시원항병원
051) 331-7275논문발표
| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 45 | Effects of Magnetic Sacral Root Stimulation on Anorectal Pressure and Volume [2001년 12월 DCR] | 2011-11-17 | 3478 |
|
G. L. Morren, M.D., S. Walter, M.D., O. Hallbook, M.D., Ph.D.,R. Sjodahl, M.D., Ph.D., F.R.C.S
From the Departments of Colorectal Surgery and Gastroenterology, University Hospital, Linkdping, Sweden
PURPOSE: Electrical sacral root stimulation induces defecation in spinal cord injury patients and is currently under examination as a new therapy for fecal incontinence. In contrast to electrical stimulation, magnetic stimulation is noninvasive. To gain more insight into the mechanism of action of sacral root stimulation, we studied the effects of magnetic sacral root stimulation on anorectal pressure and volume in both fecal incontinence and spinal cord injury patients.
METHODS: Three groups were examined: 14 healthy volunteers, 18 fecal incontinence patients, and 14
spinal cord injury patients. Repetitive magnetic sacral root stimulation was performed bilaterally using bursts of five seconds at 5 Hz. Anal and rectal pressure changes and rectal volume changes were measured. RESULTS: An increase in anal pressure was seen in 100 percent of the control subjects, in 86 percent of the spinal cord injury patients, and in 73 percent of the fecal incontinence patients (P = 0.03). The overall median pressure rise after right-sided and leftsided stimulation was 12 (interquartile range, 8-18.5) and 13 (interquartile range, 6-18) mmHg at the mid anal level. A decrease in rectal volume was provoked in 72 percent of the control subjects, in 79 percent of the spinal cord injury patients, and in 50 percent of the fecal incontinence patients. Overall median volume changes after right-sided and left-sided stimulation were 10 (range, 5-22) and 9 (range, 5-21) percent from baseline volume. An increase in rectal pressure could be measured in 56 percent of the control subjects, 77 percent of the fecal incontinence patients, and 43 percent of the spinal cord injury patients. Median pressure rises after right-sided and left-sided stimulation were 5 (range, 3-12) and 5 (range, 3-5) mmHg.
CONCLUSIONS: Magnetic sacral root stimulation produces an increase in anal and rectal pressure and a decrease in rectal volume in healthy subjects and patients with fecal incontinence or a spinal cord injury.
The effects of electrical sacral root stimulation (SRS) on bladder function are well known. Electrical SRS produces b l a d d e r evacuation in patients with a supraconal spinal injury and modulates bladder function in various forms of voiding isorders in patients with an intact spinal cord.
Not only the bladder, urethral sphincters, and pevic floor, but also the distal colon, rectum, and anal sphincters are innervated via the same sacral roots. Therefore, electrical SRS also has an effect on
distal bowel function. Sacral anterior root stimulators can be programmed to achieve complete unassisted defecation in patients with spinal cord injuries (SCI), and short-term sacral nerve neuromodulation decreases episodes of fecal incontinence (FI) in patients with an intact spinal cord. Electrical SRS requires percutaneous or open positioning of one or more electrodes at the sacral
foramina or on the anterior sacral roots. However, the sacral roots can also be stimulated using a magnetic stimulator. Magnetic stimulation applies Faraday's law, which states that a changing magnetic field induces an electrical field. This field creates a current flow in conductive tissue sufficient to produce a membrane d e p o l a r i z a t i o n in nerves. The magnetic field passes without significant attenuation through highly resistant tissues such as skin, fat, and bone. Magnetic stimulation is a noninvasive technique. The cerebral cortex, the spinal cord, and the d e e p - l y i n g p e r i p h e r a l nerves can be stimulated with only minor discomfort for the subject. Magnetic stimulation of the sacral roots has primarily been u s e d to test nerve integrity in neurophysiologic studies. The development of more powerful magnetic stimulators made it possible to study the effects of magnetic SRS on bladder function. To our knowledge, only one group has investigated its effects on the human rectum. The aim of this study was to examine the effect of magnetic SRS on the anal sphincter and rectum by measuring anal and rectal p r e s s u r e changes and rectal volume changes during stimulation. DISCUSSION
This study has shown that magnetic SRS produces an increase in anal and rectal pressure and a decrease in rectal volume in a high percentage of subjects. The sacral roots contain fast conducting myelinated fibers to the striated pelvic sphincters and pelvic floor muscles. These large diameter fibers are most sensitive to magnetic stimulation. Their excitation will provoke external anal sphincter and pelvic floor contractions and therefore a rise in anal pressure at different levels. In more than a quarter of the F1 patients, we could not provoke a rise in anal pressure. There were no failures in the control group, indicating that the stimulation technique itself is not the limiting factor. Neuropathy of the pudendal nerves or anal sphincter damage may cause failure. In the limited number of FI patients, no relation between failure and the presence of pudendal neuropathy or a sphincter defects could be found.
A valid assessment of pressure changes between groups is difficult. In analogy with standard manometry studies, the range of anal pressure changes was very large in all groups. A statistical difference between groups was not found. There were also many more women in the FI group than in the control group, making comparison less valid.
Opposite to our findings, Shafik and El-Sibai observed a fall instead of a rise of pressure at the proximal anal canal during stimulation. They used a higher frequency of stimulation (40 Hz). The influence of stimulation frequency on anal sphincter response needs further study.
Rectal volume changes could be measured in 65 percent of all subjects. Measuring volume changes
with a barostat system is only an indirect way of measuring rectal contractility and tone. Pelvic floor contractions may also cause a decrease of rectal volume. We consider the measured volume changes to be caused by rectal contractions and not by pelvic floor contractions. This is because the rectal bag was positioned proximal to the pelvic floor and because in 9 of 16 subjects without rectal response, pressures at the level of the puborectal muscle ranged from 25 to 183 mmHg during stimulation. Two SCI patients evacuated the inflated bag and one patient had a bowel movement immediately after the onset of magnetic stimulation. It is well known that stimulation of the rectal wail itself may provoke a reflex contraction. But in all of our SCI patients, the insertion or inflation of the rectal bag only induced minor rectal volume changes. Magnetic SRS itself probably produced a massive rectal contraction in these three patients. Shafik and El-Sibai induced rectal balloon evacuation in control subjects. This could not be reproduced in our study. The mechanism of action of magnetic SRS on rectal contractility is unknown. It seems unlikely that magnetic SRS directly activates the parasympathetic motor nerves to the distal bowel because these small unmyelinated fibers are relatively insensitive to magnetic stimulation. Magnetic SRS may have both an inhibitory and an excitatory effect on the bladder. Experimental work showed that sacral nerve stimulation induced excitatory and inhibitory effects on the bladder depending on the frequency and intensity of stimulation. These effects were identified as reflex responses because they were abolished after transection of the dorsal roots. Based on these findings, we postulate that magnetic SRS stimulates the large sensory nerves from the pelvic floor, which produces rectal contractions through a somatovisceral reflex at the level of the lumbosacral spine.
In only half of the patients, rectal pressure changes could be measured during stimulation. Rectal contractions do not necessarily cause a rise of rectal pressure because the rectum is a tube with a proximal open end. Rectal pressures were mainly recorded to control the position of the bag by monitoring the respiratory abdominal pressure changes and to identify artifacts caused by coughing or movement as a sudden rise of pressure outside the stimulation period.
Our experimental setup had some technical limitations. The considerable slowness of the barostat system, caused by the small-caliber tubing, probably decreased the amplitude of the volume changes. Repetitive stimulation heated the coil rapidly. Therefore we limited the stimulation periods to five seconds. The slow response of the rectal smooth muscle to electrical stimulation as observed by MacDonagh et al. 3 might have required a longer stimulation period in some subjects. The maximal magnetic field sn'ength was reduced significantly when using stimulation frequencies above 5 Hz. Therefore we did not apply higher frequencies. Failure to produce volume changes was related to a body mass index above 30, indicating that in this group of subjects a higher stimulation output may be needed. The recent development of very powerful magnetic stimulators with a cooling system and more sensitive barostat devices may overcome the technical limitations encountered in this study.
|
|||