| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
ORIGINAL RESEARCH |
From the Departments of 1Reproductive Medicine, 2Internal Medicine, 3Radiology, and 4Neurology, The Pelvic Floor Function and Disorder Group, University of California, San Diego, San Diego, California.
 |
ABSTRACT |
|---|
TOP
 ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
METHODS: Eleven nulliparous women without symptoms of anal or urinary incontinence were studied before and after pudendal nerve blockade with vaginal manometry, electromyography of the external anal sphincter and puborectalis muscle, and 3-dimensional transperineal ultrasound imaging of the urogenital hiatus during rest and squeeze.
RESULTS: After pudendal nerve blockade, mean vaginal resting pressures decreased from 19 ± 10 mm Hg to 15 ± 10 mm Hg (P < .05), and mean vaginal squeeze pressures decreased from 61 ± 29 mm Hg to 37 ± 24 mm Hg (P < .05). After pudendal nerve blockade, the anterior–posterior length of the urogenital hiatus increased from 51 ± 4 mm to 55 ± 5 mm at rest (P < .05) and increased from 47 ± 3 mm to 52 ± 5 mm during squeeze (P < .05). Resting and squeeze electromyography amplitude of the external anal sphincter and puborectalis muscle was markedly reduced by pudendal nerve blockade.
CONCLUSION: Pudendal nerve blockade decreases vaginal pressures, increases length of urogenital hiatus, and decreases electromyography activity of the puborectalis muscle, all of which suggest that the pudendal nerve does innervate the levator ani muscle.
LEVEL OF EVIDENCE: II-2
There is controversy over the innervation of the levator ani muscles. For many years, investigators stated that the levator ani had dual innervation, pudendal nerve and direct branches from the S3 and S4 motor roots.1,2 Cadaveric dissection studies described branches of the pudendal nerve innervating the levator ani from its caudal surface.3 Frenckner and Euler,4 in 1975, demonstrated the loss of electromyographic activity of the puborectalis muscle after pudendal nerve blockade in men. However, a group of investigators from St. Mark's Hospital performed nerve stimulation and conduction studies that showed different innervation patterns between the puborectalis and the external anal sphincter and concluded that these 2 muscles have different innervations. There is no controversy about the innervation of the external anal sphincter; it comes from the pudendal nerve. Additional anatomic dissection studies described innervation of the levator ani coming only from its visceral surface in the form of direct branches of the S3 and S4 nerve roots.8,9 These studies did not find any branches of the pudendal nerve traveling to the levator ani.
Anal pressures could theoretically come from either the external anal sphincter or the puborectalis muscle; therefore, a decrease in anal pressures after pudendal nerve blockade would not answer whether the levator ani is innervated by the pudendal nerve. The urethra has its own sphincteric muscles, which are also thought to be innervated by the pudendal nerve. However, the vagina does not have any true sphincter itself. Vaginal pressure is thought to be derived entirely from the levator ani and possibly the pubococcygeus and puborectalis muscle. Effects of pudendal nerve block on the vaginal pressure could provide evidence for the innervation of levator ani muscles by the pudendal nerve. We found no literature on the effects of pudendal nerve block on the vaginal pressure and the length of the urogenital hiatus.
The aim of this study was to investigate the possible pudendal nerve innervation of the levator ani muscle by measuring vaginal pressures before and after pudendal nerve blockade. Because the innervation of the external anal sphincter is undoubtedly from the pudendal nerve, we used anal manometry and electromyography of the external anal sphincter as a control. Three-dimensional transperineal ultrasonography allows for imaging of the urogenital hiatus.10 We included direct imaging and measurements of the urogenital hiatus before and after pudendal nerve block to quantify the effect of pudendal nerve blockade on levator ani muscle contraction. Our hypothesis was that pudendal nerve block would decrease external anal sphincter electromyography activity and anal pressures (our control) but would not decrease vaginal pressures or affect urogenital hiatus measurements.
|
MATERIALS AND METHODS |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Electromyography was recorded using concentric needle electrodes (Cephalon A/S, Nørresundby, Denmark) placed transcutaneously in the external anal sphincter and the puborectalis muscles, 1–2 cm from the anal verge. The external anal sphincter needle was placed at a depth of approximately 1.5 cm at the 10 o'clock position, and the needle for the puborectalis muscle was placed about 3.5 cm deep at the 7 o'clock position with respect to the anus. As the puborectalis muscle needle was inserted, electrical quiescence was noted between the external anal sphincter and the puborectalis muscle, which ensured correct placement of the electrode in the puborectalis muscle.13 The electromyogram (EMG) signals were amplified (EMG M-57, J&J Engineering, Poulsbo, WA) and recorded as integrated and enveloped signals. These needles remained in placed throughout the study.
Vaginal manometry was performed with a 6-cm-long, reverse-perfused sleeve sensor.14 Two side-holes, 1 at 2 cm from the distal end of the sleeve sensor and another positioned at its proximal end recorded pressures at the 2 ends of the sleeve sensor (Fig. 1). When the catheter was placed in the vagina, the distal side hole was located in the upper vagina. The sleeve transversed the length of the vagina, crossing the zone of maximal pressure15 and the introitus. The proximal side hole lay outside the vagina. Thus, the distal side hole approximated intra-abdominal pressure, the sleeve sensor measured the highest pressure along its length, and the proximal side hole measured atmospheric pressure.
|
Anal manometry was performed with a 4.5-mm diameter catheter with 4 side-holes placed circumferentially (90 degrees apart) at the same axial level. The catheter was placed in the anal canal and was withdrawn at a constant speed of 8 mm/sec using a motorized puller.16 Three sets of pull-through recordings were performed with the subjects at rest and during maximal squeezes of the pelvic floor.
Transperineal ultrasound imaging of the pelvic floor was performed before and after pudendal nerve blockade in 8 subjects. For these studies, a 3-dimensional ultrasound imaging system was used (Voluson 730, General Electric Medical Systems, Milwaukee, WI). A 5–9 MHz transducer was placed at the perineal body, and imaging was performed at rest and during squeeze.
The pudendal nerve blockade was performed transvaginally with injection of 10 mL of 1% lidocaine bilaterally,17 approximately 8 mm medial to the tip of the ischial spine and to a depth of approximately 1 cm using a standard pudendal nerve block needle without the one-quarter–inch spacer (Pharmaseal Paracervical/Pudendal Block Tray, Allegiance Healthcare Corp., McGaw Park, IL). The effect of the block was assessed with sharp–dull discrimination testing on the perineal area. All the manometric recordings and transperineal ultrasound images were repeated after the bilateral pudendal nerve blockade. Subjects were observed until the EMG activity of the puborectalis muscle and external anal sphincter returned. EMG activity was measured in arbitrary units. All pressures and EMG activities were recorded using Polygram HR (Medtronic, Inc., Minneapolis, MN) and a PC computer.
All pressure measurements were made relative to atmospheric pressure. For resting data, the 3 measurements were averaged for each subject and then averaged across the group. For the squeeze data, the highest pressure from each subject was used to control for variation in the squeeze effort.
The 3-dimensional ultrasound allowed a volume of image data to be captured. These volumes were stored on the hard drive of the ultrasound computer system for off-line data analysis. The ultrasound volumes were reloaded and displayed on a personal computer with the software program, 3D View 2000 (General Electric Medical Systems, Milwaukee, WI), which allows manipulation of the 3-dimensional volume. The 3-dimensional volume was rotated to view the urogenital hiatus in the plane of the pelvic floor muscles. In this plane, the distance between the lower end of the pubic bone and the anorectal angle was measured and defined as the anterior–posterior length of the urogenital hiatus (Fig. 2 and Fig. 3). Two independent investigators (N.G. and J.L.) measured this distance, and the interobserver correlations were determined.
|
|
Data were examined for normality using a statistical software program (Number Cruncher Statistical System and Power Analysis and Sample Size). Data are shown as mean ± standard deviation unless otherwise noted. Student paired t test was used to compare differences in means where the data were normally distributed. The Wilcoxon signed-rank test was used to compare differences in medians for nonnormally distributed data. A P 0.05 was considered significant.
|
RESULTS |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The effectiveness of the pudendal nerve blockade was assessed by sensory and motor testing. The sensory testing was based on the sharp–dull discrimination in the perineal area, and the motor efficacy was based on the reduction in the EMG activity of the external anal sphincter and puborectalis muscles. Based on the sensory examination, 6 subjects were thought to have complete bilateral block. The pudendal nerve blockade reduced the EMG activity of both the external anal sphincter and the puborectalis muscles in all subjects. The mean reduction in the EMG during voluntary squeeze was 73% (41% to 94%) for the external anal sphincter and 55% (14% to 92%) for the puborectalis muscle (Fig. 2).
An example of sleeve sensor recording for a subject before and after pudendal nerve blockade is shown in Figure 3. The summary data for all 11 subjects is shown in Figure 4. Before pudendal nerve blockade there is a significant increase in the pressure recorded by the sleeve sensor, from 19 ± 10 mm Hg at rest to 61 ± 29 mm Hg with squeeze (P < .05). Following pudendal nerve blockade, the rest pressure decreased significantly to 15 ± 10 mm Hg (P < .05) and squeeze pressure decreased to 37 ± 24 mm Hg (P < .05).
|
As our pudendal nerve control, pressure was measured in the anal canal, where peak pressure is thought to be from the external anal sphincter. The pudendal nerve blockade reduced maximum resting pressure in the anal canal from 98 ± 24 to 51 ± 17 mm Hg and squeeze pressure from 144 ± 43 to 70 ± 38 mm Hg (P < .05).
As stated earlier, only 6 of the 11 subjects demonstrated a complete bilateral block as determined by sensory examination (sharp–dull discrimination). We calculated the changes in pressure measurements and compared the results in subjects with complete with those with incomplete blocks. The resting and squeeze vaginal pressures in subjects with complete pudendal nerve blockade were lower (median 8 ± 7 mm Hg for resting and median 25 ± 12 mm Hg for squeeze) as compared with subjects with incomplete pudendal nerve blockade (median 10 ± 6 mm Hg for resting and median 31 ± 26 mm Hg for squeeze). The resting and squeeze anal pressures in subjects with complete pudendal nerve blockade were lower (median 42 ± 11 mm Hg for resting and median 63 ± 18 mm Hg for squeeze) as compared with subjects with incomplete pudendal nerve blockade (median 55 ± 21 mm Hg for resting and median 71 ± 53 mm Hg for squeeze). These comparisons show a trend for greater decrease in pressure with complete block, but the there was no statistically significant difference due to the small number of subjects in each group. Because all of the subjects showed some decrease in EMG activity after pudendal nerve blockade, we felt it was appropriate to include data for all 11 subjects regardless of their sensory results.
Ultrasound images were performed in the last 8 subjects (because of the availability of the equipment). These images were collected at rest and during squeeze. The axial (Fig. 5) and sagittal images (Fig. 6) reveal that the anal canal, vagina, and urethra are layered against each other inside the urogenital hiatus. The anorectal angle can be clearly seen in these sagittal images at the junction between the anal canal and the rectum. Because the anorectal angle is formed by the puborectalis muscle, a line drawn from the lower end of the pubic bone to the apex of the anorectal angle represents the anterior–posterior length of the urogenital hiatus (‘‘A-P hiatus length'’) within the plane of the pelvic floor muscles. This A-P hiatus length was measured at rest and during squeeze, before and after the pudendal nerve blockade (Fig. 7). Before pudendal nerve blockade, the mean A-P hiatus length decreased from 51 ± 4 mm at rest to 47 ± 3 mm with squeeze (P < .05). After pudendal nerve blockade, the mean A-P hiatus length at rest was 55 ± 5 mm and it shortened to 52 ± 5 mm with squeeze (P < .05). For both the resting and squeeze states, the mean A-P hiatus length is significantly longer after pudendal nerve blockade (P < .05). There is no difference between the mean A-P lengths at rest before the pudendal nerve blockade as compared with the mean A-P hiatus length during squeeze after the pudendal nerve blockade. There is a strong correlation between the puborectalis muscle length measurements made by the 2 investigators (Spearman correlation coefficient of 0.79, P < .001).
|
|
|
|
DISCUSSION |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The most important finding of our study is that pudendal nerve blockade significantly reduced vaginal pressures, increased resting length of the urogenital hiatus, and reduced shortening of the urogenital hiatus during contraction. Our hypothesis that pudendal nerve does not innervate pelvic floor muscles was not proven. We expected that if the levator ani were innervated by direct sacral branches and not the pudendal nerve, pudendal nerve blockade would have no effect on vaginal pressures or urogenital hiatus measurements. The implication of our study is that pudendal nerve injection affects both the levator ani and the external anal sphincter. Therefore, our data provide strong evidence that the pudendal nerve innervates the levator ani muscle.
In the past few decades, studies have produced conflicting data on whether the pudendal nerve innervates the levator ani muscles. Our results are consistent with Frenckner and Euler,4 who measured anal pressures and puborectalis EMG activity before and after pudendal nerve blockade and concluded that the pudendal nerve innervated the puborectalis muscle. His results could be criticized because most of the subjects were men, and the pudendal block was administered with a perineal technique and with large volumes (40–75 mL) of local anesthetic that possibly could have directly anesthetized the puborectalis muscle or sacral nerves. With a transvaginal approach and injection of smaller volumes (10 mL each side), our pudendal block technique is more likely to block the pudendal nerve only. We are quite confident that our technique did anesthetize the pudendal nerve, because the small volumes of anesthetic were injected transvaginally, far from the external anal sphincter, yet we noticed significant reduction in both anal pressure and external anal sphincter EMG.
Dissection studies have produced conflicting results. Shafik et al3 described branches of the pudendal nerve that innervated the levator ani from its caudal surface. Other investigators have described innervation of the levator ani coming only from its visceral surface, in the form of direct branches from the S3 and S4 nerve roots.8,9 In the pelvic floor, the most cephalad (visceral) structures are the pubococcygeus and iliococcygeus muscles. The puborectalis muscle is caudal to the pubococcygeus and is usually not visualized from the abdominal or the visceral surface of the pelvic floor. A possible explanation for these discrepant dissection studies is that the pubococcygeus and iliococcygeus are innervated by direct branches of S3 and S4 nerve roots, but the puborectalis is innervated by the pudendal nerve and it is the puborectalis muscle that contributes significantly to vaginal pressures and urogenital hiatus length. We have further studies planned to study the role of the puborectalis muscle in proximal anal pressures and pelvic floor function. Our results are not consistent with studies from the St. Mark's Hospital group, who performed nerve stimulation and conduction studies that showed different innervation patterns between the puborectalis and external anal sphincter. These studies did not find any branches of the pudendal nerve traveling to the levator ani.
The levator ani muscles are thought to play a crucial role in preserving urinary continence, anal continence, and pelvic organ support. Snooks et al18 and Smith et al19,20 have demonstrated the association between pudendal nerve injury during childbirth and pelvic floor dysfunction. Our study suggests that the pudendal nerve does innervate pelvic floor (levator ani) muscle and therefore damage to the pudendal nerve could lead to pelvic floor (levator ani) dysfunction.
There are 2 possible limitations to our study. It is possible that a conventionally performed transvaginal ‘‘pudendal nerve block'’ affects more than the pudendal nerve. Theoretically this block could affect the direct branches of sacral nerve roots S3 and S4 that are thought to innervate the visceral surface of the levator ani. Our injection was placed approximately 8 mm medial to the ischial spine. Anatomic and ultrasound studies have suggested that this location is unique to the pudendal nerve. The sacral nerve roots innervating the visceral surface of the levator ani branch off several centimeters before the pudendal nerve travels under the coccygeus muscle (sacrospinous ligament) near the ischial spine. We intentionally injected a relatively small volume (10 mL on each side) of anesthetic agent to minimize risk of spread to the sacral nerves and therefore think that it is unlikely that the more proximal sacral nerve roots were blocked by our technique.
The second possible limitation is that we cannot separate the possible effect of muscle fatigue from the effect of pudendal nerve block because the pudendal nerve block pressure measurements were always performed second. However, each subject had a resting period of at least 15 minutes after the pudendal block was placed while we waited for the block to take effect. Our clinical impression was that these patients were not fatigued; they were just not able to contract their pelvic floor as well after the pudendal nerve blockade. The EMG findings were quite dramatic in almost all cases.
In summary, pudendal nerve blockade decreases resting and squeeze pressures in the vagina, increases the length of the urogenital hiatus, and decreases EMG activity of the puborectalis muscle. Our findings provide evidence that the pudendal nerve does innervate the pelvic floor muscles (levator ani). The clinical significance of these findings is that the damage to the pudendal nerve, either due to delivery or other reasons, is likely to affect the pelvic floor function. The latter is thought to be important for the urinary and fecal continence mechanism, and vaginal prolapse.
|
Footnotes |
|---|
Corresponding author: R. K. Mittal, MD, Professor of Medicine, University of California San Diego, 3350 La Jolla Village Drive, La Jolla CA 92161; e-mail: rmittal{at}ucsd.ed.
doi:10.1097/01.AOG.0000175165.46481.a8
|
REFERENCES |
|---|
|
TOP
ABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
2. Wester C, Brubaker L. Normal pelvic floor physiology. Obstet Gynecol Clin North Am 1998;25(4):707–22.[Medline]
3. Shafik A, el-Sherif M, Youssef A, Olfat ES. Surgical anatomy of the pudendal nerve and its clinical implications. Clin Anat 1995;8:110–5.[Medline]
4. Frenckner B, Euler CV. Influence of pudendal block on the function of the anal sphincters. Gut 1975;16:482–9.
5. Percy JP, Neill ME, Swash M, Parks AG. Electrophysiological study of motor nerve supply of pelvic floor. Lancet 1981;1:16–7.[Medline]
6. Snooks SJ. Damage to the innervation of the pelvic floor musculature in chronic constipation. Gastroenterology 1985;89:997–81.
7. Snooks SJ, Swash M. The innervation of the muscles of continence. Ann R Coll Surg Engl 1986;68:45–9.[Medline]
8. Juenemann KP, Lue TF, Schmidt RA, Tanagho EA. Clinical significance of sacral and pudendal nerve anatomy. J Urol 1988;139:74–80.[Medline]
9. Barber MD, Bremer RE, Thor KB, Dolber PC, Kuehl TJ, Coates KW. Innervation of the female levator ani muscles. Am J Obstet Gynecol 2002;187:64–71.[Medline]
10. Dietz HP, Steensma AB, Hastings R. Three-dimensional ultrasound imaging of the pelvic floor: the effect of parturition on paravaginal support structures. Ultrasound Obstet Gynecol 2003;21:589–95.[Medline]
11. Uebersax JS, Wyman JF, Shumaker SA, McClish D, Fantl JA. Short forms to assess life quality and symptom distress for urinary incontinence in women: the Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Continence Program for Women Research Group. Neurourol Urodyn 1995;14:131–9.[Medline]
12. Vaizey CJ, Carapeti E, Cahill JA, Kamm MA. Prospective comparison of faecal incontinence grading systems. Gut 1999;44:77–80.
13. Bartolo DC, Jarratt JA, Read MG, Donnelly TC, Read NW. The role of partial denervation of the puborectalis in idiopathic faecal incontinence. Br J Surg 1983;70:664–7.[Medline]
14. Sivri B, Mittal RK. Reverse-perfused sleeve: an improved device for measurement of sphincteric function of the crural diaphragm. Gastroenterology 1991;101:962–9.[Medline]
15. Guaderrama NM, Nager CW, Liu J, Pretorius DH, Mittal RK. The vaginal pressure profile. Neurourol Urodyn 2005;24:243-7.[Medline]
16. McHugh SM, Diamant NE. Anal canal pressure profile: a reappraisal as determined by rapid pullthrough technique. Gut 1987;28:1234–41.
17. Cunningham FG, MacDonald PC, Gant NF, Leveno KJ, Gilstrap LC, editors. Williams obstetrics. 20th ed. Stamford (CT): Appelton & Lange; 1997.
18. Snooks SJ, Swash M, Henry MM, Setchell M. Risk factors in childbirth causing damage to the pelvic floor innervation. Int J Colorectal Dis 1986;1:20–4.[Medline]
19. Smith AR, Hosker GL, Warrell DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96:29–32.[Medline]
20. Smith AR, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: a neurophysiological study. Br J Obstet Gynaecol 1989;96:24–8.[Medline]
This article has been cited by other articles:
|
|
 |
|
  J. A. Kruger, S. W. Heap, B. A. Murphy, and H. P. Dietz Pelvic Floor Function in Nulliparous Women Using Three-Dimensional Ultrasound and Magnetic Resonance Imaging Obstet. Gynecol., March 1, 2008; 111(3): 631 - 638. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. S. Damaser, M. K. Samplaski, M. Parikh, D. L. Lin, S. Rao, and J. M. Kerns Time course of neuroanatomical and functional recovery after bilateral pudendal nerve injury in female rats Am J Physiol Renal Physiol, November 1, 2007; 293(5): F1614 - F1621. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. S. Padda, S.-A. Jung, D. Pretorius, C. W. Nager, D. Den-Boer, and R. K. Mittal Effects of pelvic floor muscle contraction on anal canal pressure Am J Physiol Gastrointest Liver Physiol, February 1, 2007; 292(2): G565 - G571. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Wallner, C. P. Maas, N. F. Dabhoiwala, W. H. Lamers, and M. C. DeRuiter Innervation of the Pelvic Floor Muscles: A Reappraisal for the Levator Ani Nerve. Obstet. Gynecol., September 1, 2006; 108(3): 529 - 534. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
