Intraoperative nerve stimulation with measurement of urethral sphincter pressure changes during radical retropubic prostatectomy: a feasibility study

PURPOSE: We evaluated the feasibility of using intraoperative nerve stimulation and real-time urodynamic monitoring to identify the intrapelvic innervation of the urethral sphincter during radical retropubic prostatectomy. MATERIALS AND METHODS: Using an intraurethral balloon pressure transducer and nerve stimulator changes in urethral pressure were measured in response to stimulation of the neurovascular bundles, pelvic side wall, bladder neck, rectus muscle and other structures in 8 patients undergoing nerve sparing radical retropubic prostatectomy. Intraurethral pressure changes were charted on an urodynamic monitor and correlated with the anatomical location of stimulation. RESULTS: Stimulation of the neurovascular bundles resulted in measurable and significant (greater than 10 cm. H(2)O) increases in intraurethral pressure in all 8 patients. The mean pressure increase was 22 cm. H(2)O. Neither control structure, that is the bladder neck or rectus, resulted in pressure changes with stimulation. In 60% of the subjects pelvic side wall stimulation resulted in urethral pressure increases, while in 40% this stimulation caused pelvic contraction floor but no pressure increase. The mean pressure changes with side wall stimulation was 14 cm. H(2)O. CONCLUSIONS: Intraoperative stimulation of pelvic neural structures and measurement of changes in urethral pressure in response to stimulation are feasible during radical retropubic prostatectomy. Stimulating the neurovascular bundle consistently results in significant increases in urethral pressure. The finding of an intrapelvic urethral innervation supports the previously published observation that nerve sparing radical retropubic prostatectomy may result in improved continence postoperatively.     

Restoration of external urethral sphincter function after pudendal nerve end-to-end anastomosis in the male rabbit

PURPOSE: In this study we rehabilitated external urethral sphincter function by pudendal nerve end-to-end anastomosis after experimental pudendal nerve axotomy in male rabbits. MATERIALS AND METHODS: A total of 17 animals were included in this study, including group 1-a control group of 5 (29.4%), group 2-6 (35.3%) and group 3-6 (35.3%). Animals from group 2 underwent bilateral axotomy and group 3 underwent pudendal nerve end-to-end anastomosis. In all groups we performed urodynamic investigations prior to axotomy, after axotomy or anastomosis, and 14, 42 and 90 days after axotomy or nerve anastomosis. RESULTS: In untreated group 1 control sphincter pressure was 28.5 cm H2O. In group 2 average urethral sphincter pressure was 5.6 cm H2O 14 days after axotomy with only a slight increase to 11.05 cm H2O by day 90. In group 3 external urethral pressure increased to 8.26 cm H2O after 14 days and to 21.32 cm H2O by postoperative day 90. CONCLUSIONS: External urethral sphincter deficiency after bilateral pudendal nerve axotomy demonstrates the primacy of the pudendal nerve in the innervation of the external urethral sphincter. We were able to rehabilitate external urethral sphincter function by performing pudendal nerve end-to-end anastomosis.     

Pelvic autonomic nerve mapping around the prostate by intraoperative electrical stimulation with simultaneous measurement of intracavernous and intraurethral pressure

PURPOSE: In previous studies we noted that the neurovascular bundle was not identical to the bundle of the cavernous nerve fibers. In this study we sought to prove these anatomical findings electrophysiologically and map the autonomic nerve fibers by intraoperative simultaneous measurement of intracavernous pressure and intraurethral pressure. MATERIALS AND METHODS: Between January 2004 and May 2005 electrical stimulation was performed in 27 open pelvic surgeries, including 26 radical retropubic prostatectomies and 1 radical cystectomy, using an original bipolar electrode before prostate removal. Nerve stimulation was performed at the base of the so-called neurovascular bundle (point A) and the rectal wall about 1 cm posterolateral, apart from the neurovascular bundle (point B). Intracavernous pressure and intraurethral pressure were measured simultaneously. RESULTS: The mean +/- SD increase in intracavernous pressure was 9.8 +/- 6.3 cm H2O at point A and 13.5 +/- 7.3 cm H2O at point B. Intracavernous pressure at point B was significantly higher than at point A (p = 0.0240). The mean increase in intraurethral pressure was 17.0 +/- 9.4 cm H2O at point A and 11.2 +/- 8.1 cm H2O at point B. Intraurethral pressure at point A was significantly higher than at point B (p = 0.0353). CONCLUSIONS: The course of the cavernous nerves did not always agree with the surgically identified neurovascular bundle. The distribution of cavernous nerves was wider than our image of the neurovascular bundle and it existed on the rectal wall posterolateral, apart from the neurovascular bundle rather than the neurovascular bundle itself. The surgically identified neurovascular bundle contained the nerve fibers contributing to urinary continence.     

Extradural cold block for selective neurostimulation of the bladder: development of a new technique

PURPOSE: Cryotechnique for selective block of the urethral sphincter and simultaneous activation of the bladder was developed to achieve physiological micturition during sacral anterior root stimulation (SARS). MATERIALS AND METHODS: In ten foxhounds SARS of S2 was carried out while extradurally both spinal nerves S2 were cooled down from positive 25C in a stepwise fashion until a sphincter block was observed. Subsequently, SARS of S2 was performed while the pudendal nerves were cooled down from + 15C. The effects of spinal and pudendal nerve cold block on the urethral sphincter and bladder during SARS and the recovery time were monitored by urodynamic investigation. RESULTS: A complete cold block of the urethral sphincter during spinal nerve cooling was achieved in all cases. During pudendal nerve cooling, the sphincter was completely blocked in two, and incompletely blocked in four dogs. Cold block temperature of the spinal nerves averaged +11.7C and of the pudendal nerves +6.2C. During SARS and spinal nerve cooling, an increase in intravesical pressure up to 13 cm. water was recognized, and recovery time was on average 6.6 minutes. Intravesical pressure remained unchanged during pudendal nerve cooling, with recovery time being less than 1 minute. The cold block was always reversible. CONCLUSIONS: Cryotechnique is an excellent method for selective and reversible block of the urethral sphincter during SARS to avoid detrusor-sphincter-dyssynergia. The application of cryotechnique in functional electrical stimulation leads to an improvement of quality of life in para- or tetraplegic patients because of selective nerve stimulation with optimization of micturition, standing, walking and grasping and does so without the necessity of surgical dorsal root rhizotomy.     

两种去神经支配压力性尿失禁模型的比较

目的 比较两种去神经支配压力性尿失禁(SUI)模型的效果.方法 30只雌性Wistar大鼠随机分为3组.测漏尿点压力(LPP),3组分别切断坐骨神经、阴部神经和只游离不切断,术后2周测LPP,行喷嚏试验.术后1月行尿道组织学检查.解剖坐骨、阴部神经.结果 3组术前LPP差异无统计学意义(P>0.05).对照组手术前后LPP分别为(27.567 70±5.434 89)、(30.132 20±5.790 94)cm H_2O,差异无统计学意义(P>0.05);坐骨神经组为(30.911 00±5.467 62)、(30.400 80±5.515 54)cm H_2O,差异无统计学意义(P>0.05);阴部神经组为(27.84930±5.23036)、(9.588 30±2.342 55)cm H_2O,差异有统计学意义(P<0.01).阴部神经组术后喷嚏时漏尿,镜检尿道括约肌萎缩.解剖证明坐骨、阴部神经各自独立,支配尿道括约肌的是阴部神经.结论 切断阴部神经可以建立大鼠去神经支配SUI模型,切断坐骨神经则不能.     

Voiding reflex in chronic spinal cord injured cats induced by stimulating and blocking pudendal nerves

AIMS: To induce efficient voiding in chronic spinal cord injured (SCI) cats. METHODS: Voiding reflexes induced by bladder distension or by electrical stimulation and block of pudendal nerves were investigated in chronic SCI cats under alpha-chloralose anesthesia. RESULTS: The voiding efficiency in chronic SCI cats induced by bladder distension was very poor compared to that in spinal intact cats (7.3 +/- 0.9% vs. 93.6 +/- 2.0%, P < 0.05). In chronic SCI cats continuous stimulation of the pudendal nerve on one side at 20 Hz induced large amplitude bladder contractions, but failed to induce voiding. However, continuous pudendal nerve stimulation (20 Hz) combined with high-frequency (10 kHz) distal blockade of the ipsilateral pudendal nerve elicited efficient (73.2 +/- 10.7%) voiding. Blocking the pudendal nerves bilaterally produced voiding efficiency (82.5 +/- 4.8%) comparable to the efficiency during voidings induced by bladder distension in spinal intact cats, indicating that the external urethral sphincter (EUS) contraction was caused not only by direct activation of the pudendal efferent fibers, but also by spinal reflex activation of the EUS through the contralateral pudendal nerve. The maximal bladder pressure and average flow rate induced by stimulation and bilateral pudendal nerve block in chronic SCI cats were also comparable to those in spinal intact cats. CONCLUSIONS: This study shows that after the spinal cord is chronically isolated from the pontine micturition center, bladder distension evokes a transient, inefficient voiding reflex, whereas stimulation of somatic afferent fibers evokes a strong, long duration, spinal bladder reflex that elicits efficient voiding when combined with blockade of somatic efferent fibers in the pudendal nerves.     

Ipsilaterality of motor innervation of canine urethral sphincter

The functional activity of the sphincter muscle of the urethra is known to be controlled largely by the hypogastric and pudendal nerves. It remains unknown, however, whether innervation of the muscle by these peripheral nerves is ipsi- or bilateral. In an attempt to answer this question urethral closure pressure was determined simultaneously in the anterior, posterior, right and left portions of urethral wall in dogs. The pressure measurements were stereographed with the aid of a computer (stereo-UPP) and by this means the effect of unilateral section or electrical stimulation of hypogastric and pudendal nerves on the intraurethral pressure profile was analyzed. Unilateral section or electrical stimulation of the hypogastric nerve, distal to its division, produced a fall and a rise primarily in proximal intraurethral pressure, respectively, in all four directions. There was no significant difference in this response between the involved and uninvolved sides. Unilateral section of the pudendal nerve resulted in a fall primarily in distal intraurethral pressure in all four directions. No significant difference was present between the injured and noninjured sides. In contrast, electrical stimulation of the pudendal nerve distal to the point of its division caused a rise in intraurethral pressure in all four directions, with a significantly greater pressor response on the stimulated than on the nonstimulated side. These observations suggest decussating motor innervation of the urethra by the hypogastric nerves and also the possibility of the distal urethra being ipsilaterally innervated by the pudendal nerve.     

Neuroanatomy of the human female lower urogenital tract

PURPOSE: The neuroanatomy of the female lower urogenital tract remains controversial. We defined the topographical anatomy and differential immunohistochemical characteristics of the dorsal nerve of the clitoris, the cavernous nerve and the nerves innervating the female urethral sphincter complex. MATERIALS AND METHODS: A total of 16 normal female human pelvic specimens at 14 to 34 weeks of gestation were studied by immunohistochemical techniques. Serial sections were stained with antibodies raised against the neuronal markers S-100 and neuronal nitric oxide synthase (nNOS), vesicular acetylcholine transporter, calcitonin gene-related peptide and substance P. The serial sections were computer reconstructed into 3-dimensional images. RESULTS: Under the pubic arch at the hilum of the clitoral bodies the branches of the cavernous nerves joined the clitoral dorsal nerve to transform its immunoreactivity to nNOS positive. The cavernous nerves originated from the vaginal nervous plexus occupying the 2 and 10 o'clock positions on the anterolateral vagina and they traveled at the 5 and 7 o'clock positions along the urethra. The urethral sphincter complex was innervated by nNOS immunoreactive and nonimmunoreactive nerve fibers arising from the vaginal nervous plexus and pudendal nerve, respectively. CONCLUSIONS: The dorsal nerve of the clitoris receives nNOS positive branches from the cavernous nerve as a possible redundant mechanism for clitoral erectile function. The urethral sphincter complex has dual innervation, which pierces into the urethral sphincter complex at different locations. The study of the neuroanatomy of the female lower urogenital tract is germane to the strategic design of female reconstructive surgery.     

Functional and neuroanatomical effects of vaginal distention and pudendal nerve crush in the female rat

PURPOSE: We tested the hypothesis that neuroanatomical degeneration near the external urethral sphincter (EUS) would parallel urinary dysfunction after vaginal distention or bilateral pudendal nerve crush in female rats. MATERIALS AND METHODS: A total of 28 female rats underwent bilateral pudendal nerve crush or vaginal distention, or were unoperated controls. Two days later a catheter was implanted into the bladder dome and 2 days after that (4 days after injury) urethral leak point pressure testing was performed with the rat under urethane anesthesia. The pudendal nerve and urethra were then dissected and prepared for light and electron microscopy. RESULTS: Leak point pressure was significantly decreased 4 days after pudendal nerve crush and vaginal distention (29.3 +/- 3.4 and 31.0 +/- 2.5 cm H(2)O, respectively) compared with controls (44.3 +/- 3.4 cm H(2)O). The percentage of nerve fascicles with degeneration near the EUS was significantly greater in the nerve crush (13.1% +/- 1.7%) and vaginal distention (7.2% +/- 2.2%) groups than in the control group (0% +/- 0%). There were fewer nerve fascicles near the EUS in the ventral half of the urethral cross section than in the dorsal half in all 3 groups and the percent of fascicles with degeneration was greater in the ventral half than in the dorsal half in the 2 injury groups. CONCLUSIONS: These results suggest that the pudendal nerve is particularly vulnerable to injury during vaginal distention in this animal model. The 2 injury models may be useful for investigating the pathophysiology of stress urinary incontinence.     

Electrical stimulation induced sphincter fatigue during voiding.

The stimulation of the sacral nerves to induce voiding is often associated with simultaneous contraction of the striated sphincter rendering micturition difficult or impossible. Rhizotomy of some sacral nerves was found to be necessary to facilitate voiding with stimulation. An main objective in the present experiment was to evaluate the feasibility of achieving the same result using electrical stimulation to fatigue the sphincter. In order to compare the effect of rhizotomy and fatiguing striated sphincter, the bladder outlet resistance was measured. S2 nerves were stimulated with 3 V, 35 Hz and 100 microseconds duration for 5 to 10 sec. Following S2 nerves stimulation the pudendal nerve was stimulated till we obtained sphincteric fatigue. The optimal parameter to induce sphincter fatigue were 3 V, 100-500 Hz and 100 microseconds. for 15-20 sec. The combined pressure-flow studies showed that fatiguing the sphincter via the pudendal nerve using these parameters was as good as cutting it in achieving bladder emptying with stimulation.     

Urethral response to nerve stimulation measured by strain gauge force transducer

This paper presents a study of urethral responses to efferent nerve stimulation in dogs. The pelvic, hypogastric and pudendal nerves were stimulated using a programmed instrument under three different in vivo conditions. The preparations consisted of: (A) bladder, urethra, and rectum; (B) urethra and rectum, and (C) urethra only. Stimulation of the pelvic nerve in preparation A resulted in elongation and constriction of the mid and proximal urethra with a resultant rise in pressure. However, this response was reduced in preparations B and C. Similar observations were made with hypogastric nerve stimulation. The results of pudendal nerve stimulation were significantly different, in that the pressure rise occurred in the mild and distal urethra and varied in elongation response.     

Bladder inhibition or voiding induced by pudendal nerve stimulation in chronic spinal cord injured cats

AIMS: To investigate pudendal-to-bladder spinal reflexes in chronic spinal cord injured (SCI) cats induced by electrical stimulation of the pudendal nerve. METHODS: Bladder inhibition or voiding induced by pudendal nerve stimulation at different frequencies (3 or 20 Hz) was studied in three female, chronic SCI cats under alpha-chloralose anesthesia. RESULTS: Voiding induced by a slow infusion (2-4 ml/min) of saline into the bladder was very inefficient (voiding efficiency=7.3%+/-0.9%). Pudendal nerve stimulation at 3 Hz applied during the slow infusion inhibited reflex bladder activity, and significantly increased bladder capacity to 147.2+/-6.1% of its control capacity. When the 3-Hz stimulation was terminated, voiding rapidly occurred and the voiding efficiency was increased to 25.4+/-6.1%, but residual bladder volume was not reduced. Pudendal nerve stimulation at 20 Hz induced large bladder contractions, but failed to induce voiding during the stimulation due to the direct activation of the motor pathway to the external urethral sphincter. However, intermittent pudendal nerve stimulation at 20 Hz induced post-stimulus voiding with 78.3+/-12.1% voiding efficiency. The voiding pressures (39.3+/-6.2 cmH2O) induced by the intermittent pudendal nerve stimulation were higher than the voiding pressures (23.1+/-1.7 cmH2O) induced by bladder distension. The flow rate during post-stimulus voiding induced by the intermittent pudendal nerve stimulation was significantly higher (0.93+/-0.04 ml/sec) than during voiding induced by bladder distension (0.23+/-0.07 ml/sec). CONCLUSIONS: This study indicates that a neural prosthetic device based on pudendal nerve stimulation might be developed to restore micturition function for people with SCI.     

Perineal nerve and transcutaneous spinal stimulation: new methods for investigation of the urethral striated sphincter musculature

The distal motor latencies in the perineal and pudendal nerves were measured in 20 normal subjects using digitally directed pudendal nerve stimulation. The mean pudendal and perineal nerve latencies were 1.9 ms +/- 0.2 (SD) and 2.4 ms +/- 0.2 (SD) respectively. In a further eight normal subjects transcutaneous spinal stimulation was used to record the motor latency from L1 and L4 stimulation sites to the urethral striated sphincter musculature. The mean spinal nerve terminal latencies from L1 and L4 were 4.9 ms +/- 0.3 (SD) and 4.1 ms +/- 0.2 (SD) respectively. These techniques can be applied to the investigation of the nerve supply to the urethral striated musculature in stress urinary incontinence and other disorders affecting the innervation of the anterior pelvic floor musculature.     

Effects of olfactory tubercle stimulation on efferent activities in the vesical branch of the pelvic nerve and in the urethral branch of the pudendal nerve in dogs

Experiments were performed to elucidate the effects of stimulation of the olfactory tubercle on the urinary bladder and external urethral sphincter in 31 dogs anesthetized with ketamine and alpha-chloralose and immobilized with gallamine. The hypogastric nerve was severed in all dogs, and the bladder was filled with Tyrode's solution under constant pressure (15-20 cmH2O). The outflows of the pelvic vesical branch (PV) and the pudendal urethral branch (PU) and isotonic vesical contractions were recorded simultaneously. Stimulation (5-100 Hz, 3 msec, 0.2 mA) was applied through a unipolar platinum electrode (50 microns, in diameter) inserted into the olfactory tubercle from the ventral surface. Olfactory tubercle stimulation elicited PV excitation (bladder contraction) and concomitant PU inhibition (urethral relaxation), but no reverse effect. Electrical stimulation was applied to the excitatory points at varied frequencies (5-100 Hz). PV excitation and bladder contraction were produced at 10, 20, 50 and 100 Hz, but not at 5 Hz. In another group, the vesicopressor pathway from the tubercle was investigated by partial sectioning of the brain stem in dogs from which the left fore- and mid-brain had been previously removed. The vesicopressor response induced by tubercle stimulations was not abolished by sectioning of the medial preoptic area, medial hypothalamus or periaqueductal grey, but was abolished by sectioning of the lateral preoptic area, lateral hypothalamus or ventral mesencephalic tegmentum, respectively. At the rostral pontine level, the response was abolished by partial sectioning of the lateral part of the pontine reticular formation ipsilateral to the stimulation.     

人体阴茎海绵体神经一氧化氮合成酶免疫组织化学研究

目的探讨人体阴茎海绵体神经中一氧化氮合成酶的分布情况。方法采用人体组织切片苏木素-伊红(HE)染色和神经性一氧化氮合成酶(nNOS)免疫组织化学染色方法，对1具成人尸体阴茎海绵体神经及相关组织进行染色分析。结果前列腺后外侧神经束中存在nNOS神经元细胞体和神经纤维。神经元细胞胞浆内可见均匀分布棕黄色颗粒，神经纤维则可见散在棕黄色颗粒。阴茎干背神经中，4条神经纤维截面发现有棕黄色颗粒，其他神经纤维均未发现棕黄色颗粒。龟头部组织中，未发现nNOS棕黄色颗粒神经纤维。结论前列腺后外侧阴茎海绵体神经束中存在nNOS，并且包含nNOS神经节细胞，它发出nNOS神经纤维到达阴茎海绵体，与背神经同行。     

Pudendal nerve stimulation of a preparation of isolated guinea-pig urethra

OBJECTIVE: To assess the functional response of the urethral striated muscle to activation of its nerves, using a novel isolated organ-bath preparation. MATERIALS AND METHODS: The urethra of the female guinea-pig was chosen as a suitable model for investigation, as it is functionally and structurally similar to the human urethra. Female Dunkin-Hartley guinea-pigs (400-500 g) were used; for the histochemical and immunohistochemical experiments, unfixed urethras were cryo-sectioned (14 microm thick) and were stained using established methods. For in vitro experiments, whole urethras were suspended vertically, with pudendal nerves intact, for isometric tension and intraluminal pressure recording in a 40-mL organ bath. Drugs were applied directly to the bathing solution. RESULTS: In the striated muscle layer of the urethra there was positive beta-NADPH-diaphorase activity. In organ-bath studies the pudendal nerve-evoked contractions (0.2 ms pulses, 5 s trains, 70 V and 1-100 Hz) were abolished in the presence of tubocurarine (10(-6)m), and unaffected by guanethidine and atropine (both 10(-6)m). Pre-incubation with sodium nitroprusside and SIN-1 chloride significantly reduced the initial peak pressure responses (P < 0.05, anova for paired data) evoked by electrical field stimulation of the pudendal nerves at stimulus parameters of 0.2 ms pulses, 5 s trains, 70 V and 25 Hz. CONCLUSION: Electrically induced contractions were abolished by tubocurarine, confirming that the pudendal nerve innervates the striated muscle of the guinea-pig external urethral sphincter via nicotinic receptors. beta-NADPH-diaphorase histochemistry gave positive staining around guinea-pig striated muscle cells and possibly identified neuromuscular junction sites staining positively for the nitric oxide synthase marker. Together with the results of the organ-bath experiments, the results suggest that the striated muscle cells of the guinea-pig urethra have the machinery to respond to nitric oxide.     

Abnormalities of the innervation of the urethral striated sphincter musculature in incontinence

Perineal nerve and transcutaneous spinal cord stimulation have been used to study 17 patients with idiopathic neurogenic faecal incontinence, 12 of whom also had urinary incontinence. Significant increases in spinal, perineal and pudendal nerve motor latencies were demonstrated in all 17 patients. These results suggest that there is damage to the nerves innervating both the urethral and perianal sphincter musculature in these patients, including those with isolated faecal incontinence. There was evidence of both a distal (perineal nerve) and a proximal (sacral root) component to the damage to the nerve supply of the urethral striated sphincter muscle in half of the patients.     

Response of external urethral sphincter to high frequency biphasic electrical stimulation of pudendal nerve

PURPOSE: We optimized the axonal blocking effect of high frequency, biphasic stimulation on neurally evoked contractions of the external urethral sphincter (EUS) and further investigated the repeatability of the blocking effect during relatively long periods to evaluate any acute nerve damage. MATERIALS AND METHODS: Two stainless steel electrodes were positioned 5 to 10 mm apart on the decentralized pudendal nerve in alpha-chloralose anesthetized cats. The distal electrode was first tested at different frequencies (1 to 10 kHz) to search for the effective blocking frequency. At a fixed frequency (4, 6, 8 or 10 kHz) different stimulation intensities were then tested to evaluate their blocking effect. Sine waveform or biphasic pulses of a fixed pulse width were also tested. Finally, the proximal electrode was stimulated at 40 Hz for more than 40 minutes and during the same period the distal electrode (6 to 10 kHz) was repeatedly activated for 1-minute intervals in an attempt to block the EUS contraction induced by the proximal electrode. RESULTS: High frequency, biphasic stimulation (6 to 10 kHz) with a pulse width dependent on frequency is optimal to block EUS contractions compared with sine waveform or biphasic pulses of a fixed pulse width. Acute nerve damage caused by blocking stimulation was not observed on neurally evoked urethral pressure. CONCLUSIONS: Reversible block of EUS contractions by high frequency, biphasic stimulation of pudendal nerves is a potential method for suppressing detrusor-sphincter dyssynergia and improving voiding in spinal cord injured patients.     

Identification of communicating branches among the dorsal,perineal and cavernous nerves of the penis

PURPOSE: The mechanism of human erection requires the coordination of an intact neuronal system that includes the cavernous, perineal, and dorsal nerves of the penis. We defined the communication of these 3 nerves that travel under the pubic arch using specific neuronal immunohistochemical staining and 3-dimensional reconstruction imaging technique. MATERIALS AND METHODS: A total of 18 normal human fetal penile specimens at 17.5 to 32 weeks of gestation were studied by immunohistochemical techniques. Serial sections were stained with antibodies raised against the neuronal markers S-100, and neuronal nitric oxide synthase (nNOS), vesicular acetylcholine transporter (VAChT), calcitonin gene-related peptide and substance P. RESULTS: The continuation of the dorsal neurovascular bundle of the prostate was documented under the pubic arch. Two distinct nerve bundles were identified superior to the urethra and medial to the origin of the crural bodies. Nerve bundles were observed to join the corporeal bodies at the penile hilum. Proximal to the penile hilum the dorsal nerves stained only for S-100 and VAChT. From the junction of the crural bodies at the hilum to the glans penis dorsal nerve fibers stained positive for S-100, VAChT and nNOS. Calcitonin gene-related peptide and substance P demonstrated positive staining at the distal nerves, particularly at the glans. In contrast, the whole course of the cavernous nerve stained for S-100 and nNOS. Under the pubic arch at the penile hilum the cavernous nerves were found to convey nNOS positive branches to the dorsal nerve to transform its immunoreactivity to nNOS positive. Proximal nNOS negative perineal nerves were shown to stain positive for nNOS distal on the penis. Interaction between nNOS positive dorsal nerve branches and perineal nerves was at the cavernous-spongiosal junction, where the bulbospongiosus muscle terminates. CONCLUSIONS: At penile hilum, where the corporeal bodies start to separate, the cavernous nerve sends nNOS positive fibers to join the dorsal nerve of the penis, thereby, changing the functional characteristics of the distal penile dorsal nerve. Similarly the nNOS negative, ventrally located perineal nerve originating from the pudendal nerve becomes nNOS reactive at the cavernous-spongiosal junction. These 2 examples of redundant neuronal wiring in the penis may impact erectile function, especially during reconstructive surgery.     

Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck

AIMS: Pudendal nerve stimulation is known to have a potential modulative effect on bladder function. However, even if its efficiency has been established for various neurogenic and non-neurogenic bladder dysfunctions, the underlying neuronal mechanism, and the involved pathways in humans remain unknown. In this prospective study we focused on the effects of pudendal nerve stimulation in complete spinal cord injured patients to identify neuromodulative processes that occur on spinal level. METHODS: Twenty complete spinal male presenting with upper motor neuron lesion and neurogenic incontinence underwent pudendal nerve stimulation. Bladder, bladder neck (BN), and external urethral sphincter (EUS) pressures were continuously recorded with a three channel microtip pressure transducer catheter. Fifty six pudendal stimulations using biphasic rectangular impulses (0.2 ms, 10 Hz) with intensities up to 100 mA were applied to the dorsal penile nerve. In six patients, 18 stimulations were repeated after intravenous (i.v.) administration of 7 mg phentolamine. RESULTS: Mean BN and EUS pressure increased during stimulation significantly (P < 0.001). The latencies to the EUS responses range between 27 and 41 ms and those to the BN responses between 188 and 412 ms. Phentolamine decreased initial BN pressure and reduced the pressure rise during stimulation significantly (P < 0.05). CONCLUSIONS: Pudendal nerve stimulation evoked somatic responses in the EUS and autonomic responses in the smooth muscle sphincter controlling the BN. Longer latencies of the BN responses and the sensitivity to the alpha-blocking agent phentolamine suggest that sympathetic alpha-adrenergic fibers are involved. Somatic afferent fibers of the pudendal nerve are supposed to project on sympathetic thoracolumbar neurons to the BN and modulate their function. This neuromodulative effect works exclusively at the spinal level and appears to be at least partly responsible for BN competence and at least continence.