in pressures with age. 3. The pudendal nerve may not be the only nerve to sustain significant trauma during childbirth. The complexity and variability of damage to the nerves and muscles of the pelvic floor may help explain the varying results in the literature. Histologic changes of neuropathy in the EAS imply pudendal nerve damage while neuropathic changes in the IAS imply damage to the autonomic nerves. Abnormal sensation in the anal canal and in the rectum has also been reported. It seems likely that the neurologic damage associated with vaginal delivery is not limited to the pudendal nerve, but may also involve
damage to the inferior hypogastric plexus and the autonomic nerves entering or arising from it. 4. Our inability to demonstrate a direct correlation between the values for MSP and PNTML may be
caused by the characteristics of latency measurements with regard to nerve damage. Prolonged PNTML will only occur when the faster conducting fibers are damaged. 5. PNTML measurement, although clinically useful, is not the most sensitive means of detecting neurologic damage. EAS fiber density as determined by single fiber EMG is a more sensitive parameter in recognizing the degree of dysfunction of the pudendal nerve. |
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