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.     

Bladder voiding by combined high frequency electrical pudendal nerve block and sacral root stimulation

AIMS: Uncoordinated contraction of the external urethral sphincter is prevalent in individuals with spinal cord injury and can prevent bladder voiding. The aim of this study was to demonstrate that complete and reversible sinusoidal high frequency alternating current (HFAC) conduction block of the pudendal nerves (PN) can eliminate external urethral sphincter activation and produce low residual bladder voiding. METHODS: In four cats, tripolar nerve cuff electrodes were implanted bilaterally on both pudendal nerves and on both extradural S2 roots. Bladder and urethral pressures, bladder volumes and flow were recorded. Bilateral HFAC was applied to determine voltage and frequency parameters resulting in bilateral PN conduction block. Sacral root stimulation provided bladder activation. Randomized sets of voiding trials were conducted with and without HFAC PN block. Additional voiding trials were conducted following bilateral PN neurotomy to eliminate somatic sphincter resistance and provide an estimate of voiding with complete block. RESULTS: Effective bilateral PN block and voiding was obtained in three of four animals. Application of bilateral PN HFAC stimulation improved voiding from 2 +/- 4% to 77 +/- 18% of the initial bladder volume and significantly (P < 0.001) reduced maximum bladder pressure during voiding. Voiding in trials with PN block was not significantly different from voiding following PN neurotomy (82 +/- 19%, P = 0.51). CONCLUSIONS: These results demonstrate that bilateral HFAC block of the PN can produce effective voiding. Neural prostheses using this approach may provide an alternative method for producing micturition for people with spinal cord injury.     

Inhibiting the hyperreflexic bladder with electrical stimulation in a spinal animal model

Uninhibited bladder contractions are a problem in spinal cord injured patients. Accordingly, methods using electrical stimulation to inhibit the bladder were investigated in chronic spinal cord injured (C6-T1) male cats. In unanesthetized, restrained animals, spontaneous bladder contractions were observed after the bladder was filled above the micturition threshold. In 3 of the 5 cats studied, this bladder activity could be inhibited with stimulation of either sacral nerves or pudendal nerves. Pudendal nerve stimulation, however, was more selective than sacral nerve stimulation for inhibition with fewer side effects such as leg spasms. Tibial nerve stimulation was ineffective and caused leg spasms and increased bladder activity. Finally, high-frequency stimulation (1,000 Hz) of the sacral nerves was shown to block bladder contractions in 2 of 3 cats investigated. However, this method had adverse side effects such as leg flexion and secondary bladder contractions. We conclude that pudendal nerve/pelvic floor stimulation at low frequency is a relatively effective method in this model.     

Role of the pudendal nerves on the dynamics of micturition in the dog evaluated by pressure flow EMG and pressure flow plot studies

The role of the pudendal nerves on the dynamics of micturition was studied using 16 decerebrated dogs. The voiding cycles were analyzed by pressure flow EMG and pressure flow plot studies under 3 conditions: control, after unilateral, and after bilateral pudendal nerve transection. In the control condition, highly reproducible reflex micturition with bladder contraction and spasmodic rhythmic sphincter contractions was demonstrated. Two patterns were noted following pudendal nerve transection: reflex micturition and overflow incontinence. Even though reflex micturition could be achieved in 9 out of 16 dogs after bilateral transection, there was decreased bladder emptying as well as absence of spasmodic rhythmic sphincter contractions. Overflow incontinence developed in the remaining 7 dogs (5 dogs after bilateral transection and 2 dogs after unilateral transection). It appears that the pudendal nerves play an important role in emptying the bladder of the dog.     

Role of the sympathetic nerve in bladder and urethral sphincter function during the micturition cycle in the dog evaluated by pressure flow EMG study

The role of the sympathetic nerve on bladder and urethral sphincter function during the whole micturition cycle, including the collecting and emptying phases, was evaluated on 10 decerebrated dogs by pressure flow EMG study. A series of experiments was performed before and after hypogastric nerve transection. In the control condition and after hypogastric nerve transection, reflex micturition with bladder contraction and spasmodic rhythmic sphincter contractions occurred. Urodynamic parameters of the micturition cycle were statistically compared between control and nerve transection experiments. Threshold volume, threshold pressure and opening pressure showed a small but significant change after nerve transection. A decrease in voided volume seems to be secondarily accompanied with a decrease in threshold volume. It seems that adrenergic nerves play a certain role in bladder function during the collecting phase of the micturition cycle.     

Experimental and clinical studies of urethral anesthesia on etiology and treatment of detrusor-sphincter dyssynergia

We studied whether detrusor-sphincter synergia during micturition was obtained by means of urethral anesthesia with lidocaine hydrochloride in five thoracic spinal cats and eight clinical cases with detrusor-sphincter dyssynergia. In thoracic spinal cats with detrusor-sphincter dyssynergia, urethral anesthesia produced detrusor-sphincter synergia, an increase in the maximum bladder pressure and a decrease in the residual volume. In clinical cases with detrusor-sphincter dyssynergia, urethral anesthesia produced detrusor-sphincter synergia or a decrease in the external urethral sphincter activities during micturition, and a decrease in the maximum urethral closure pressure and the residual volume. There were no remarkable changes of the external urethral sphincter activities during urine storage phase before and after urethral anesthesia in both spinal cats and clinical cases. These results suggest that urethral anesthesia blocks the urethro-urethral contraction reflex and secondarily activates vesico-urethral relaxation reflex. The block of urethral sensory nerves is thought to effectively treat detrusor-sphincter dyssynergia.     

Urinary bladder control by electrical stimulation: Review of electrical stimulation techniques in spinal cord injury

Evacuation of urine in paraplegics without the need for catheters would be possible when voiding could be induced by eliciting a bladder contraction. A challenging option to obtain detrusor contraction is electrical stimulation of the detrusor muscle or its motor nerves. This article reviews the 4 possible stimulation sites where stimulation would result in a detrusor contraction: the bladder wall, the pelvic nerves, the sacral roots, and the spinal cord. With respect to electrode application, sacral root stimulation is most attractive. However, in general, sacral root stimulation results in simultaneous activation of both the detrusor muscle and the urethral sphincter, leading to little or no voiding. Several methods are available to overcome the stimulation-induced detrusor-sphincter dyssynergia and allow urine evacuation. These methods, including poststimulus voiding, fatiguing of the sphincter, blocking pudendal nerve transmission, and selective stimulation techniques that allow selective detrusor activation by sacral root stimulation, are reviewed in this paper.     

Urodynamic evaluation and electrical and pharmacologic neurostimulation

Summary We introduce a rat model that allows simultaneous or independent recording of bladder and sphincteric activity. Via a polyethylene tube inserted into the bladder dome, bladder pressure is measured in response to constant intravesical saline perfusion. The electrical activity of the intra-abdominal urethra (a well-defined striated muscular tube which, in the rat, constitutes the external urethral sphincter) is recorded simultaneously with an electromyography needle electrode. Thus, precise statements can be made about detrusor/sphincter interrelationships. Changes in urodynamic parameters with the anesthetics urethane, methoxyflurane (Metofane), and thiobutabarbital sodium (Inactin) were investigated. High-frequency oscillations in intraluminal bladder pressure could be demonstrated during micturition cycles only in rats anesthetized with urethane or Metofane. As this high-frequency activity is generated by the striated muscle of the intra-abdominal urethra, the external sphincter of the rat is the force behind urine expulsion. The anesthetic Inactin combined with a low intravesical perfusion rate attenuated spontaneous bladder and sphincteric activity and abolished micturition cycles. This rat model can provide accurate and reproducible measurements of urodynamic changes in response to electrical stimulation of the pelvic and pudendal nerves and pharmacologic stimulation with neuropeptides at the lumbosacral spinal cord level. We recommend using this model with urethane or Metofane for physiologic studies of micturition and with Inactin for meticulous neuropharmacologic and electrostimulatory evaluation of urodynamic parameters.     

膀胱出口梗阻所致逼尿肌过度活动的神经电生理研究

目的 从膀胱传入神经以及盆底相关神经肌肉角度探讨神经因素及肌源性因素在膀胱出口梗阻所致的逼尿肌过度活动发生中的作用.方法 采用耻骨上膀胱颈梗阻的方法建立逼尿肌过度活动大鼠模型,测定不稳定收缩时盆神经传入电位信号,并同步测定阴部神经运动支电位、尿道外括约肌肌电及腹肌肌电的反射反应.并观察T8段脊髓截断、双侧盆神经截断、腹交感干截断以及双侧阴部神经截断后大鼠膀胱充盈测压不稳定收缩的变化.结果 成功制作了膀胱出口梗阻逼尿肌过度活动大鼠模型,成功率62.5%.充盈性膀胱测压神经肌电生理同步记录结果显示,允盈期逼尿肌过度活动可分为两种类型,一种为收缩幅度高于10 cmH2O(1 cmH2O=0.098 kPa)的逼尿肌过度活动(B-DO),伴有同步盆神经传入的信号明显增强,且能引发阴部神经、尿道外括约和腹肌肌电图出现显著变化;一种为收缩幅度低于10 cmH2O的逼尿肌过度活动(S-DO),没有上述盆神经传入及相关神经肌电变化.T8脊髓截断后,膀胱充盈-排尿收缩周期消失,膀胱基础压显著升高,B-DO消失,S-DO仍然存在,且收缩幅度较截断前略有上升,但差异无统计学意义.依次截断控制膀胱的盆神经、交感神经和阴部神经后,膀胱失去充盈-排尿收缩周期,基础压显著升高,不稳定收缩中B-DO消失,S-DO仍然存在.结论 膀胱出口梗阻所致的逼尿肌过度活动存在不依赖于中枢和周围神经的膀胱源性因素.     

Effect of naloxone on detrusor-sphincter dyssynergia in the chronic spinal cat

Naloxone, an opioid peptide antagonist, has been reported to facilitate voiding in neurologic bladder disorders, but its effects on the neural micturition reflex arc are poorly understood. We studied the effect of naloxone in 34 male adult cats, spinalized at C5-C6 level 7 to 119 days previously. Each cat served as its own control. The following tests were performed: Urethral pressure profiles, cystosphincterograms with the urethro-vesical junction opened and closed and mechanograms of the detrusor, and the circular and longitudinal urethral muscles. The study included (1) the effects of anesthesia of the bladder and pelvic nerve, as well as that of the urethral and pudendal nerves; (2) the action of naloxone; and (3) the action of oxymorphone. Our results demonstrated that naloxone (1) increased somatic (osteotendinous and nociceptive) reflexes and aggravated spasticity; (2) increased vegetative micturitional and sexual reflexes, in particular the urethra-urethral contraction reflex, aggravating the spasmodic contractions of the external sphincter; and (3) increased the frequency and intensity of the mass reflex. In consequence, we suggest that naloxone is contraindicated in cases of spinal cord lesions with detrusor-sphincter dyssynergia syndrome.     

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.     

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.     

Pelvic nerve innervation of the external sphincter of urethra as suggested by urodynamic and horse-radish peroxidase studies

In view of the fact that the detrusor vesicae and external urethral sphincter perform closely synergic functions in micturition, experiments were conducted to explore the action of the pelvic efferent neurons on the external urethral sphincter. The pelvic efferent neurons are generally recognized, by urodynamic assessments and histochemical study with the technique of retrograde axonal transport of horse-radish peroxidase, to innervate the vesical detrusor. In 7 of 15 adult dogs studied, the external urethral sphincter continued to show a normal synergic electromyogram pattern with enhanced electrical activity on vesical distention and disappearance of discharges on vesical contraction even after bilateral transection of the pudendal nerves. The electrical discharges ceased in the sphincter only after subsequent bilateral pelvic neurotomy. Horse-radish peroxidase-positive cells were demonstrated in the intermediolateral and intermediomedial nuclei and in the Onuf nucleus of the sacral cord in approximately half the dogs whose pelvic nerve was injected with the plant peroxidase. The results suggest that the pelvic nerve may contain somatic fibers innervating the external urethral sphincter.     

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.     

Selective block of urethral sphincter contraction using a modified Brindley electrode in sacral anterior root stimulation of the dog

AIMS: Patients with spinal cord injury often present with dysfunction of urinary bladder and urethral sphincter. One treatment option is sacral rhizotomy and sacral anterior root stimulation with the Finetech Brindley stimulator. However, a major disadvantage is the lack of selective stimulation, resulting in simultaneous contraction of sphincter and bladder followed by unphysiological micturition. This study investigated the possibility of selective bladder stimulation by using a Brindley electrode. METHODS: In 11 male anaesthetized foxhounds, a complete posterior rhizotomy was perormed. The anterior S2 roots were stimulated with different quasi-trapezoidal (QT) pulses (pulse length range, 600-1,400 microsec; stimulation current, 0.1-2.0 mA; frequency, 20 Hz) by using a tripolar Brindley electrode. Sphincter and bladder pressures were measured urodynamically. RESULTS: All 11 animals showed a maximal reduction of the highest sphincter pressure over 80%, and in 6 of 11 trials, the sphincter pressure was inhibited completely (100%). With stimulations at maximal sphincter blockade, the average achievable bladder pressure was 33.48 cm H(2)O higher than the average sphincter pressure, and in three cases, a strong micturition was observed. Selective blockade of the sphincter was possible by applying QT pulses. The bladders remained uninfluenced by this blockade and kept their excitability at any time. CONCLUSIONS: This study shows that selective bladder stimulation with little or no coactivation of the sphincter is possible. A physiological micturition can be achieved by using a tripolar Brindley electrode. Introduction of this stimulation technique into clinical practice should not face major difficulties, considering that the device is an established electrode.     

Effect of baclofen and dantrolene on bladder stimulator-induced detrusor-sphincter dyssynergia in dogs

The effect of baclofen (Lioresal) and dantrolene (Dantrium) on bladder stimulation-induced detrusor-sphincter dyssynergia was studied in normal and chronic T-10 paraplegic dogs. Dantrolene, which depresses skeletal muscle contractility, had little effect on electrically evoked contractions of the urethral sphincter in dogs. Baclofen, which acts centrally by potentiating presynaptic inhibition, depressed the pudendal to pudendal nerve reflex and decreased urethral resistance during bladder stimulation.     

Functional conditions of micturition induced by selective sacral anterior root stimulation: experimental results in a canine animal model

Electrical stimulation of the sacral anterior roots using conventional rectangular current pulses results in a simultaneous contraction of the urinary bladder and the striated urethral sphincter. Using a tripolar nerve cuff electrode with quasitrapezoidal current pulses and appropriate stimulation parameters, hyperpolarization of the nerve-fiber cell membrane under the anode of the stimulating electrode can reversibly arrest action potential propagation in large myelinated nerve fibers, innervating the striated urethral sphincter, while leaving action potential propagation unaffected in small non-myelinated nerve fibers innervating the urinary bladder smooth muscle (anodal arrest). Using this technique in 19 female mongrel dogs, we studied the effect of bladder filling, level of anesthesia, and sacral deafferentation on bladder pressure, urethral pressure, and urinary flow. Effective micturition could be induced only after complete dorsal rhizotomy, abolishing reflex contraction of the striated urethral sphincter, when blocking quasitrapezoidal current pulses were used for stimulation. Stimulation with rectangular current pulses directly induced a rise in distal urethral pressure, preventing micturition during stimulation.     

Control of the unstable urinary bladder by graded thermoelectric cooling of the spinal cord

OBJECTIVE: To evaluate local lumbosacral spinal-cord cooling (a novel technique for neuromodulating urinary bladder reflexes) for its feasibility in possible clinical use, by determining the efficacy and the optimum temperature for suppressing reflex urinary incontinence in two rat models of neurogenic urinary bladder instability. MATERIALS AND METHODS: Overactivity of the detrusor muscle was induced by inflammation of the urinary bladder in a group of rats. A second group of rats was examined 6 weeks after complete midthoracic spinal cord transection, when all animals had developed neurogenic bladder hyper-reflexia. The intravesical pressure, urethral pressure and electromyographic (EMG) activity of the external urethral sphincter (EUS) were recorded simultaneously during repetitive local cooling and re-warming of the dorsal L6/S1 spinal cord segments, using a thermoelectric cooling device. RESULTS: Spinal cord cooling at L6/S1 had no influence on the recorded values at >26 degrees C, but markedly suppressed detrusor contraction frequency at 21- 25 degrees C. Cooling to <20 degrees C completely and reversibly eliminated inflammation-induced bladder contractions in rats with an intact neural axis and significantly reduced the contraction amplitudes (mean reduction 61%) and duration of contractions in spinally transected rats. Cooling simultaneously increased tonic EUS EMG activity and urethral perfusion pressure in both experimental groups, indicating closure of the urethral outlet. Cooling of adjacent spinal cord segments had no influence on bladder and urethral functions. CONCLUSION: Cooling the dorsal spinal cord at the origin of the parasympathetic innervation of the bladder can be used to reversibly suppress bladder instability with simultaneous closure of the urethral outlet. Therefore, local spinal cord cooling, e.g. as an implantable thermoelectric device, may offer a suitable method to treat detrusor overactivity and restore continence.     

Reduction of bladder outlet resistance by selective stimulation of the ventral sacral root using high frequency blockade: a chronic study in spinal cord transected dogs.

PURPOSE: The use of electrical neural stimulation as treatment for neurogenic bladder is complicated by simultaneous contraction of the striated sphincter. This result is due to the composition of the ventral sacral roots, which contain somatic fibers innervating the external urethral sphincter and preganglionic parasympathetic fibers innervating the detrusor, among others. The somatic fibers have a larger caliber than the parasympathetic fibers and, as large diameter fibers, need a lower stimulus amplitude for activation than smaller fibers. Activation of the smaller fibers is always accompanied by activation of the larger fibers. We studied the effect of chronic application of selective combined low and high frequency current stimulation of the ventral sacral root on bladder evacuation and urethral resistance in chronically spinalized (spinal cord transected above the spinal micturition center) male dogs for daily bladder evacuation. MATERIALS AND METHODS: A total of 14 male mongrel dogs weighing 20 to 25 kg. underwent transection of the spinal cord at the T10 vertebra. The S2 ventral sacral root was wrapped with a bipolar electrode connected to a subcutaneous microstimulator. Daily bladder evacuation by neural stimulation with determination of the voided and residual urine volumes was done for 8 months. The animals were stimulated only with low frequency current during the 1-month spinal shock phase. Selective parameters of combined low frequency stimulation and high frequency blockade currents were subsequently applied for 6 months. For the last study month the animals were again stimulated by low frequency current alone. Bladder and urethral pressure as well as electromyography of the external urethral sphincter and pelvic floor muscles were evaluated monthly. Histopathological testing of the chronically stimulated nerve and external sphincter was performed. RESULTS: Of the 14 dogs 12 completed the followup study. During the shock phase with the application of low frequency only stimulation the animals voided 26% of mean functional bladder capacity with the early return of detrusor activity. Mean detrusor pressure plus or minus standard error of mean was 76.4 +/- 21.6 cm. water, while mean urethral pressure was 83.6 +/- 16.8 cm. water. During the application of selective combined low and high frequency stimulation 7 animals (58%) evacuated the bladder completely with post-void residual urine less than 10% of mean individual functional bladder capacity and 5 (42%) had mean post-void residual urine less than 20% of mean individual bladder capacity. Mean detrusor pressure was 73.5 +/- 20 cm. water and mean urethral pressure was 44 +/- 7.3 cm. water. There was a 45.19% reduction in the mean electromyography activity of the external sphincter. Stimulation of the dogs for the last month by low frequency current resulted in the voiding of 33% of mean bladder capacity with an increase in mean urethral pressure and electromyography activity. CONCLUSIONS: These results of reducing external sphincter activity by the simultaneous application of high frequency current blockade of the somatic fibers and activation of the autonomic fibers of the bladder by low frequency stimulation are promising.     

Use of anal sphincter electromyography during operations on the conus medullaris and sacral nerve roots.

The mechanical activity of the anal sphincter can be translated into electrical activity and recorded on graph paper or an oscilloscope. The activity of the anal sphincter may be extrapolated to activity of the external urethral sphincter because both are striated muscles innervated by the pudendal nerve that arises from S-2, S-3, and S-4. Stimulation of these nerves causes contraction of the sphincter muscles, and a deflection of the recording device occurs. This technique was employed intraoperatively in monitoring operations on the conus medullaris and sacral nerve roots in 10 patients with spinal dysraphism (age range, 3 weeks to 15 years). Their diagnoses were tethered conus, 4; lipomeningocele, 3; spinal hamartoma, 1; syringocele, 1; and sacral arachnoiditis, 1. With general anesthesia, and the patient in the prone position, an electrode-containing anal plug was inserted or two needle electrodes were inserted into the anal sphincter muscle. The electrodes were connected to the electromyography recording stylus of the urodynamic bladder diagnostic unit. During the spinal operation, whenever a structure could not be identified clearly, it was stimulated with the disposable electrical stimulator and, if oscillations of the stylus occurred (indicating contraction of the anal sphincter), the structure was preserved. This technique permitted spinal operations in these 10 patients without changes in neurological or urological function.