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| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 23 | Sacral Nerve Stimulation for Treatment of Fecal Incontinence [2001년 5월 DCR] | 2011-11-17 | 3519 |
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A Novel Approach for Intractable Fecal Incontinence
Ezio Ganio, M.D., AltSerto Realis Luc, M.D., Giuseppe Clerico, M.D.,Mario Trompetto, M.D.
From the Colorectal Epordienisis Cente15 tvrea, Italy
PURPOSE: Many patients with fecal incontinence demonstrate a functional deficit of the internal anal sphincter or the external sphincter muscles without any apparent structural defects. Few patients are amenable to repair or substitution of the sphincter. However, sacral nerve stimulation appears to offer a valid treatment option for fecal incontinence. The objectives of this study were: to evaluate the efficacy of temporary stimulation of the sacral nerve roots (percutaneous nerve evaluation) in patients with functional fecal incontinence; to determine the mechanisms of possible improvement; and to evaluate if temporary stimulation could be reproduced and maintained by implanting a permanent neurostimulation system.
METHODS: Twenty-three patients with fecal incontinence, 18 females and 5 males, median age of 54.9 years (range 28-71), underwent a percutaneous nerve evaluation test. Eleven patients (47.8 percent)
also had urinary disorders: urge incontinence (4), stress incontinence (3), and retention (4). Associated disorders included perineal and rectal pain (1), spastic paraparesis (1), and syringomyelia (1). All patients underwent a preliminary evaluation using stationary anal manovohimetry, pudendal nerve terminal motor latency measurements, and anal ultrasound. A percutaneous electrode for the stimulation of the sacral nerve roots was positioned at the level of the third sacral foramen (S3) in 20 patients and S2 in 2 patients (1 patient missing). Stimulation parameters used were: pulse width 210/xsec, frequency 25 Hz, and average amplitude of 2.8 V (range 1-6). The electrode was left in place for a minimum of 7 days. Five patients were successively implanted with a permanent sacral electrode with a stimulation frequency of 16 to 18 Hz and amplitude of 1.1-4.9 V. RESULTS: Seventeen of the 19 patients (89.4 percent) who completed the minimum percutaneous nerve evaluation period of 7 days (median 10.7 (range 7-30)), had a reduction of liquid or solid stool incontinence by more than 50 percent, and fourteen (73.6 percent) were completely continent for stool. The most important changes revealed by manovohimetl T were an increase in resting pressure (P
< 0.001) and voluntary contraction (P = 0.041), reduction of initial pressure for first sensation (P = 0.049) and urge to defecate (P = 0.002), and a reduction of the rectal volume for urge sensation (P = 0.006). The percutaneous nerve evaluation results were reproduced at a median follow-up of 19.2 months (range 5 to 37) in the 5 patients who received a permanent implant. CONCLUSIONS: Temporary stimulation of the sacral roots (percutaneous nerve evaluation) can be of help in those patients with fecal incontinence, and the results are reproduced with permanent implantation. The positive effect on continence seems to be derived from not only the direct efferent stimulation on the pelvic floor arid the striated sphincter muscle, but also from modulating afferent stimulation of the autonomous neural system, inhibition of the rectal detrusor, activation of the internal anal sphincter, and modulation of sacral reflexes that regulate rectal sensitivity and motility.
Fecal continence is the result of coordinated activity of the rectum and the anal sphincters. Adequate
rectal compliance and sensitivity are important, as is the volunta W and reflex activity of the anal sphincters. Both the smooth muscle sphincter (internal anal sphincter) and the striated sphincters (external sphincter and puborectalis muscle sling) contribute to continence. The smooth muscle sphincter maintains a pressure gradient between the rectum and the anal canal at rest, and the external sphincter and the puborectalis present basal activity at rest that contributes to the anorectal gradient and assures voluntary contraction to postpone defecation. Until recently, treatment of fecal incontinence has focused on the sphincters. Muscular lesions of the striated sphincters can be repaired surgically or corrected with the use of autologous or artificial
materials. Dynamic graciloplasty is now a standard procedure, although it remains complex and requires experience to obtain good results. The artificial anal sphincter constitutes another option but it is an invasive procedure which requires the implant of foreign material. Many patients present functional defects of the internal anal sphincter or of the striated muscle with no identifiable structural defects, which represent a therapeutic dilemma. Attempts at surgical correction (posterior and/or anterior anoplasty) have led to an improvement of continence in no more than 50 to 60 percent of cases; the results are often transient because of mechanical correction of a dynamic problem. In these patients it may be possible to improve continence by modifying the neural control of the sphincter and the proximal bowel rather than attempting to substitute the sphincter mechanism. Electrical control of urinary dysfunction began in the 1950s. Initial attempts to provoke artificial micturition
involved direct stimulation of the spinal cord, the detrusor muscle, and the striated sphincter. None of these methods produced satisfactory bladder voiding. Research was then focused on electrical stimulation of the sacral nerve roots to treat serious bladder voiding dysfunctions. Tanagho and Schmidt of the University of California in San Francisco applied the principles of sacral nerve stimulation to patients affected by voiding dysfunction or incontinence because of bladder instability. In 1981, they performed the first sacral nerve stimulation implant. Currently, stimulation of the sacral nerve roots is used successfully to control voiding difficulties and urinary incontinence. The aims of this study were to evaluate whether temporary stimulation of the sacral nerve roots modifies the symptoms of functional fecal incontinence, determine the mechanisms of possible improvement, and evaluate if temporary stimulation could be reproduced and maintained when implanting a permanent sacral nerve stimulation system. DISCUSSION
The goal of sacral roots stimulation is to reduce fecal incontinence. According to Matzel et al.,stimulation of the efferent motor nerves to the anal sphincters increases the pressure in the anal canal by contraction of the pelvic floor and the anal sphincter muscles. This could be aided by a conversion of fast twitch fibers into slow twitch fibers in the striated sphincter as suggested by Tanago and Matzel et al. and the pelvic floor muscle, increasing the closing capacity. At a follow-up of six months, using a stimulation frequency of 15 Hz, Matzel reported a complete recovery of continence in two cases and soiling in one patient with definitive implant of a sacral electrode. Vaizey et al. reported total continence during PNE in seven of nine patients using a stimulation frequency of 15 Hz. Matouf et al. reported an improvement on the Wexner incontinence scale from 16 to 20 to 3 to 6 in four patients with definitive implant of a sacral electrode with a stimulation frequency of 15 Hz and a follow-up of 12.5 to 25 months. In our experience, electrical stimulation of sacral roots 2 and 3 was associated with an improvement in fecal continence.
We found a significant increase in resting pressure (P < 0.001) and a slight increase on the squeeze
pressure. This may result from the extrinsic innervation of the internal anal sphincter via the sacral parasympathetic supply, and to a direct effect on the striated anal sphincter. In relation to type of incontinence, only the patients with urge incontinence showed benefit from sacral
neurostimulation and again patients with complete nervous lesions don't show advantages from sacral neurostimulation. Sacral nerve stimulation seems to have an effect on rectal sensitivity and motility, which could be of clinical importance. The interaction between the autonomic and somatic nervous system is an integral part of the nerve control of the mechanisms of continence and evacuation. Functional incontinence may be associated with reduced resting tone or reduced squeeze tone, reduced rectal sensitivity and compliance. Swash evidenced damage to the pudendal nerves as the cause of incontinence but some areas still need to be clarified The cause of internal sphincter failure- damage to the efferent somatic fibers does not explain the basal hypotony, so there is either contemporary damage to the nerve fibers of the internal sphincter or there is damage to the afferent fibers necessary for control of the basal tone of the internal sphincter. With regard to the role of the rectal muscle and sensitivity, with innervation linked to the pelvic and sympathetic nerves, a reduction in compliance can be linked to a reflex or lack of reflex of somatic afferents, rather than only the mechanical effect of an absence of distention because of the
reduction in anal pressure. Recent personal observations have demonstrated that patients with rhizotomy of the posterior sacral
roots do not recover sphincteric tone during rectoanal inhibitory reflex and stimulation of the anterior roots causes a contraction of the ampulla recti. In a feline model, Schuttz-Lampel et al. demonstrated an effect on bladder detrusor that was dependent on the frequency and intensity of stimulation, with excitation at low frequencies (2-5 Hz) and low voltage (0.8-1.4 times the threshold for the contraction of the striated muscles), and relaxation at high frequencies (7-10 Hz) and high voltage (1.4-2 times the threshold for the contraction of the striated muscles). During rectoanal manovolumetry in humans, the rectal volume decreases with high frequency acute sacral roots stimulation or stays the same at low frequency, and increases during the subchronic phase of low intensity stimulation (unpublished observations). The level of stimulation needed to activate the afferent fibers is 1.5 times that necessary to activate the somatic motoneurons. The efferent autonomic B fibers need 3 to 5 times the stimulation required by the motoneurons, while the C fibers, responsible for pain, show an even higher threshold. The increase in rectal volume observed in the subchronic phase can be attributed to the inhibitory action linked to the stimulation of afferent A/3-y sensory fibers in the sacral nerves rather than an efferent stimulation of the B fibers. The mechanism of continence may involve not only the efferent motor fibers, but also the afferent sensory fibers. These fibers are capable of inhibiting the contraction of the detmsor through the medullary or pontine centers, with a positive effect on rectal compliance and motility, in addition to modulating positive feedback on the striated fibers and probably on the internal sphincter. The effect demonstrated on the behavior of the ampulla is similar to the afferent inhibitory influence of the efferent parasympathetic nerves on the bladder detmsor, demonstrated by Tanagho and Schmidt. Improvement of rectal sensation with a reduction of the rectal distention pressure for the feeling threshold
(P = 0.049) and urgency (P = 0.002) as well as the rectal volume needed for urge sensation (P = 0.006) is of particular interest because this allows the individual to take measures to avoid an incontinent episode. Also, Vaizey et al. discovered an effect on rectal sensation during PNE. Although there is no explanation for this observation, it may be secondary to a change in the sacral reflexes mediated by the afferent stimulation. Sacral nerve stimulation is interesting because it is the most peripheral location for bilateral control of
the nervous system support of the striated muscles. Even though the mechanism of action is not known, electrical stimulation of the sacral roots could restore continence through 1. A direct voluntary contraction of the sphincter;
2. An inhibition, mediated by the sympathetic and parasympathetic fibers through the pontine center or through a sacral interneuron arch, of contractions of the rectal muscle 3. An activation of the internal sphincter, mediated by sympathetic and parasympathetic fibers with a stabilization of the sphincteric pressure; or 4. An activation of the afferents in the local reflex arcs to maintain the tone of the striated sphincter. These results on sacral nerve stimulation for fecal incontinence are similar to those obtained with sacral
nerve stimulation for urinary dysfunctions. Unfortunately, it is difficult to directly compare the results of sacral nerve stimulation for bladder and rectal disorders. The qualitative difference in content and, above all, the frequency, modality, and variability of defecation require longer observation periods. The median duration of observation in this study, 10.7 days, was more than the 5-day duration used by urologists to assess the effects of stimulation on the bladder. The present classifications of fecal incontinence aim to quantify the importance of the problem but do
not provide any information on the pathogenic mechanisms, with the exception of the presence of anatomic sphincteric lesions. A distinction between passive (stress) incontinence and urge incontinence could indicate that rectal motility to play a more important role in the mechanism of fecal incontinence. |
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