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Neuroregeneration and voiding behavior patterns after pudendal nerve crush in female rats.

Since the pudendal nerve innervates the external urethral sphincter, pudendal nerve injury and resultant neuroregeneration should affect voiding behavior. In this study, neuroregenerative activity of pudendal nerve was correlated to the changes in urinary behavior in female rats. Eighteen female rats underwent bilateral pudendal nerve crush, and 17 to 21 age-matched rats were used as unoperated controls. Urinary volume and frequency were recorded 6 and 13 days post-operatively (dpo). Initiation of pudendal nerve regeneration was indicated by an upregulation of beta(II) tubulin mRNA in the dorsolateral motoneurons (DLM), as measured at 7 and 14 dpo by in situ hybridization with radio-labeled beta(II) tubulin cDNA. At 6 dpo, mean volume voided by the crush group was significantly decreased compared to the control group during the light cycle (P < 0.05). At 7 dpo, the DLM mRNA level was significantly increased in the nerve crush group compared to the control group (P < 0.05). At 13 dpo, there were no differences in volume or frequency between the two groups, suggesting a return to normal voiding behavior. At 14 dpo, there was no significant difference in DLM mRNA levels between crush and control groups. Initiation of nerve regeneration occurs before normalization of voiding behavior after pudendal nerve crush. This data suggest that treatments to accelerate nerve regeneration would improve functional recovery of neurologically based incontinence.

Animals↗

The utility of pudendal nerve terminal motor latencies in idiopathic incontinence.

PURPOSE: Pudendal nerve terminal motor latency testing has been used to test for pudendal neuropathy, but its value remains controversial. We sought to clarify the relationship of pudendal nerve terminal motor latency to sphincter pressure and level of continence in a cohort of patients with intact anal sphincters and normal pelvic floor anatomy. METHODS: We reviewed 1,404 consecutive patients who were evaluated at our pelvic floor laboratory for fecal incontinence. From this group, 83 patients had intact anal sphincters on ultrasound and did not have internal or external rectal prolapse during defecography. These patients were evaluated by pudendal nerve terminal motor latency testing, a standardized questionnaire, and anorectal manometry, which measured resting and squeeze anal pressures. Incontinence scores were calculated by using the American Medical Systems Fecal Incontinence Score. Values were compared by using the Fisher's exact test and Wilcoxon's rank-sum test; and significance was assigned at the P < 0.05 level. RESULTS: 1) Using a 2.2-ms threshold, 28 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 12 percent bilaterally. 2) At a 2.4-ms threshold, 18 percent of patients had prolonged pudendal nerve terminal motor latency unilaterally and 8 percent bilaterally. 3) Bilaterally prolonged pudendal nerve terminal motor latency was significantly associated with decreased maximum mean resting pressure and increased Fecal Incontinence Score, but not decreased maximum mean squeeze pressure, at both 2.2-ms and 2.4-ms thresholds. 4) Unilaterally prolonged pudendal nerve terminal motor latency was not associated with maximum mean resting pressure, maximum mean squeeze pressure, or fecal incontinence score at either threshold. CONCLUSIONS: The majority of incontinent patients with intact sphincters have normal pudendal nerve terminal motor latency. Bilaterally but not unilaterally prolonged pudendal nerve terminal motor latency is associated with poorer function and physiology in the incontinent patient with an intact sphincter.

Aged↗

Pudendal nerve palsy after femoral intramedullary nailing.

Pudendal nerve palsy after femoral intramedullary (IM) nailing was retrospectively reviewed in 65 nailings performed on 63 patients. Ten pudendal nerve palsies (15%) were noted in eight male patients and two female patients. Three male patients had autonomic involvement affecting erections. All palsies were transient (3-173 days), and occurred in patients done in the supine position as opposed to the lateral position. A possible etiology is the smaller perineal post used in the supine position that may penetrate the pelvis deeper, compressing the pudendal nerve. Other factors may be operating time and amount of traction. As prevention, the perineal post must always be adequately padded, and the operating time and amount of traction should be minimized to decrease the incidence of pudendal nerve palsy. Because pudendal nerve palsy appears to be a common complication in femoral IM nailing, the patient must be informed of this possibility.

Adolescent↗

Identification of neuropeptides in pelvic and pudendal nerve afferent pathways to the sacral spinal cord of the cat.

The distribution of several neuropeptides, including vasoactive intestinal polypeptide (VIP), substance P, somatostatin, leucine enkephalin, methionine enkephalin, and cholecystokinin, in sacral afferent pathways of the cat was examined by immunohistochemical techniques. Certain peptides (substance P, somatostatin, and leucine enkephalin) could be demonstrated in normal dorsal root ganglion cells; however, topical administration or injections of colchicine solution into ganglia 36-56 hours prior to removal markedly increased the number of cells labeled and the intensity of staining. Other peptides (VIP, cholecystokinin, and methionine enkephalin) were only detected in significant numbers of cells following intraganglionic injections of colchicine. The distribution of peptides in dorsal root ganglion cells projecting to the pelvic nerve (visceral) and the pudendal nerve (somatic) was examined by retrograde dye labeling combined with immunohistochemistry. Fluorescent dyes were applied to the cut ends of the nerves 2 weeks prior to removal. A considerably higher percentage of pelvic nerve afferent neurons than pudendal nerve afferent neurons exhibited peptide immunoreactivity; e.g., VIP (42% vs. 10%), cholecystokinin (29% vs. 12%), substance P (24% vs. 21%), leucine enkephalin (30% vs. 24%), and methionine enkephalin (10% vs. 3%). Somatostatin was present in only a small percentage of either type of afferent neuron (0.3-2%). The total percentage of peptide-containing pelvic afferent neurons exceeded 100% (137%), suggesting that more than one peptide is present in some visceral afferent neurons. This has been confirmed in preliminary experiments. The peptide-containing cells were in general less than 40 micron in average diameter; however, a significant percentage of substance P and cholecystokinin neurons ranged from 40 to 60 micron in average diameter. VIP cells had the smallest average diameter (30 micron) whereas somatostatin cells had the largest average diameter (36 micron). Statistical analysis of cell sizes revealed that substance P cells projecting to the pelvic nerve were smaller than substance P cells sending axons into the pudendal nerve. On the other hand, VIP cells in the two afferent pathways were not significantly different in size. Sacral visceral and somatic afferent neurons contain a wide spectrum of neuropeptides, some of which (e.g., VIP and cholecystokinin) seem to be preferentially distributed in the visceral afferent systems.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Pudendal nerve function in idiopathic fecal incontinence.

PURPOSE: The study was undertaken to determine whether idiopathic fecal incontinence in middle-aged and elderly females is likely to be a result of pudendal nerve damage (neurogenic incontinence) or merely a consequence of aging. METHODS: One hundred seventy-eight females over the age of 50 years with fecal incontinence were studied. The incontinence was classified as idiopathic because none of the patients related the incontinence to trauma (including obstetric trauma) or other events or diseases. All had an anal physiology examination, including determination of nerve conduction velocity of both pudendal nerves (pudendal nerve terminal motor latency). RESULTS: With a cutoff value of 2.4 msec, 79 percent (95 percent confidence limit, 73-85) had normal pudendal nerve terminal motor latency on both sides, 13 bilaterally prolonged latency (7 percent; 4-11), and 25 unilaterally prolonged latency (14 percent; 9-19). With a cutoff value of 2.2 msec, 66 percent (59-73) had normal latency on both sides, 15 percent (9-20) bilaterally prolonged pudendal nerve terminal motor latency, and 20 percent (14-26) unilateral prolongation. No relationship between the groups with normal, bilateral, or unilateral prolongation of pudendal nerve terminal motor latency and anal resting and squeeze pressure was found. Anal resting pressure decreased with increasing age (P < 0.05). CONCLUSION: Our data support the view that idiopathic fecal incontinence in the majority of females is likely to be a result of the aging process and that only a limited number may suffer from anal incontinence of neurogenic origin. Furthermore, unilateral prolongation of pudendal nerve terminal motor latency probably is without clinical significance.

Age Factors↗

The central conduction time in posterior tibial and pudendal nerve somatosensory evoked potentials.

The somatosensory evoked potentials (SEPs), following stimulation of both the posterior tibial nerve (PTSEP) and pudendal nerve (PNSEP), comprise of the lumbar negative, subcortical and cortical potential. These can be used to assess the long somatosensory pathway, including peripheral, intraspinal and intracranial conduction along the entire length. This study aimed to compare the central conduction time between the PTSEP and the PNSEP, and to investigate the relationship between the intraspinal and intracranial conduction time in the SEP pathway. The SEPs following stimulation of the posterior tibial nerve at the ankle and the pudendal nerve at the shaft of the penis were analyzed in 20 normal male subjects. The central conduction of the PNSEP was found to be slower than that of the PTSEP (p <0.05). This difference is due to a delay in conduction rather than that of intracranial conduction.

Adolescent↗

Evidence for a spinal site of action of clonidine on somatic and viscerosomatic reflex activity evoked on the pudendal nerve in cats.

Reflex activation of the pudendal nerve from bladder and urethral afferent fibers is believed to contribute to maintaining normal urinary continence under stress and to the pathophysiologic behavior seen in the urethral sphincter after suprasacral spinal cord injury. We sought to determine whether clonidine could influence, at a central level, somatic and viscerosomatic reflexes on the pudendal nerve independent of actions on the sympathetic nervous system. The expected central antisympathetic activity of clonidine could be demonstrated by near maximal lowering of the blood pressure at 5 micrograms/kg of clonidine. The drug had no influence on urethral constriction evoked by stimulation of the peripheral cut end of the pudendal nerve. However, central effects on the pudendal (somatic) nerve outflow could be demonstrated in both functional and electrophysiological experiments. Clonidine (5-50 micrograms/kg) inhibited the urethral constriction produced by stimulation of the central cut end of the pudendal nerve. Similarly, the compound action potentials recorded on the pudendal nerve in response to stimulation of the central cut end of the contralateral pelvic or pudendal nerves were reduced by as much as 75 to 85% by clonidine. The clonidine effect on the reflexes was resistant to acute transection of the spinal cord at T10; however, the antagonistic activity of prazosin was reduced dramatically. Yohimbine (0.5 mg/kg) but not prazosin (0.2 mg/kg) reversed the clonidine effect. There was no relationship between the action of clonidine on blood pressure and its action on the reflexes. We conclude that clonidine acts in the sacral spinal cord at alpha-2-adrenoceptors to depress a viscerosomatic and a somatic reflex associated with external urethral sphincter function.

Action Potentials↗

Magnetic stimulation of the pudendal nerve.

UNLABELLED: Electroneurography of the pudendal nerve is extremely important in the diagnosis of neurogenic fecal incontinence and a pudendal canal syndrome. PURPOSE: The aim of this study was to determine pudendal nerve motor latency of the overall distance by stimulation of nerve root S3 by discharging a magnetic coil. METHODS: This can be achieved by positioning an earth electrode between the site of stimulation and the registration electrode. We investigated 18 volunteers by this method. RESULTS: The average latency period was 2.51 milliseconds (SD = 0.32) on the right and 2.49 milliseconds (SD = 0.33) on the left side. CONCLUSION: This method enables precise diagnosis in neuropathies of the pudendal nerve more so than with conventional electric stimulation.

Adult↗

The overlapping innervation of the two sides of the external anal sphincter by the pudendal nerves.

Unilateral pudendal neurectomy in the monkey results in histological changes consistent with partial denervation on both sides of the external anal sphincter muscle, but much more marked ipsilaterally than contralaterally. Histological features consistent with reinnervation developed during the 9-13 weeks after unilateral neurectomy in the anterior parts of the muscle on both sides. These observations suggest that there is a substantial overlap in the pudendal innervation of the external anal sphincter muscles on the 2 sides. This derives from interdigitation of muscle fascicles across the midline in this circular muscle. This functionally overlapping innervation enables reinnervation to be partially accomplished from the contralateral side. This is important in understanding the results of electrophysiological and histopathological studies of this muscle in patients with idiopathic faecal incontinence, itself a neurogenic disorder.

Anal Canal↗

New, simple, ultrasound-guided infiltration of the pudendal nerve: topographic basics.

PURPOSE: We report the topographic relationship of the pudendal nerve to the accompanying pudendal vessels and the ischial spine and provide the basics for an ultrasonographic depiction of these structures. METHODS: Twenty-nine female and 29 male adult human cadavers were positioned prone to expose the deep gluteal region. In 58 left and 58 right pelves the course of the pudendal nerve and vessels at the ischial spine were evaluated and analyzed statistically (n = 116). RESULTS: Multitrunked pudendal nerves were found in 40.5 percent with a left-vs.-right ratio of 1:1.5. The diameters of the single-trunked nerves ranged from 1.3 to 6.8 (mean 3.6 +/- 1.1) mm. In 75.9 percent the pudendal nerve was found medial to the accompanying internal pudendal artery. The distance to the artery ranged from 17.2 mm medial to 8 mm lateral (mean, 3.4 mm medial +/- 4.1 mm). The distance to the tip of the ischial spine ranged from 13.4 mm medial to 7.4 mm lateral (mean, 2.1 mm medial +/- 3.7 mm). CONCLUSIONS: The knowledge of the close spatial relationship between the pudendal nerve and the internal pudendal artery is important for any infiltration technique and even surgical release. It demands real-time, visually controlled infiltration techniques, such as with ultrasound.

Aged↗

Pudendal nerve function in normal and encopretic children.

BACKGROUND: Abnormal pudendal nerve function contributes to fecal retention and incontinence in adults. To determine the role of pudendal neuropathy in childhood, we prospectively evaluated pudendal nerve function in normal and encopretic children. METHODS: We studied pudendal nerve terminal motor latency in 23 encopretic children and in an equal number of similarly aged, normal children. Anal manometry and electromyography were also obtained in all children. RESULTS: Pudendal nerve latency in the encopretic children equaled 1.58 +/- 0.33 msec, which was the same as that in control children. Of the 75 pudendal nerves tested, latency was prolonged in only one encopretic child. In contrast, anal electromyography demonstrated nonrelaxation of the external anal sphincter in 75% of the encopretic children but in only 13% of the normal children (p < 0.001). Anorectal manometry demonstrated, on average, lower and sphincter pressures at rest and with squeezing in the encopretic children (p < 0.01), but only 17% had sphincter pressures more than two standard deviations below normal. CONCLUSIONS: Other than poor relaxation response of the external anal sphincter during evacuation, these data reveal a paucity of functionally important abnormalities in encopretic children. In particular, we find no evidence that abnormal pudendal nerve function is important in the etiology or pathogenesis of encopresis in children.

Anal Canal↗

Topographic anatomy of a new posterior approach to the pudendal nerve for stimulation.

OBJECTIVES: To describe a new approach to the pudendal nerve from a dorsal direction in terms of topographic anatomy and to discuss pudendal nerve neurophysiology in light of the rationale behind pudendal nerve stimulation to treat lower urinary tract disorders. MATERIALS AND METHODS: Cadavers of four women aged 78-87 yr were studied. After placing the cadavers in prone position with a 40 degrees -60 degrees flexion of the hips and determining anatomic landmarks, a 20-G insulated needle was inserted close to the pudendal nerve. Then the topographic relationships of the puncture with the pudendal canal were explored by dissection. RESULTS: The mean points of insertion of the needle were 14 cm inside the great trochanter, 9 cm above the ischiatic tuberosity, and 6 cm outside the gluteal fold. If the needle was inserted 6.5 cm under the previous with an orifice of 60 degrees and this route was followed, the needle could have a contact area with the pudendal nerve larger, leading to a greater stimulation efficacy with less stimulation intensities. The rectum was so far away that a rectal injury with the needle seemed unlikely. No vascular structure was at the contact of the nerve. CONCLUSIONS: The described new puncture technique to reach the pudendal nerve provides easy and safe accessibility of the nerve for stimulation. In light of our increasing understanding of the rationale behind neuromodulative stimulation, the pudendal nerve could be a promising target for continuous lower urinary tract neuromodulation by implant.

Aged↗

Early structural effects of oestrogen on pudendal nerve regeneration in the rat.

OBJECTIVE: To determine the early effects of oestrogen on the ultrastructure of the pudendal nerve and distal nerve fascicles near the external urethra sphincter (EUS) after a pudendal nerve crush injury. The pudendal nerve is one of the pelvic floor tissues injured during vaginal delivery, possibly contributing to the development of stress urinary incontinence (SUI) in women, the symptoms of which often do not appear until menopause, implicating hormonal factors. MATERIALS AND METHODS: Twenty-seven virgin female Sprague-Dawley rats were anaesthetized and underwent ovariectomy. Three days later, they had one of four procedures: bilateral pudendal nerve crush plus implant of a subcutaneous oestrogen-containing capsule (NC+E); nerve crush plus implant of a sham saline-containing capsule (NC+S); no nerve crush with an oestrogen capsule; or no nerve crush with a sham capsule. After 2 weeks the pudendal nerves and urethral tissues were prepared for light and electron microscopy. The number of axons, myelin figures and endoneurial nuclei in the pudendal nerve segment distal to the lesion were counted. Nerve fascicles near the EUS were also counted and categorized as normal or showing signs of degeneration and/or regeneration. The location of each nerve fascicle was specified as either ventral or dorsal. RESULTS: As there were no significant differences between the two control groups they were combined to form a single control group. In the distal pudendal nerve there were significantly fewer myelinated axons and large myelinated axons in the NC+E and NC+S groups than in the control group. There were three times as many large unmyelinated axons in the NC+E group than in either the NC+S or control groups (P < 0.05). There were only half as many nerve fascicles near the ventral side of the EUS in the NC+S group than in both the control and NC+E groups (P < 0.05). CONCLUSION: Oestrogen appears to affect large unmyelinated axons in both the injured pudendal nerve and at the denervated EUS target. After pudendal nerve crush, nerve fascicles with evidence of degeneration or regeneration near the EUS appear to be spared with oestrogen treatment, particularly in the ventral region. These observations may reflect the early stages of a neuroregenerative effect of oestrogen. Additional studies are needed to confirm these results at later periods and with functional methods.

Animals↗

Anatomy of pudendal nerve at urogenital diaphragm--new critical site for nerve entrapment.

OBJECTIVES: To investigate the relations of the pudendal nerve in this complex anatomic region and determine possible entrapment sites that are accessible for surgical decompression. Entrapment neuropathies of the pudendal nerve are an uncommon and, therefore, often overlooked or misdiagnosed clinical entity. The detailed relations of this nerve as it exits the pelvis through the urogenital diaphragm and enters the mobile part of the penis have not yet been studied. METHODS: Detailed anatomic dissections were performed in 10 formalin preserved hemipelves under 3.5x loupe magnification. The pudendal nerve was dissected from the entrance into the Alcock canal to the dorsum of the penis. The branching pattern of the nerve and its topographic relationship were recorded and photographs taken. RESULTS: The anatomic dissections revealed that the pudendal nerve passes through a tight osteofibrotic canal just distal to the urogenital diaphragm at the entrance to the base of the penis. This canal is, in part, formed by the inferior ramus of the pubic bone, the suspensory ligament of the penis, and the ischiocavernous body. In two specimens, a fusiform pseudoneuromatous thickening was found. CONCLUSIONS: The pudendal nerve is susceptible to compression at the passage from the Alcock canal to the dorsum of the penis. Individuals exposed to repetitive mechanical irritation in this region are especially endangered. Diabetic patients with peripheral neuropathy can have additional compression neuropathy with decreased penile sensibility and will benefit from decompression of the pudendal nerve.

Cadaver↗

High frequency electrical conduction block of the pudendal nerve.

A reversible electrical block of the pudendal nerves may provide a valuable method for restoration of urinary voiding in individuals with bladder-sphincter dyssynergia. This study quantified the stimulus parameters and effectiveness of high frequency (HFAC) sinusoidal waveforms on the pudendal nerves to produce block of the external urethral sphincter (EUS). A proximal electrode on the pudendal nerve after its exit from the sciatic notch was used to apply low frequency stimuli to evoke EUS contractions. HFAC at frequencies from 1 to 30 kHz with amplitudes from 1 to 10 V were applied through a conforming tripolar nerve cuff electrode implanted distally. Sphincter responses were recorded with a catheter mounted micro-transducer. A fast onset and reversible motor block was obtained over this range of frequencies. The HFAC block showed three phases: a high onset response, often a period of repetitive firing and usually a steady state of complete or partial block. A complete EUS block was obtained in all animals. The block thresholds showed a linear relationship with frequency. HFAC pudendal nerve stimulation effectively produced a quickly reversible block of evoked urethral sphincter contractions. The HFAC pudendal block could be a valuable tool in the rehabilitation of bladder-sphincter dyssynergia.

Animals↗

A new approach for pudendal nerve exposure and its clinical significance.

Analgesia of the pudendal nerve is used in patients undergoing gynecologic, obstetric and penile surgery. Stimulation techniques are used to determine the functions of the nerve. In these interventions, different landmarks are used to describe the localization of this nerve. Although some authors use perineal approaches, others prefer a transvaginal (rectal in males) approach. Knowledge regarding the anatomy of the pudendal nerve and its blockade allows an easy approach to the clinical problems like perineal neuralgia, neurogenic bladder dysfunction and penile implant operations. However, in the descriptions of these different approaches, there is no clear information regarding the depth of the nerve and the branches of the pudendal nerve that are blocked. The aim of the present study was to determine the depth and location of the pudendal nerve and, thus, describe certain and easily identified surface landmarks for clinical use. According to our examinations, the distance between the ischial tuberosity and the coccyx (the base of a triangle defined by the ischial tuberosity, coccyx and ischial spine) was 8.62 +/- 0.92 cm (range 6.74-9.77 cm). The distance between the ischial tuberosity and the ischial spine was 5.23 +/- 0.33 cm (range 4.76-5.81 cm) and the distance from the ischial spine to the coccyx was 5.42 +/- 0.52 cm (range 4.02-6.32 cm). Because the pudendal nerve intersected the distance between the posterior superior iliac spine and the ischial tuberosity, the distance between these two landmarks was also measured and found to be 13.31 +/- 0.91 cm (range 10.58-15.13 cm); the depth of the nerve was 4.14 +/- 0.83 cm (range 3.13-5.25 cm).

Anesthesia, Epidural↗

Pudendal nerve "complete" motor latencies at four different levels in the anal sphincter system in young adults.

PURPOSE: Pudendal nerve complete motor latency, or the sum of the conduction time from the root of the sacral nerve to the end of the pudendal nerve and the synaptic delay, varied in length (from shortest to longest) in the puborectalis, the deep external anal sphincter, and the superficial/subcutaneous external anal sphincter, in that order, for middle-aged people. The aim of this study was to elucidate whether such a phenomenon was physiologic or pathologic. METHODS: In 20 young adults (21.9 +/- 1.37 years old, 10 females), pudendal nerve complete motor latencies were measured after magnetic stimulation to the sacral region. Electromyographic recordings were taken at depths of 5, 3.8, 2.6, and 1.5 cm from the perineal skin using a needle electrode and at 3 cm from the anal verge using surface electrodes within the anal canal. The data were compared with the data of the middle-aged cohort (65.4 +/- 7.70 years old) in our previous study. RESULTS: The pudendal nerve complete motor latencies were 3.85 +/- 1.24 ms at 5 cm, 3.97 +/- 1.25 ms at 3.8 cm, 5.41 +/- 2.42 ms at 2.6 cm, 9.98 +/- 4.01 ms at 1.5 cm, and 3.45 +/- 0.52 ms while using surface electrodes. The pudendal nerve complete motor latencies at 5, 3.8, and 2.6 cm were significantly shorter in the young adults than in the middle-aged subjects. The pudendal nerve complete motor latency using surface electrodes was significantly shorter than the pudendal nerve complete motor latency at 2.6 and 1.5 cm (mean +/- standard deviation). CONCLUSIONS: Because pudendal nerve complete motor latency was progressively longer at 5, 3.8, 2.6, and 1.5 cm, in that order, in young adults as well as in middle-aged people, this phenomenon was considered to be physiologic and may be mechanically reasonable and safe in shutting the anal canal and might be useful for milking the residual mucus out of the anal canal to prevent soiling. Aging disturbed the innervation of the upper three levels of the anal sphincter system. Pudendal nerve complete motor latency using intra-anal surface electrodes approximated that at the highest of the anal sphincters.

Adult↗