External Urethral Sphincter EMG Research Articles

Changes in excitability of midbrain micturition control circuitry during alterations in sleep-like brain states in rats – implications for nocturnal enuresis

In humans micturition typically does not occur during sleeping but the bladder may accumulate a large volume of urine, which during wakefulness would be suprathreshold for triggering a need to void. The mechanism underlying this effect is not known but could include inhibition of sensory input from the bladder during sleep and/or a resetting of the excitability of the micturition control circuit. Micturition requires the functional integrity of a spino-midbrain-spinal loop that relays in the caudal ventrolateral periaqueductal grey (vlatPAG). We investigated whether the excitability of the micturition circuitry within the vlatPAG changed with arousal state. The urethane anaesthetised rat preparation was used, which shows spontaneous cyclical changes in EEG waveform that resemble changes in sleep state in unanesthetised animals. During infusion of saline into the bladder (6ml h−1) we found that transition from ‘arousal’ (desynchronised, low amplitude high frequency (3-5Hz) EEG) to synchronized high amplitude, slow wave (1Hz) activity (slow wave ‘sleep’) was accompanied by increases in micturition bladder pressure threshold and voided volume, and decreased end filling compliance, typical of natural sleep. The spontaneous firing of single units in the vlatPAG also slowed (8.0±3.2-3.0±1.9 Hz, n=15, p<0.01). These included 7 ‘micturition control’ neurons, which showed phasic changes in firing time-locked to changes in bladder pressure or external urethral sphincter EMG activity that were also depressed (n=6) or completely abolished (n=1) during SWS-like EEG activity. The results suggest that the micturition reflex is reset centrally during sleep. Failure of this mechanism could contribute to the development of nocturnal enuresis.

Differential effects of Diabetes mellitus on Nerve Fibers by Type of Diabetes

spinal loop that relays in the caudal ventrolateral periaqueductal grey (vlatPAG). We investigated whether the excitability of the micturition circuitry within the vlatPAG changed with arousal state. The urethane anaesthetised rat preparation was used, which shows spontaneous cyclical changes in EEG waveform that resemble changes in sleep state in unanesthetised animals. During infusion of saline into the bladder (6ml h) we found that transition from ‘arousal’ (desynchronised, low amplitude high frequency (3-5Hz) EEG) to synchronized high amplitude, slow wave (1Hz) activity (slow wave ‘sleep’) was accompanied by increases in micturition bladder pressure threshold and voided volume, and decreased end filling compliance, typical of natural sleep. The spontaneous firing of single units in the vlatPAG also slowed (8.0±3.2-3.0±1.9 Hz, n=15, pb0.01). These included 7 ‘micturition control’ neurons, which showed phasic changes in firing time-locked to changes in bladder pressure or external urethral sphincter EMG activity that were also depressed (n=6) or completely abolished (n=1) during SWS-like EEG activity. The results suggest that the micturition reflex is reset centrally during sleep. Failure of this mechanism could contribute to the development of nocturnal enuresis.

Contribution of the external urethral sphincter to urinary void size in unanesthetized unrestrained rats.

In anesthetized rats, voiding is typically associated with phasic activation (bursting) of the external urethral sphincter (EUS). During spontaneous voiding in unanesthetized, unrestrained rats, EUS bursting is the most common form of EUS activity exhibited, but it is not necessary for productive voiding to occur. The aim of the present study was to determine which aspects of EUS activity contributed to void size during bursting and non-bursting voiding in conscious, freely moving rats. Female rats were implanted with electrodes adjacent to the EUS for recording electromyographic activity (EMG). EUS EMG recordings were performed during 24-hr sessions in a metabolic cage while voided urine was continuously collected and weighed. Void size was positively correlated with the duration of the intra-burst silent and active periods and variables reflecting the overall intensity and duration of bursting, particularly at lower frequencies within the 3-10 Hz range of EUS bursting. In addition, void size was inversely related to the frequency of bursting and to the average EMG amplitude during voiding, both in voids with and without bursting. EUS bursting contributes to productive voiding when bursting is present. Lower bursting frequencies elicit more productive voiding than do higher frequencies. In the absence of bursting, the association of increased void size with smaller average EUS EMG amplitude suggests that conscious rats can perform synergic voiding (i.e., bladder contraction with EUS relaxation) that is comparable to that seen in humans and other typically non-bursting species. Neurourol. Urodynam. 35:696-702, 2016. © 2015 Wiley Periodicals, Inc.

Long-term recording of external urethral sphincter EMG activity in unanesthetized, unrestrained rats

The external urethral sphincter muscle (EUS) plays an important role in urinary function and often contributes to urinary dysfunction. EUS study would benefit from methodology for longitudinal recording of electromyographic activity (EMG) in unanesthetized animals, but this muscle is a poor substrate for chronic intramuscular electrodes, and thus the required methodology has not been available. We describe a method for long-term recording of EUS EMG by implantation of fine wires adjacent to the EUS that are secured to the pubic bone. Wires pass subcutaneously to a skull-mounted plug and connect to the recording apparatus by a flexible cable attached to a commutator. A force transducer-mounted cup under a metabolic cage collected urine, allowing recording of EUS EMG and voided urine weight without anesthesia or restraint. Implant durability permitted EUS EMG recording during repeated (up to 3 times weekly) 24-h sessions for more than 8 wk. EMG and voiding properties were stable over weeks 2-8. The degree of EUS phasic activity (bursting) during voiding was highly variable, with an average of 25% of voids not exhibiting bursting. Electrode implantation adjacent to the EUS yielded stable EMG recordings over extended periods and eliminated the confounding effects of anesthesia, physical restraint, and the potential for dislodgment of the chronically implanted intramuscular electrodes. These results show that micturition in unanesthetized, unrestrained rats is usually, but not always, associated with EUS bursting. This methodology is applicable to studying EUS behavior during progression of gradually evolving disease and injury models and in response to therapeutic interventions.

Neural pathways of somatic and visceral reflexes of the external urethral sphincter in female rats

The external urethral sphincter (EUS) plays a crucial role in maintaining urinary continence. The activity of the EUS is modulated by bladder and urethra sensory neurons. However, a complete understanding of the somatic or visceral sources that modulate the EUS is lacking. The aims of the present study were to characterize the response of the EUS to perineal skin, genital, rectal, and urethral mechanical stimulation, as well as to determine the peripheral neural pathways of the reflex. EUS reflex electromyographic activity (EMG), innervation of pelvic and perineal structures, and the anatomy of afferent and efferent nerves were determined in anesthetized female rats. The EUS responds to cutaneous as well as genital and rectal stimuli. However, the EUS EMG response is significantly larger when induced by genital stimulation. The dorsal nerve of the clitoris and the cavernous nerve both innervate the distal urethra and the distal vagina, as well as the clitoris and perigenital skin and are the main afferent pathways for the genito-sphincteric reflex. Efferent axons travel through the pudendal nerve and the lumbosacral trunk and converge in the motor branch of the lumbosacral plexus, which innervates the EUS. Because the nerves are located on the vaginal walls, they are susceptible to damage during childbirth. Physiology and anatomy of the different neural pathways that regulate EUS activity are important to consider when inducing nerve damage to create models of urinary incontinence.

255 DRAMATIC REDUCTION IN URETHRAL SPHINCTER ACTIVITY FOLLOWING PELVIC NERVE CRUSH IN THE RAT

You have accessJournal of UrologyBladder and Urethra: Anatomy, Physiology and Pharmacology I1 Apr 2012255 DRAMATIC REDUCTION IN URETHRAL SPHINCTER ACTIVITY FOLLOWING PELVIC NERVE CRUSH IN THE RAT Christopher Chermansky, Qiang Wu, J. Christian Winters, and Matthew Fraser Christopher ChermanskyChristopher Chermansky New Orleans, LA More articles by this author , Qiang WuQiang Wu New Orleans, LA More articles by this author , J. Christian WintersJ. Christian Winters New Orleans, LA More articles by this author , and Matthew FraserMatthew Fraser Durham, NC More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2012.02.312AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES There is no established rat model for euglycemic non-obstructive underactive bladder (UAB). We present such a model for the purpose of testing therapies aimed at improving bladder emptying in patients with this condition. METHODS 44 female SD rats were divided into two experimental groups: bilateral pelvic nerve crush (PNC) and control. PNC was performed in 23 rats under isoflurane anesthesia. A straight Jacobson micro mosquito clamp was used to crush each pelvic nerve for 30 seconds. The crush was performed proximal to each pelvic nerve's entry into the major pelvic ganglion. Prior to crushing, the identity of the pelvic nerve was verified by electrical stimulation with a bipolar electrode to confirm visual bladder contraction. 21 control rats underwent a sham operation where pelvic nerves were exposed but not crushed. At 1, 2, and 4 weeks following PNC or sham surgery, the rats underwent continuous cystometry and external urethral sphincter (EUS) EMG testing under urethane anesthesia (1.2g/kg) using a PE90 transvesical catheter and a saline infusion rate of 0.04 ml/min. Periurethral EUS EMG fine wire electrodes were inserted percutaneously. Finally, isovolumetric cystometry was performed to measure bladder contractile strength by tying off the urethra. Data were collected using PowerLab from AD Instruments. Statistical comparisons between groups were performed using two-way ANOVA with GraphPad from Prism. RESULTS Following PNC, intercontraction interval (ICI) increased at 1 week and remained doubled at 4 weeks during continuous CMG. This was paralleled by similar increases in bladder compliance. A striking reduction (50%) in EUS EMG activity during filling was also seen with PNC. Isovolumetric CMG in the PNC groups revealed a 40% reduction in peak bladder contraction pressures over baseline and a 30% reduction in isovolumetric bladder contraction areas under the curves. CONCLUSIONS In this preliminary study, we have shown that bilateral pelvic nerve crush in the rat is a promising, long-lasting model of UAB, demonstrating both bladder and outlet dysfunction consistent with pelvic nerve denervation. Increased ICI, bladder compliance, and decreased EUS activity are consistent with decreased afferent sensitivity with PNC. Decreased bladder contraction strength is consistent with compromised efferent function. By establishing a chronic rat model for UAB in otherwise normal animals, we can test potential therapies for treating UAB and voiding dysfunction, thereby addressing both afferent and efferent dysfunction. © 2012 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 187Issue 4SApril 2012Page: e103-e104 Peer Review Report Advertisement Copyright & Permissions© 2012 by American Urological Association Education and Research, Inc.MetricsAuthor Information Christopher Chermansky New Orleans, LA More articles by this author Qiang Wu New Orleans, LA More articles by this author J. Christian Winters New Orleans, LA More articles by this author Matthew Fraser Durham, NC More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Urethral sphincter EMG-controlled dorsal penile/clitoral nerve stimulation to treat neurogenic detrusor overactivity

The goal of this study was to investigate whether real-time external urethral sphincter (EUS) EMG-controlled dorsal genital nerve (DGN) stimulation can suppress undesired detrusor bladder contractions in patients with both neurogenic detrusor overactivity (NDO) and detrusor sphincter dyssynergia (DSD). Detrusor pressure (Pdet) and EUS EMG were recorded in 12 neurogenic patients who underwent two filling cystometries. The first one was without stimulation and was intended to confirm the NDO and DSD and to set the EMG detection threshold. The second one was with real-time EMG-controlled stimulation of DGNs. Two detection methods were analyzed to detect bladder contractions. The first method was a Kurtosis-scaled root mean square (RMS) detector and was used on-line. The second was a simple RMS detector and was used off-line. Of 12 patients included, 10 patients showed both NDO and DSD. In nine of these ten patients relevant EMG concomitant to detrusor activity was detected and stimulation could suppress at least one detrusor contraction. The second filling compared to the first one showed an increase of 84% in bladder capacity (p = 0.002) and a decrease of 106% in Pdet (p = 0.002). Nine false-positive detections occurred during the ten fillings with electrical stimulation. The mean increases of both time and Pdet between stimulation and bladder contraction onsets for method 1 were 1.8 s and 4 cmH2O and for method 2 were 0.9 s and 2 cmH2O, respectively. This study shows that EUS EMG can be used in real time to detect the onset of a bladder contraction. In combination with DGN stimulation has been shown to be feasible to suppress undesired bladder contractions and in turn to increase bladder capacity in subjects with both NDO and DSD.

GABAergic control of micturition within the periaqueductal grey matter of the male rat.

In urethane-anaesthetised rats continuous infusion of saline into the bladder (6 ml h⁻¹) evoked periodic sharp rises in intravesicular pressure accompanied by rhythmic bursting of external urethral sphincter (EUS) EMG and expulsion of urine from the urethral meatus. Microinjection of the GABA agonist muscimol (250 pmol) into the caudal ventrolateral periaqueductal grey (PAG), but not at other sites in the PAG, either depressed reflex voiding frequency (-60%, n = 7) and tonic EUS EMG activity (-38%, n = 6) or completely inhibited voiding (four sites). Microinjection of the GABA antagonist bicuculline (BIC; 1 nmol) into the same region, to reduce ongoing GABA tone, increased reflex voiding frequency (+467%, n = 16) and tonic activity in the EUS (+56%, n = 7) whilst bursting activity in the EUS became desynchronised. Although muscimol failed to change reflex micturition when microinjected into the dorsal caudal PAG, microinjection of BIC at these sites evoked pronounced autonomic arousal and increased reflex voiding frequency (+237%, n = 34). The results demonstrate that the functional integrity of synapses in the caudal ventrolateral PAG is essential to permit micturition. Transmission through the region is normally regulated by a tonic GABAergic inhibitory influence. In contrast, the functional integrity of the dorsal caudal PAG is not essential for reflex micturition. However, micturition may be initiated from this region via projections to the caudal ventrolateral PAG, as part of the behavioural response to psychological threat or other stressful stimuli.

Organization of external urethral sphincter recruitment during micturition in the female rat.

The goal of this study was to examine the activation patterns of individual external urethral sphincter (EUS) motor units (MUs) during micturition in rats. To this end, bladder intravesical pressure (BP) and EUS EMG activity were recorded in urethane anesthetized adult female Sprague Dawley rats during continuous infusion of saline into the bladder. Individual EUS MU activity was recorded using a tungsten microelectrode (1 MΩ) inserted in the EUS or by placing an L6 ventral root filament, dissected in continuity, on platinum electrodes. Four different EUS MU recruitment patterns were observed. (1) Low threshold/sustained MUs were recruited prior to bladder contraction and exhibited sustained firing. (2) Medium threshold/not sustained MUs were recruited at the beginning of bladder contraction and stopped firing at the end of bladder contraction. (3) Medium threshold/sustained MUs were recruited at the beginning of bladder contraction and exhibited sustained firing. (4) High threshold/burst only MUs were recruited shortly before EUS bursting and stopped firing shortly after EUS bursting. Every EUS MU exhibited EUS bursting at the peak of bladder contraction. Among medium threshold MUs, derecruitment varied inversely with conduction velocity with slowly conducting units exhibiting longer sustained activity. This project is supported by the New York State Spinal Cord Injury Research Board.

Role of spinal metabotropic glutamate receptors in regulation of lower urinary tract function in the decerebrate unanesthetized rat

The role of spinal metabotropic glutamate receptors (mGluRs) in control of lower urinary tract functions was evaluated in rats using an mGluR antagonist administered via the intrathecal route. Cystometrograms in combination with external urethral sphincter (EUS) EMG recordings were performed on 13 decerebrate unanesthetized Sprague-Dawley female rats (n=6 for spinal cord intact rats; n=7 for spinal cord transected rats). In spinal cord intact rats, a group I/II mGluR antagonist, (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG), at doses of 3-30 microg, changed neither bladder nor EUS EMG activity, whereas a larger dose (100 microg) produced a significant facilitation of EUS EMG activity (41% increase in the peak activity) with little effect on bladder contractions. In chronically spinal cord transected rats, MCPG (3-100 microg) had no effect on bladder and EUS EMG activity. The results suggest that group I/II mGluRs are likely to be involved in inhibition of the excitatory pathway to the EUS but not involved in the control of the bladder. The lack of effect of MCPG on the EUS EMG activity in chronic spinal cord transected rats indicates that mGluR-mediated inhibitory control of the EUS was eliminated after spinal cord injury.

Interaction between D2 Dopaminergic and Glutamatergic Excitatory Influences on Lower Urinary Tract Function in Normal and Cerebral-Infarcted Rats

Previous studies showed that bladder hyperactivity after cerebral infarction in Sprague–Dawley (SD) rats was mediated in part by D2 dopaminergic and NMDA glutamatergic mechanisms. In the present experiments, the interaction between dopaminergic and glutamatergic excitatory mechanisms in the control of bladder and external urethral sphincter (EUS) reflexes was investigated in urethane-anesthetized sham-operated (SO) and cerebral-infarcted (CI) SD rats. Occlusion of the left middle cerebral artery or a sham operation was performed under halothane anesthesia. Two hours after either of the two procedures, rats were anesthetized with urethane. Dizocilpine, an N-methyl-d-aspartate (NMDA) glutamatergic antagonist, was administered intravenously in doses of 0.3 or 3 mg/kg to CI rats and 3 mg/kg to SO rats. These doses completely inhibited bladder and EUS activity. The effects of apomorphine (a dopamine agonist with greater efficacy at D2 than D1 receptors) or quinpirole (a selective D2 dopamine receptor agonist) were examined on the dizocilpine-induced depression of bladder contractions and EUS EMG activity. Apomorphine did not antagonize the dizocilpine depression of EUS activity, but it did reestablish the micturition reflex after dizocilpine blockade and did increase the amplitude of bladder contractions and voided volume in a dose-dependent manner (0.0001–10 mg/kg, iv), in both CI rats and SO rats pretreated with dizocilpine. There were no differences between SO rats and CI rats in the apomorphine responses in rats pretreated with doses of 0.3 or 3 mg/kg dizocilpine. A larger dose of dizocilpine (10 mg/kg) did not affect the bladder contractions after apomorphine administration. Quinpirole (0.001–1 mg/kg, iv) also partially reversed the dizocilpine depression of bladder activity in SO and CI rats. These results indicate that NMDA glutamatergic and D2 dopaminergic mechanisms exert independent excitatory influences on bladder activity in both SO and CI rats. D2 dopamine receptor agonists can reverse the effect of NMDA receptor blockade on bladder activity but were ineffective in reversing the block of sphincter activity.

Effects of GYKI 52466 and CNQX, AMPA/kainate receptor antagonists, on the micturition reflex in the rat

GYKI 52466, a non-competitive AMPA/kainate glutamate receptor antagonist, administered in graded doses (0.5–8 mg/kg, i.v.) at 10 min intervals, decreased the amplitude and duration of reflex bladder contractions (maximal inhibition = 63%), the intercontraction interval (maximal inhibition = 83%) and external urethral spincter activity (maximal inhibition = 91%) in urethane-anesthetized (1.2 g/kg, s.c.) intact rats during continuous transurethral cystometrograms. On the other hand, in unanesthetized decebrate rats, the drug did not alter reflex bladder activity but did produce a significant depression of sphincter activity (maximal inhibition = 59%). The depressant effects of single doses of GYKI 52466 (4 mg/kg, i.v.) on external urethral sphincter EMG activity occurred with similar time courses in both urethane-anesthetized (1.2 g/kg, s.c.) intact and unanesthetized decerebrate rats during continuous transurethral cystometrograms. In urethane-treated (0.6 g/kg, i.p.) decerebrate rats, GYKI 52466 (0.5-4 mg/kg, i.v.) depressed bladder contraction amplitude and sphincter EMG activity, similar to the effects in urethane-anesthetized (1.2 g/kg, s.c.) intact rats. CNQX (0.01-1 mg/kg, i.v.), a competitive AMPA/kainate receptor antagonists, administered to urethane-anesthetized (1.2 g/kg. s.c.) intact or unanesthetized decerebrate rats did not alter the bladder or the external urethral sphincter activity during continuous transurethral cystometrograms, possibly due to the inability of the drug to readily cross the blood-brain barrier. The present results indicate that glutamatergic excitatory transmission mediated by AMPA/kainate receptors is essential for the activation of external urethral sphincter activity during micturition in anesthetized and unanesthetized preparation. However, the depressant effect of GYKI 52466 on reflex bladder activity is only unmasked by urethane anesthesia, raising the possibility that urethane interacts with AMPA/kainate glutamate receptors in the spinobulbospinal micturition reflex pathway.

Stress urinary incontinence: An alternative concept of pathogenesis

A urodynamic study was done on 14 normal subjects and 24 with stress urinary incontinence (SUI), aiming to elucidate SUI etiology. All were multiparous women; 8 of the SUI patients also had partial fecal incontinence. The investigations comprised measuring the vesical and urethral pressures before and after testing external urethral sphincter anesthesia, determination of the functional urethral length and recording of the external urethral sphincter EMG, the straining-urethral reflex and the perineal nerve terminal motor latency (PNTML). The results in both normal and SUI subjects showed that coughing caused both vesical and urethral pressure increase, while an increase in vesical pressure only on external urethral sphincter anesthesia. In SUI patients, the urethral pressure at rest and on coughing was significantly lower (P<0.001) and the functional length shorter than in normal subjects (P<0.01). The external urethral sphincter EMG activity was below normal. The latency of the straining-urethral reflex as well as the PNTML were longer than normal (P<0.01). Results suggest that urethral pressure increase on coughing is effected by external urethral sphincter contraction and is not transmitted by increased intraabdominal pressure, as evidenced by the urethral sphincter anesthesia test and physioanatomic studies. The vesical and urethral descent in SUI is likely to be related to levator subluxation and sagging, which causes levator dysfunction. The cause of the weak external urethral sphincter and the prolonged straining-urethral reflex latency seems to be neurogenic, due probably to stretch of the pudendal nerve in the pudendal canal, as evidenced by the prolonged PNTML.

Effects of LY274614, a competitive NMDA receptor antagonist, on the micturition reflex in the urethane-anaesthetized rat.

1. The effects of 3 competitive N-methyl-D-aspartate (NMDA) receptor antagonists, LY274614, LY233536 and LY235723, on the micturition reflex and external urethral sphincter EMG activity, were examined either under isovolumetric conditions or during continuous filling cystometry in urethane-anaesthetized (1.2 g kg-1, s.c.) rats. 2. Intravenous administration of LY274614 (3-30 mg kg-1) inhibited in a dose-dependent fashion both bladder and sphincter activity in the intact rats. In addition, the volume threshold for inducing micturition was increased and voided volume was decreased. 3. Intrathecal administration of LY274614 (0.06-30 micrograms) similarly inhibited bladder and sphincter activity during cystometry in intact rats. 4. In chronic spinal cord (T6-T8) transected rats LY274614 (0.1-30 mg kg-1, i.v.) did not alter bladder activity under isovolumetric conditions but decreased the amplitude of micturition contractions and sphincter EMG activity during cystometry at a dose of 10-30 mg kg-1. 5. The inhibitory effects of i.v. administration of LY274614, on bladder and sphincter activity induced by infusion of chemical irritant (0.1% acetic acid) or saline, were similar; except that a slightly larger dose was needed to inhibit sphincter activity during acetic acid infusion. 6. Peak amplitude of micturition contractions recovered to 50% of control 3 h following i.v. (30 mg kg-1) or i.t. (6 micrograms) administration of LY274614. 7. Two other chemically related NMDA antagonists, LY233536 and LY235723 produced similar but less potent effects than LY274614 when given i.v. 8. These data indicate that glutamatergic transmitter mechanisms at the level of the spinal cord are important in modulating bladder activity in the intact animal, but that these mechanisms do not contribute to bladder reflexes in the chronic spinal rat. These mechanisms may, however, contribute to sphincter activity in both intact or chronic spinal rats.

Modulation of the bulbocavernosus reflex during voiding: loss of inhibition in upper motor neuron lesions.

The bulbocavernosus reflex (BCR) is a sacral segmental reflex which is suppressed throughout most of micturition. The BCR was evaluated by recording the associated EMG activity using a concentric needle electrode placed in the external urethral sphincter. The influence of the central nervous system (CNS) on the BCR was studied in 29 neurologically normal individuals and in 33 patients with upper motor neuron (UMN) lesions and voiding dysfunction. Ninety percent (26/29) of the neurologically normal patients did not have a BCR during most of micturition. By comparison, all the patients with an UMN lesion had a positive BCR beginning early during voiding. The finding of suprasegmental modulation of the BCR during voiding demonstrated by external urethral sphincter EMG was a more sensitive although slightly less specific sign of UMN bladder dysfunction than detrusor sphincter dyssynergia; uninhibited bladder contractions were neither sensitive nor specific for UMN lesions.