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ORIGINAL RESEARCH |
From the Departments of 1Anatomy & Embryology and 2Urology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and the Departments of 3Anatomy & Embryology and 4Gynaecology, Leiden University Medical Center, Leiden University, Leiden, The Netherlands.
| ABSTRACT |
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METHODS: Ten female pelves were dissected and a pudendal nerve blockade was simulated. The course of the levator ani nerve and pudendal nerve was described quantitatively. The anatomical data were verified using (immuno-)histochemically stained sections of human fetal pelves.
RESULTS: The levator ani nerve approaches the pelvic-floor muscles on their visceral side. Near the ischial spine, the levator ani nerve and the pudendal nerve lie above and below the levator ani muscle, respectively, at a distance of approximately 6 mm from each other. The median distance between the levator ani nerve and the point of entry of the pudendal blockade needle into the levator ani muscle was only 5 mm.
CONCLUSION: The levator ani nerve and the pudendal nerve are so close at the level of the ischial spine that a transvaginal "pudendal nerve blockade" would, in all probability, block both nerves simultaneously. The clinical anatomy of the levator ani nerve is such that it is prone to damage during complicated vaginal childbirth and surgical interventions.
LEVEL OF EVIDENCE: II-3
| MATERIALS AND METHODS |
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To further help characterize the anatomical relationship of the LAN and the pudendal nerve, we also studied (immuno-)histochemically stained sections of human fetal pelves. The fetuses were obtained after legal abortion, and the study was approved by the medical-ethical committee of the Leiden University Medical Center. Two female fetal pelves (female, 14 and 19 weeks of gestation) were stained for the presence of striated muscle tissue, using a monoclonal antibody directed against myosin heavy chain (clone A4.1025; Upstate Cell Signaling Solutions, Charlottesville, VA), and for the presence of nerve tissue, using a polyclonal antibody directed against neurofilament 68 kD (AB1983; Chemicon International, Temecula, CA), as well as with hematoxylin-azophloxin. To verify the data obtained from these two fetuses, we also undertook investigations on existing fetal pelvic sections from the collections of the departments of Anatomy & Embryology, Leiden University Medical Center, and from the Academic Medical Center, Amsterdam. These fetuses (11 females and 7 males, ranging from 65 mm crown-rump length [CRL, 10 weeks of gestation] to 260 mm CRL [27 weeks of gestation]) were stained with hematoxylin and either azophloxin or eosin. Male fetuses were used to show that the levator ani nerve is present in both sexes. Three-dimensional reconstructions were prepared using Amira 3.0 (TGS Template Graphics Software, San Diego, CA; available at: http://www.tgs.com).
| RESULTS |
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The pudendal nerve, by contrast, coursed behind the sacrospinous ligament and the overlying coccygeal muscle before passing around the ischial spine. In the area of the ischial spine, the distance between the pudendal nerve and levator ani nerve (positioned inferior and superior to the levator ani muscle, respectively) was 6 mm (95% CI 411 mm). The tip of the needle, inserted during the mock pudendal nerve blockade maneuver, effectively reached the pudendal nerve in all specimens. The distance between the levator ani nerve and the passage of the needle through the levator ani muscle was 5 mm (95% CI 18 mm). In the fetuses the close topographic relationship of the levator ani nerve and the pudendal nerve as found in the adult specimens could be confirmed and elegantly demonstrated by using nerve and striated musclespecific immunohistochemistry (Fig. 3).
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The levator ani nerve, originating from the third and/ or fourth sacral foramen and innervating the levator ani muscle on its visceral side, was demonstrable in female as well as male fetal pelves (Fig. 4A). Figure 4B shows the course of the nerves in a female fetal pelvis in a three-dimensional reconstruction.
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| DISCUSSION |
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In contrast, our anatomical data reveal that the topographical relation of the levator ani nerve to the pudendal nerve is so close at the point of injection that even the small amount of lidocaine that is used reaches both nerves. Moreover, literature data show the distribution area of anesthetics administered through pudendal nerve blockade to be large. A study in which spread of anesthetics during transvaginal pudendal nerve blockade was visualized with X-rays showed that anesthetics spread widely. The X-rays showed diffusion retrogradely up to the sacral roots of origin of the pudendal nerve.6
A limitation of our analysis could be that we studied cadavers as opposed to live subjects. One might argue that the age of our cadavers may have influenced the thickness of the pelvic floor muscles, because the pelvic floor in the elderly is frequently less functional, and that our assessment of the distance between the levator ani nerve and the pudendal nerve in cadavers is therefore an underestimate. Because the pelvic floor, both in the fetus and the adult, consists of one layer of muscle bundles only, we think that the possible differences in thickness in the pelvic floor are marginal. Also, although embalming of cadavers can cause distortion of anatomical relations, this distortion is probably minimal in the area of the ischial spine and the sacrospinous ligament because these are firm structures that resist the pressures created in embalming.
A second argument against our hypothesis could be that the levator ani muscle functions as an effective diaphragm and divides the space above and below the pelvic floor into separate compartments, which inhibits diffusion of lidocaine to the levator ani nerve. Only a study in which the diffusion pattern of the anesthetic is assessed could clarify whether the levator ani muscle does indeed prevent spreading of the anesthetic to the levator ani nerve.
Our findings confirm and extend earlier findings. Several studies argue that direct sacral branches are responsible for innervation of the levator ani muscle on its visceral side and that the pudendal nerve innervates the external anal sphincter only.3,7,8 This pattern is also seen in other primates and in rats.12 Furthermore, neurectomy of the levator ani nerve or the pudendal nerve in rats12 and squirrel monkeys9 shows that only denervation of the levator ani nerve affects the levator ani muscle, whereas denervation of the pudendal nerve affects the external anal sphincter. Neurostimulation of the levator ani nerve or the pudendal nerve in humans also shows muscle-specific effects on the levator ani and the external anal sphincter, respectively.7,13 Together, these studies convincingly demonstrate that the levator ani muscle and the external anal sphincter are innervated by different nerves.
The clinical implications of the innervation of the pelvic floor are evident: denervation of the pelvic floor muscles and the accompanying muscle dysfunction could cause urinary and/or anal incontinence, and pelvic organ prolapse. The concept of neural damage due to stretching and pressure during complicated vaginal childbirth or pelvic surgical procedures is more easily conceivable with the nerve to the levator ani muscle being located on the superior, visceral side of the pelvic floor. In contrast, the pudendal nerve is better protected in these situations because it lies on the inferior side of the pelvic floor, within Alcocks canal. The same considerations apply to transvaginal sacrospinous ligament fixation for vault prolapse. One or more permanent stitches are put through the ligament by placing them 1 cm medial to the ischial spine.14 As can be concluded from our morphological findings, this procedure holds a risk of levator ani nerve entrapment or disruption, either immediately or as a delayed response to surgery. Documentation of recurrence rates of vaginal vault prolapse after sacrospinous ligament fixation is poor due to lack of follow-up studies with standardized parameters14,15 but is repeatedly mentioned in the literature as a clinical problem associated with this surgical procedure.3,14,15 Pelvic floor muscle denervation due to disruption of the levator ani nerve could explain these recurrent prolapses.
Given the clinical impact of a denervation of the levator ani muscles, all obstetricians, gynecologists, and pelvic surgeons should be aware of the levator ani nerve and its clinical anatomy. Although we fully realize that the functional assessment of the levator ani nerve is not trivial, our data clearly show that a pudendal blockade with an anesthetic is not the proper approach because it fails to distinguish between the pudendal and the levator ani nerves.
| Footnotes |
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Corresponding author: M. C. DeRuiter, PhD, Department of Anatomy & Embryology, Leiden University Medical Center, Building 2, S-1-P, P.O. BOX 9600, 2300 RC Leiden, The Netherlands; e-mail: M.C.DeRuiter{at}lumc.nl.
doi:10.1097/01.AOG.0000228510.08019.77
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