Management of neurogenic bladder dysfunction in the adult

MANAGEMENT

OF NEUROGENIC

DYSFUNCTION

IN THE ADULT

ALAN J. WEIN,

M.D.

DAVID M. RAEZER, GEORGE

BLADDER

S. BENSON,

M.D. M.D.

From the Division of Urology, Department of Surgery, University of Pennsylvania School of Medicine, and the Veterans Administration Hospital, Philadelphia, Pennsylvania

ABSTRACT -A review of the management of neurogenic bladder dysfunction in the adult is presented. The various modes of therapy are classi$ed according to their effects on bladder contractility and outlet resistance, providing a logical framework fm discussion.

The purpose of this review is to discuss methods of managing traumatic and nontraumatic neurogenie bladder dysfunction in adults. Except in the case of a malignant spinal cord lesion or a progressive neuropathy, there is little difference in the prognosis or management of neuropathic bladder dysfunction of traumatic or nontraumatic etiology after the first three months have elapsed. lz Therefore, these modes of therapy are applicable to any such patient in whom balanced bladder function has not developed spontaneously after the period of spinal shock (if present initially) has passed. Although the goals of management are similar for adults and children, particular approaches vary (especially in the case of myelomeningocele), and the treatment of children with neurogenic bladder dysfunction will not be specifically discussed in this article.

General Principles It is important to adopt a flexible approach that recognizes the importance of certain priorities and goals while taking into account the practicality of each proposed solution for the individual patient. 3,4 Although collective experience is valuable, no single schema, classification, protocol, or model is always reliable and appropriate. The patient’s total life situation and capabilities must be considered for example:

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Prognosis of underlying disease, especially progressive or malignant disease Limiting factors: inability to perform certain tasks (use of hands, mobility) Motivation Reliability Intelligence, education, and educability Psychosocial environment: interest, reliability, and cooperation of family Economic resources. The same therapeutic measures may not be applicable to all patients with the same type of bladder dysfunction. Hospital resources and bed-use efficiency must also be considered, especially in situations in which the demand for rehabilitation beds is great. Although no two authors agree completely on specific goals in the management of neuropathic bladder dysfunction, the following common objectives are evident:5-16 Upper urinary tract preservation or improvement Absence or control of infection Adequate emptying at low intravesical pressure Avoidance of overdistention Adequate storage to prevent or lessen incontinence Adequate control No catheter or stoma Social acceptability/adaptability Vocational acceptability/adaptability.

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2. Interruption of innervation (a) Subarachnoid block (b) Sacral rhizotomy

From these objectives, the following indications for changing or augmenting a particular regimen are derived: Upper urinary tract deterioration Recurrent sepsis or fever of urinary origin Lower urinary tract deterioration Inadequate emptying Inadequate storage Inadequate control Skin changes secondary to incontinence or to a collecting device. A useful classification of the various types of therapy is based on how well the bladder performs its two functions - urine storage and emptying.5,“,8,‘5-‘7 The following outline summarizes measures to facilitate bladder emptying: A. Increase intravesical pressure 1. External compression 2. Promotion or initiation of reflex contractions (a) Trigger zones or maneuvers (b) Bladder training, tidal drainage 3. Pharmacologic manipulation (a) Parasympathomimetic agents (b) Blockers of inhibition (?) 4. Electrical stimulation (a) Directly to bladder (b) To nerve root or spinal cord B. Decrease outlet resistance 1. At level of bladder neck resection of bladder (a) Transurethral neck Y-V-plasty of bladder neck Pharmacologic inhibition level of distal mechanism (a) External sphincterotomy Urethral overdilation Pudendal nerve interruption Pharmacologic inhibition (1) External sphincter/pelvic floor (2) Urethra C. Circumvent problem 1. Intermittent catheterization 2. Urinary diversion. Therapy

to facilitate

urine storage is as follows:

A. Inhibit bladder contractility 1. Pharmacologic manipulation Anticholinergic agents Beta-adrenergic stimulation Musculotropic relaxants Polysynaptic inhibitors

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B. Increase outlet resistance 1. At level of bladder neck stimulation (a) Alpha-adrenergic Mechanical compression (b) 2. At level of distal mechanism manipulation (a) Pharmacologic Mechanical compression C Electrical stimulation of pelvic floor i”l C. Circumvent problem 1. Intermittent catheterization 2. Urinary diversion Almost any pathologic alteration of micturition secondary to neurogenic dysfunction can be broadly categorized in this manner. This approach stems from the simple but practical idea” that the efficiency of micturition represents a balance between (1) the forces of bladder expulsion, and (2) the forces of resistance, comprising the bladder neck and the “distal urethral mechanism” I9 (the intrinsic urethral smooth muscle and the extrinsic striated musculature of the pelvic floor). A combination of therapeutic maneuvers can sometimes be used to achieve a particular end, especially if they act through different mechanisms. This approach often succeeds when a single method has failed. One should consider the possible effect of any therapeutic measure on related intact functions, such as sexual function, and its potential reversibility. The simplest and least destructive mode of therapy should generally be tried first. Well-balanced bladder function may become unbalanced in response to relatively minor trauma, such as nonurinary sepsis or infection, or surgery.6 In such a situation the previous degree of bladder function will normally be regained spontaneously, but additional therapeutic maneuvers may be required even after the effects of the injury have disappeared. Finally, in considering the merits of various types of therapy, one must remember that there are no universal criteria by which the terms success, improvement, and failure are applied. Long-term practical fulfillment of as many of the goals of management as possible with the least number of unpleasant side effects should be the standard by which all forms of treatment are judged.

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Therapy to Facilitate Bladder Emptying increasing

intravesical

pressure

Voiding by abdomiExternal compression. nal straining, Valsalva, Crede, or with the use of an expression belt is unphysiologic and is resisted by the same forces that normally resist stress incontinence (the bladder neck and the intrinsic urethral mechanism). 5,6,8,15To increase intravesical pressure in this manner requires voluntary control of the abdominal wall and diaphragmatic muscles or, in the case of Crede, ,adequate hand control. Crede is more readily performed in a child than in an adult and is easier if the abdominal wall is lax rather than taut and lean rather than obese. External compression is most effective in those patients with a hypotonic or atonic bladder who can generate a pressure greater than 50 cm. water with this maneuver.20 If adequate emptying does not occur, procedures to decrease outlet resistance may be required, especially at the level of the bladder neck, which often does not open adequately with external compression. Vesicoureteral reflux is a relative contraindication to this form of voiding, as upper tract damage can result if concomitant infection exists. Promotion or initiation Manual stimulation tions.

of rejex

contrac-

of the sacral and lumbar dermatomes (squeezing the glans penis or clitoris, pulling the skin or hair of the pubis, scrotum, or thigh, or digital rectal stimulation) can be used by patients with supranuclear lesions in an attempt to provoke reflex bladder contraction.5p6~8 According to Glahn20 the most effective method consists of rhythmic suprapubic manual pressure (seven or eight pushes every three seconds), which is thought to produce a summation effect on the tension receptors in the bladder wall and activation of the reflex arc via the afferent discharge produced. The optimal intravesical pressure so produced is 60 to 70 cm. water. This procedure may have to be combined with measures to decrease outlet resistance, especially at the level of the distal urethral mechanism, where functional obstruction often exists in these patients. Some manual dexterity and the presence of an external collecting device or excellent mobility are required. There is no evidence that the establishment of a rhythmic pattern of intake or output by periodically clamping and unclamping an in-

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dwelling catheter and maintaining a copius fluid intake either “conditions” the detrusor reflex or prevents bladder contracture. Such a regimen benefits the patient primarily by focusing his attention on his bladder and insuring an adequate fluid intake. 6-8 Pharmacologic manipulation. Since the final common pathway in physiologic bladder contraction is stimulation of the cholinergic receptor sites at the postganglionic parasympathetic neuromuscular junction, it stands to reason that parasympathomimetic agents should be useful in the management of certain types of neurogenic bladder dysfunction.21-24 Acetylcholine, thought to be the parasympathetic neurohumoral transmitter, cannot be used because of its diffuse action (ganglionic and central effects) and its rapid hydrolysis by acetylcholinesterase and nonspecific cholinesterase.25 Bethanechol chloride (Myotonachol, Urecholine) is cholinesterase resistant and has a relatively selective action on the smooth muscle of the gut and urinary bladder. It causes a contraction in vitro of smooth muscle from all areas of the bladder.26 This agent is useful in alleviating postoperative urinary retention and may be helpful in the management of chronic hypotonic bladder dysfunction if irreversible changes of bladder muscle decompensation have not occurred.21-25 It is most effective when given subcutaneously in doses of 5 to 10 mg. Oral doses of less than 50 mg. are probably ineffective in the adult.22*27 The use of bethanechol chloride is generally contraindicated in cases of known bladder outlet obstruction, but theoretically it can be combined with procedures designed to decrease outlet resistance. We, as well as others2* have been generally unimpressed with the long-term effect of oral bethanechol chloride on bladder emptying. We are also unable to rationalize its use in combination with intermittent catheterization in patients with supranuclear lesions who are in spinal shock unless it proves to facilitate the micturition reflex arc. Since voiding produced by this drug is unphysiologic, additional measures may be necessary to achieve adequate emptying.

If the sympathetic nervous system can exert an inhibitory effect on parasympathetic ganglionic transmission2’ and directly inhibit bladder muscle contractility,30-32 adrenergic blocking agents may be effective in increasing bladder contractility. Guanethidine has been used with this rationale, although a subsequent report of its efficacy has not appeared.33

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Electrical stimulation. Clinical trials of direct electronic vesical stimulation originated in 194034 but have met with only partial success and intermittent enthusiasm since that time.35-3g Recently, Merrill and Conway,40-42 and Halverstadt and Parry43 reviewed the literature and reported the results of clinical trials of newer, more reliable equipment. Direct electrical stimulation was most effective in patients with hypotonic, areflexic bladders. A low postvoiding residual and sterile urine were initially achieved in 5 of the 10 patients in Halverstadt and Parry’s series and in 3 of the 5 patients in Merrill’s series. Secondary failure, usually related to equipment malfunction, occurred in three of Halverstadt’s patients. The primary failure rate is higher in patients with supranuclear lesions who have reflex detrusor contractions, and direct electrical stimulation is not recommended for this group unless conversion to an areflexic bladder is first achieved neurosurgically. Side effects and complications are frequent and are generally related to equipment failure. The spread of current to other pelvic structures whose stimulus thresholds are lower than that of the detrusor can result in abdominal, pelvic, and perineal pain, a desire to defecate, contraction of pelvic and leg muscles, and erection and ejaculation. Since the increase in intravesical pressure is not coordinated with bladder neck opening or pelvic floor relaxation, concomitant measures to accomplish these ends may be necessary. A very interesting approach to this problem has been adopted by Grimes and his associates.44’45 In a series of 10 carefully selected they applied a stimulator paraplegic patients, directly to the sacral cord, taking advantage of the remaining intact motor pathways to initiate voiding. Since this stimulus is also unphysiologic, many of the side effects seen with direct bladder stimulation occurred. However, 6 of these patients were successfully treated by this procedure, although 2 required ancillary treatment to decrease outlet resistance.

tients: (1) those with weak or absent detrusor contractions, and (2) those with anatomic or functional obstruction at the level of the bladder neck and proximal urethra which prevents emptying even with a sustained detrusor contraction.5~8,‘2~‘5=47~4g The ideal patient is one with a sacral lesion and an areflexic bladder who can achieve a measurable increase in intravesical pressure by straining and/or Credit but who cannot empty the bladder adequately by these maneuvers. Some urologists still prefer to resect the bladder neck whenever signs of outlet obstruction are associated with a neuropathic bladder, and treat other areas of outlet resistance later, if this proves necessary.20,48 In a patient with a suprasacral lesion whose bladder is still areflexic after three months, but in whom reflex contractions are expected to develop eventually, resection may be done to facilitate early catheter removal; this can be followed, if necessary, by a procedure to decrease resistance at the level of the distal mechanism.13J5 Techniques of resection include: (1) a thorough circumferential resection of all tissue between the internal orifice and the verumontanum; (2) a limited resection of dorsal tissue from the 3-o’clock through 9-o’clock position; (3) a resection further limited to the posterior lip; and (4) transurethral incisions of the bladder neck at the 5-o’clock and ‘i-o’clock positions. It is generally agreed that any prostatic tissue prolapsing into the lumen after the resection should be removed. Under-resection rather than overresection is generally advised, since multiple resections involve little morbidity. Satisfactory results occur in 60 to 90 per cent of patients selected and treated in this manner 78,47,48 comprising 10 to 20 per cent of all patients with neurogenic bladder dysfunction in most authors’ series. Hemorrhage, extravasation, epididymo-orchitis, and other complications are uncommon. The operation can be performed in children.50 It is seldom necessary in females.

performed the first transurethral bladder neck resection in a patient with neurogenic bladder dysfunction in 1937, and for years this procedure represented the first line of surgical attack in cases of poorly balanced bladder function. The current view is that this operation is useful primarily for two groups of pa-

Y-V-plasty of bladder neck. A simple Y-Vplasty of the bladder neck can accomplish the same effect as a transurethral resection and is especially appropriate when an open surgical procedure is required to correct a concomitant disorder, such as vesicoureteral reflux.8*48,50 It is rarely performed as an independent procedure. A radical Y-V-plasty of the bladder neck can be used to render a refractory, poorly emptying bladder totally incontinent, a condition which can then be managed by an external collection

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Decreasing outlet resistance Transurethral Emmett46 neck.

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device or by the implantation sphincter. 51,52

of a prosthetic

Pharmacologic inhibition of bladder neck. The fact that certain sympatholytic drugs (reserpine and phenoxybenzamine hydrochloride) may facilitate voiding in certain patients was first noted in 1970 by Kleeman.53 Krane and 01sson54,55 subsequently further described a physiologic internal sphincter which is contributed to at least partly by a tonic neurogenic effect on alpha-adrenergic receptors in the smooth muscle of the bladder neck and They successfully used proximal urethra. phenoxybenzamine, an alpha-adrenergic blocking agent, to correct a specific type of emptying failure secondary to neuropathic bladder dysfunction. Six patients without prostatic hypertrophy and without a spastic external sphincter who could not void effectively with cholinergic stimulation were treated with phenoxybenzamine, 10 to 30 mg. daily, alone or together with bethanechol chloride. All but one of these patients established good voiding patterns that persisted for up to fifteen months. Additional reports of successful alpha-adrenolytic therapy, both in adults and in children (given 0.3 to 0.5 mg. of phenoxybenzamine per kilogram body weight per day) have appeared,50,56,57 and the number will undoubtedly increase. Side effects include drowsiness and orthostatic hypotension, both of which tend to lessen with time, and loss of ejaculatory ability. External sphincterotomy. Therapeutic destruction of the external urethral sphincter was first performed in 193658 in a patient with nonspastic obstruction. Although this procedure was mentioned again in 1943,5g the first large clinical series was reported in 1958 by Ross, Gibbon, and Damanski.” Their series has subsequently been expanded to more than 150 patients,61,62 and other large63+!5 and smalleP6* series have been reported. The primary indication for this procedure is the failure of the bladder to empty in a patient with a suprasacral lesion and good detrusor contractions where prostatic obstruction and obstructive inflammatory lesions at the bladder neck have been ruled out.62 Cystourethrograp hit demonstration of obstruction at the level of the external sphincter in these patients 61 has been confirmed by urethral pressure profile studies pre- and postoperatively. 6g,70In patients with sacral lesions, if procedures designed to decrease resistance at the bladder neck fail to produce adequate emptying at low intravesical pressures,62 external

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sphincterotomy may be used as an adjunct to measures to increase intravesical pressure. Techniques of resection vary. Gibbon13,62 makes incisions at the 5-o’clock and 7-o’clock positions with a knife electrode using minimal coagulating current. Schellhammer, Hackler, and Bunts64,65 recommend making incisions from just proximal to the verumontanum to the proximal bulbous urethra at the &o’clock and 9-o’clock positions with a cutting current followed by coagulation. Other techniques include incisions at 2, 4, 8, and 10 o’clock;14 at 11 and 1 o’clock;71 and a single incision at the I2-o’clock position. ‘* The presence of collapsed apical prostatic tissue in the fossa after posterolateral incisions have been made usually calls for resection. Repeat sphincterotomy may be necessary due to initial or late failure. A substantial improvement in bladder emptying has occurred in 70 to 90 per cent of reported cases. 13~14,61-68 Upper tract deterioration is rare after a successful sphincterotomy, and vesicoureteral reflux, if present, often disappears because of lower voiding pressures and the reduced incidence of infection in a catheterless patient with a low residual urine. An external collecting device is generally worn postoperatively. Disagreement exists, however, as to the incidence of total dripping incontinence or severe stress incontinence. Some authors62,73 claim that these conditions are rare, other?* report an incidence approaching 80 per cent, and many make no comment whatever about postoperative incontinence. Since most of the patients selected to undergo this procedure have preoperative incontinence secondary to reflex contractions only, and have a competent bladder neck and intrinsic urethral mechanism, the occurrence of these types of incontinence after division of only the external striated sphincter is puzzling. In fact, reflex incontinence may be less likely postoperatively, since with better emptying the threshold pressure for eliciting a reflex contraction will be reached less frequently. Other complications of sphincterotomy include hemorrhage and urinary extravasation (both uncommon). Recently, erectile impotence has been reported. In one retrospective study74 impotence was noted in 8 of 25 patients. Kiviat’l reported a 29-per cent incidence of permanent impotence after a 3- and 9-o’clock sphincterotomy and attributed it to injury to the deep and dorsal corporal arteries. None of his patients who had incisions at the ll- and I-o’clock posi-

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tions was impotent postoperatively. Since reflexogenic erections, either spontaneous or due to external stimulation, occur in more than 90 per cent of patients with suprasacral spinal and proscord injuries, ‘5 further retrospective pective investigation into the true incidence of iatrogenic impotence with different techniques and types of current is definitely warranted. If only the external sphincter is severed, it is difficult to theorize a mechanism whereby the ability to achieve an erection would be compromised. UrethruZ overdilation. External sphincterotomy is seldom necessary in females, since urethral overdilation to 40 to 50 F usually achieves the same objective. I3 In young boys a similar stretching of the posterior urethra can be accomplished through a perineal urethrostomy, obviating or postponing the need for a sphincterotomy. 5o Pudendal nerve interruption. Relief of an obstruction at the level of the striated external sphincter can also be achieved by a pudendal in 1899 by neurectomy, first d escribed Rochet.‘6 This procedure can be used especially in children, in whom external sphincterotomy may be difficult, 76,77 and is also useful in adults.7”-81 According to Engel and Schirmer,‘l the most suitable patient is one with a supranuclear lesion, a good detrusor reflex, clear evidence of outflow obstruction, and a voiding pattern that improves after a unilateral pudendal block. In their series of 23 such patients, 18 had excellent results after a unilateral pudendal neurectomy that severed only the median branch of the nerve supplying the external urethral sphincter. Bilateral nerve section results in an unacceptably high rate of impotence and sometimes in fecal and urinary incontinence 8,13,15,81 Pharmacologic inhibition of distal urethral mechanism. Unfortunately, there is no pharmaceutical agent that will selectively relax the musculature of the pelvic floor. Although centrally acting muscle relaxants, such as diazepam (Valium) and chlordiazepoxide hydrochloride (Librium), methocarbamol (Rbbaxin), and orphenadrine citrate (Norflex), are used to inhibit skeletal spasm,8’82 spasticity of the external urethral sphincter is rarely controlled on a longterm basis with any of these drugs alone. Though free of autonomic side effects, all of them commonly produce sedation and drowsiness, especially when taken in the large oral

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doses required to control the skeletal spasticity associated with suprasacral spinal cord lesions. Dantrolene sodium (Dantrium), a relatively new skeletal muscle relaxant, has a direct action on skeletal muscle and appears to alleviate the spasticity associated with upper motor neuron lesions.82 It has no autonomic side effects, but it does tend to induce a generalized weakness of the skeletal musculature, which may be severe enough to compromise its therapeutic benefits. Whether or not it will prove useful in treating spasticity of the periurethral striated muscle remains to be seen. Some patients with an areflexic bladder and a flaccid pelvic floor due to a conus or cauda equina lesion can open the bladder neck by straining but are unable to empty the bladder because of a functional obstruction in the posterior urethra. In a recent report of such patients, alpha-adrenergic blockade with phentolamine (Regitine) resulted in relaxation of this area and adequate emptying.83 This result indicates that at least some of the outflow resistance in the posterior urethra involves smooth muscle under alpha-adrenergic stimulation, an idea originally suggested by Donker, Ivanovici, and Noach.84 More sophisticated methods of diagnosing the level of functional obstruction may help to identify those patients likely to benefit by this form of treatment. lntermittent

catheterization

Intermittent catheterization has proved to be the most effective means of attaining a catheterfree state in the majority of patients with acute spinal cord lesions. 85-88 It is also an effective method of treating the adult or child whose bladder fails to empty, especially when efforts to increase intravesical pressure and decrease outlet resistance have been unsuccessfu18’ In those patients who have inadequate urine storage or reflex or stress incontinence with inadequate emptying, it may also be used successfully if the dysfunction can be converted pharmacologically or surgically solely to one of emptying.8g-g3 Intermittent catheterization requires a cooperative, well-motivated patient or family. It is difficult to accomplish if the patient lacks hand control or cannot achieve adequate urethral exposure because of pronounced spasticity of the leg muscles. We have been satisfied with clean rather than sterile catheterization. Close follow-up is necessary. Patients should be maintained on urinary suppressive medication, and

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acute symptomatic infections should promptly and appropriately managed.

be

store urine adequately to one that fails to empty, a condition that can then be corrected by external compression maneuvers or by intermittent catheterization. 16*go,g8The usual dosage of imipramine is 25 mg. four times daily in adults and 5 to 10 mg. four times daily (not to exceed 1.5 to 2 mg. per kilogram per dose) in children. Side effects include dry mouth, blurred vision, constipation, tachycardia, excessive sweating, fatigue, tremor, and headache.

Urinary diversion As a last resort, continuous catheterization or urinary diversion may be necessary to circumvent emptying or storage failure. Therapy to Facilitate Urine Storage

Ephedrine, which causes the peripheral release of norepinephrine as well as direct stimulation of alpha and beta receptors,lo4 would be expected to facilitate urine storage in the same manner as imipramine. Its clinical effectiveness in the treatment of incontinence has been ascribed to stimulation of alpha receptors in the urethra, lo5 and no effect on detrusor hypertonicity has been reported. Perhaps the effect of imipramine on hypertonicity is due to the intracellular inhibition previously mentioned rather than to a beta-adrenergic effect on the musculature of the bladder corpus.

Inhibiting bladder contractility Pharmacologic manipulation. Atropinic and antimuscarinic agents produce a competitive blockade of acetylcholine receptors, primarily at postganglionic autonomic effector sites.94 Propantheline bromide (Pro-Banthine) is the agent most commonly used to achieve this effect; it does, however, possess some ganglionic blocking (nicotinic) activity. Propantheline bromide is used primarily to block uninhibited bladder contractions in adults and children.23,94,g5 The usual initial dosage is 15 mg. every four to six hours in adults and 7.5 mg. every four to six hours in children. Imipramine hydrochloride (Tofranil) has proved useful in decreasing detrusor hypertonicity in adults and children,g6-g8 as well as in the management of enuresis. gg~looIts peripheral action on the bladder may be due to a block of norepinephrine reuptake by adrenergic nerve terminals (an effect as yet demonstrated only in the central nervous system). lo1 Theoretically, stimulation of the predominantly betaadrenergic receptors in the bladder corpus would decrease smooth muscle tone and increase the accommodation capacity.26,2g-32 A similar stimulation of the bladder base and proximal urethra, where alpha receptors predominate, would augment the activity of the physiologic internal sphincter. 26,53V55*102,103 Both of these effects would tend to promote urine storage. Imipramine may also have a direct inhibitory intracellular effect, for it has been shown to block the response of bladder muscle in vitro to both bethanechol chloride and barium chloride.‘03 In our experience it has been especially useful when inadequate urine storage has been secondary to bladder hypertonicity rather than to uninhibited contractions. 16,g8 If both conditions exist, imipramine may be administered along with propantheline bromide. We have found this combination especially useful in converting a bladder that fails to

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Musculotropic relaxants such as flavoxate hydrochloride (Urispas)‘06~‘07 and oxybutynin chloride (Ditropan)‘08*10g are thought to act directly on smooth muscle at an intracellular site distal to the cholinergic receptor mechanism.lo3 Polysynaptic inhibitors such as hydramitrazine (Lisidonil)23 and lioresol, a derivative of gamma aminobutyric acid, ‘lo are thought primarily to exert an inhibitory effect on shinal interneurones without affecting neuromuscular transmission. Although some clinical success23,110 has been claimed with both classes of inhibitors, additional double-blind studies are needed to prove their value in the treatment of uninhibited contractions and detrusor hypertonicity in neuropathic bladder disease.

Interruption of innervation. Subarachnoid alcohol block is not used solely for urologic indications but is used to convert a state of severe somatic spasticity to flaccidity and to abolish autonomic dysreflexia. 5-8 As a byproduct, a reflex neurogenic bladder will usually be converted to an areflexic autonomous one which can be emptied by methods described previously or by intermittent catheterization. In 8 of 29 patients in Gibbon’s7 series and in 7 of 11 patients in that of Misak et al. ‘11 an autonomous bladder developed that emptied without further surgical or medical treatment. Additional therapy, when necessary, was directed at increasing intravesical pressure and decreasing outlet resistance. The presence of a well-balanced reflex bladder

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is a contraindication to this nonselective procedure, as is the ability to achieve an erection, a function usually lost as a result.5-8 In most cases bilateral anterior and posterior sacral rhizotomy or conusectomy will also conhypertonic bladder to an vert a hyperreflexic, autonomous one.“1,“2 Adequate emptying was achieved in 23 of 28 such patients treated by Misak et al.“’ but 13 required subsequent catheterization because of persistent vesicoureteral reflux, or hypersensitivity to or technical difficulty with the required collecting device. Erections were lost or impaired in 85 per cent of patients who were potent preoperatively. A temporary impairment of bowel function, lasting six to twelve weeks, also occurred postoperatively. Selective sacral nerve section is thought to increase bladder capacity by abolishing only the motor supply responsible for uninhibited contractions, leaving sphincter and sexual function intact. The initial use of this procedure followed the observation by Heimburger, Freeman, and Wilde in 1948113 that the third sacral anterior root provides the dominant motor innervation of the human bladder. To enhance the clinical response and minimize side effects, differential sacral rhizotomy should be preceded by stimulation and blockade of the individual sacral roots with cystometric and sphincterometric control. Rockswold, Bradley, and Chou114 and Torrens and Griffithn5 described their experiences with differential sacral rhizotomy. Of Torrens’ 9 cases, 2 were unequivocal failures, 2 were successes, and 5 were “improved.” No significant postoperative disturbance of bowel or sexual function occurred. This procedure would appear, however, to be of limited value in treating patients with increased outflow resistance unless this, too, is reduced or eliminated. Increasing

outlet resistance

Pharmacologic manipulation directed at the bladder neck and urethra (alpha-adrenergic stimulation) has already been mentioned. A prosthetic sphincter may be used to produce continence by means of mechanical compression at the level of the bladder neck or urethra.116,117 However, all 7 failures in Scott’s”6 initial series of 34 patients occurred in those with neurogenic bladder dysfunction. Marked detrusor hyperreflexia will cause cuff deflation and leakage, and satisfactory results are achieved in these patients only if they are first rendered totally incontinent.

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There is no drug available that will selectively increase the contractility of the striated pelvic floor and periurethral musculature. Electrical stimulation of these structures to produce continence has been tried since 1963.“* Since, as Merrill, Conway, and DeWolfng have pointed out, the stimulation is not to the pelvic floor musculature directly but indirectly through the motor pudendal nerve, the lack of success in treating patients with lower motor neuron lesions is not surprising. Such a device would also be of limited use in patients with complete upper motor neuron lesions, who are incontinent because of reflex contractions and usually already have pelvic floor spasticity. Merrill and his associates do not recommend the use of electronic stimulation to produce continence in patients with paraplegia and myelomeningocele. Spotty disease of the corticoregulatory tracts with uninhibited contractions appears to be the only type of neuropathic bladder dysfunction to which this technique is applicable. Problem

of Vesicoureteral

Reflux

The potentially deleterious effects of vesicoureteral reflux on the upper tracts of patients with neuropathic bladder dysfunction, especially those with poor voiding ability and infection, are emphasized by Donnelly, Hackler, and Buntseg The true incidence of reflux in these patients is unknown, and estimates range from as low as 7 per cent to as high as 38 per cent8-10 Reflux is usually reversible if infection is eradicated and efficient voiding at low intravesical pressures restored. 13~15~120Hackler,” however, estimated that there is a 15-per cent incidence of irreversible reflux after five to ten years of paraplegic life. If conservative therapy fails, surgical intervention is indicated in selected cases, even though the success rate is not as great as in patients without neuropathic bladders.‘20J21 Using a modification of the Hutch I procedure in patients with good bladder capacities (150 cc.), well-balanced bladder function, and normal upper tracts, Reece and Hackler12* achieved an impressive success rate of 73 per cent in 92 refluxing units. The serious potential of vesicoureteral reflux is demonstrated by the fact that in 80 per cent of the 27 renal units that continued to reflux in this series, upper tract deterioration developed despite catheter drainage. In those patients having a successful antireflux procedure, more than 90 per cent of the renal units remained stable. If

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reflux persists on one side, a transureteroureterostomy can be done. Hackle?’ reported renal deterioration in only 1 of 11 such cases. Advocacy of antireflux procedures in patients with neuropathic bladder dysfunction is by no means universal, however. Bors and Comarr* are among those who advise against this mode of treatment. Place of Continuous Catheter Drainage and Urinary Diversion Continuous catheter drainage or urinary diversion is seldom necessary in patients with neurogenic bladder disease and is considered a last resort. Unequivocal indications include upper urinary tract deterioration or deleteriously poor emptying that cannot be reversed or stabilized by more conservative therapy directed at the bladder or outlet.‘3~15~‘22~123 Unmanageable vesicoureteral reflux with infection usually leads to renal deterioration and therefore necessitates some form of continuous drainage. The presence of an abscess or fistula that makes the lower urinary tract unusable as a reservoir or conduit obviously calls for supravesical diversion. Intractable, intolerable incontinence, especially in a female, may also be a reasonable indication for diversion or catheter drainage. For patients who have progressive or malignant disease or uremia, or who are unable or unwilling to undergo certain surgical procedures, a permanent indwelling catheter may be necessary and preferable. Gibbon13 found this to be necessary in 4 per cent of his patients. If a cutaneous ureterostomy is not possible, ureteroileostomy, first performed in 1935 and popularized in 1950, lz4 has become the standard by which all other forms of supravesical diversion are judged. lz2 Although numerous wellknown complications of the urinary and intestinal tracts may occur, this procedure is usually satisfactory in terms of upper tract stabilization or improvement. 122-127 The colonic conduit, especially with an antireflux ureteroenteral anastomosis (possible only with undilated ureters), may prove to have fewer complications. l**13* It should be noted, however, that the percentage of patients having subsequent upper tract deterioration (determined by radiographic and chemical criteria) after an ileal conduit depends on the length of the postoperative follow-up period. 133 Ten to fifteen years must elapse before the final attributes of any supravesical diversion can be evaluated, especially

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since this time period represents the peak incidence of renal deterioration, at least after spinal cord injuries.* In most recently reported large series, the percentage of adults undergoing urinary diversion for neurogenic bladder dysfunction is low, ranging from 1 to 3 per cent.10,‘3,14 This procedure can be expected to remain infrequent owing to a more sophisticated appreciation of the neuromuscular and neuropharmacologic factors responsible for inadequate bladder emptying or storage and more precise methods of diagnosis and treatment. Hospital of the University of Pennsylvania Suite W-310 White Building Philadelphia, Pennsylvania 19104 (DR. WEIN) References 1. TRIBE, C. R., and SILVER, J. R.: Renal Failure in Paraplegia, London, Pitman Co., 1969. 2. JAMESON, R. M.: Management of the bladder in non-traumatic paraplegia, Paraplegia 12: 92 (1974). 3. BOYARSKY, S. : The neurogenic bladder (editorial comment), in Boyarsky, S., Ed.: The Neurogenic Bladder, Baltimore, Williams and Wilkins Company, 1967, p. 183. 4. TALBOT, H. S.: The physiological approach to neurogenic vesical dysfunction, in Boyarsky, S., Ed. : ibid. ,3 pp. 183-186. 5. BORS, E.: Neurogenic bladder, Urol. Surv. 7: 177 (1957). 6. COMARR, A. E.: The practical urologic management of the patient with spinal cord injury, Br. J. Urol. 31: 1 (1959). 7. GIBBON, N.: Management of the bladder in acute and chronic disorders of the nervous system, Acta Neurol. Stand. [Suppl.] 42: 133 (1966). 8. BORS, E., and COMARR, A. E.: Neurological Urology, Baltimore, University Park Press, 1971. 9. DONNELLY, J., HACKLER, R. H., and BUNTS, R. c.: Present urologic status of World War II paraplegic: 25-year followup. Comparison with status of the 20-year Korean War paraplegic and 5-year Vietnam paraplegic, J. Urol. 108: 558 (1972). 10. HACKLER, R. H.: Spinal cord injuries: urologic care, Urology 2: 13 (1973). 11. LAPIDES, J.: Neurogenic bladder: principles of treatment, Urol. Clin. North Am. 1: 81 (1974). 12. ROSSIER, A. B.: Neurogenic bladder in spinal cord injury: management of patients in Geneva, Switzeribid. 1: 125 land and West Roxbury, Massachusetts, (1974). 13. GIBBON, N. 0. K.: Neurogenic bladder in spinal cord injury: management of patients in Liverpool, England, ibid. 1: 147 (1974). 14. O’FLYNN, I. D.: Neurogenic bladder in spinal cord injury: management of patients in Dublin, Ireland, ibid. 1: 135 (1974). 15. GIBBON, N. 0. K.: Later management of the paraplegic bladder, Paraplegia 12: 87 (1974). 16. DUCKETT, J. W., JR., and RAEZER, D. M.: Neuromuscular dysfunction of the urinary bladder, in

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Kelalis, P. P., and King, L. R., Eds.: Pediatric Urology, Philadelphia, W. B. Saunders, in press. QUESADA, E. M., SCOTT, F. B., and CARDUS, D.: Functional classification of neurogenic bladder dysfunction, Arch. Phys. Med. Rehabil. 49: 692 (1968). EMMETT, J. L.: Urinary retention from imbalance of detrusor and vesical neck: treatment by transurethral resection, J. Urol. 43: 692 (1940). TURNER-WARWICK, R. T., and WHITESIDE, C. G.: Investigation and management of bladder neck dysfunction, in Riches, E., Ed.: Modern Trends in Urology - 3, New York, Appleton-Century-Crofts, 1970, pp. 295-311. GLAHN, B. E.: Neurogenic bladder in spinal cord injury: management of patients in Hornback, Denmark, Urol. Clin. North Am. 1: 163 (1974). LEE, C. W.: The clinical use of urecholine in dysfunction of the bladder, J. Urol. 62: 300 (1949). LAPIDES, J., et al. : Further observations on pharibid. 79: 707 macologic reactions of the bladder, (1958). PEDERSEN, E., and GRYNDERUP, V.: Clinical pharmacology of the neurogenic bladder, Acta Neurol. Stand. [~uppl.] 42: 111 (1966). URSILLO, R. C.: Rationale for drug therapy in bladder dysfunction, in Boyarsky, S., Ed., ibid. ,3 pp. 187- 190. KOELLE, G.: Parasympathomimetic agents, in Goodman, L. S., and Gilman, A., Eds.: The Pharmacologic Basis of Therapeutics, New York, Macmillan Company, 1975, pp. 467-476. RAEZER, D. M., WEIN, A. J., JACOBOWITZ, D., and CORRIERE, J. N.,_ JR.: Autonomic innervation of canine urinary bladder, Urology 2: 211 (1973). LAPIDES, J., FRIEND, C. R., AJEMMIAN, E. P., and SONDA, L. P.: Comparison of action of oral and parenteral bethanechol chloride upon the urinary bladder, Invest. Urol. 1: 94 (1963). GIBBO~V, N. 0. K: Urinary incontinence in disorders of the nervous system, Br. J. Ural. 37: 624 (1965). DE GROAT, W. C., and SAUM, W. R.: Adrenergic inhibition in mammalian parasympathetic ganglia, Nature New Biol. 231: 188 (1971). EDVARDSEN, P.: Nervous control of the urinary bladder in cats, Acta Neurol. Stand. 43: 343 (1967). LEONI, J. V., WEIN, A. J., RAEZER, D. M., and SCHOENBERG, H. W.: The effect of beta adrenergic stimulation on the contractile response of canine detrusor muscle, Invest. Ural. 10: 419 (1973). WEIN, A. J., et al. : Sympathetic innervation and chemical sympathectomy of canine bladder, Urology 4: 27 (1974). HARTVIKSEN, K.: Discussion, Acta Neurol. Stand. [Suppl.] 42: 180 (1966). DEES, J. D.: Contraction of the urinary bladder produced by electric stimulation: preliminary report, Invest. Urol. 2: 539 (1965). BRADLEY, W., CHOU, S., and FRENCH, L.: Further experience with the neurotransmitter receiver unit for the neurogenic bladder, J. Neurosurg. 20: 953 (1963). BOYCE, W. H., LATHEM, J. E., and HUNT, L. D.: Research related to the development of an artificial electrical stimulator for the paralyzed human bladder: a review, J. Urol. 91: 41 (1964).

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M., CARDUS, D., and LASKOWSKI, T. : Electronic bladder stimulation: dog and human experiments, Invest. Urol. 3: 231 (1965). HALD, T., et (I/. : Clinical experience with a radio linked bladder stimulator, J. Urol. 97: 73 (1967). STENBERG, C. C., BURNETTE, H. W., and BUNTS, R. C.: Electrical stimulation of human neurogenic bladders: experience with four patients, ibid. 97: 79 (1967). MERRILL, D. C., and CONWAY, C. J.: Clinical experience with the Mentor bladder stimulator. I. Patients with upper motor neuron lesions, ibid. 112:52 (1974). MERRILL, D. C.: Clinical experience with the Mentor bladder stimulator. II. Meningomyelocele patients, ibid. 112:823 (1974). IDEM: Clinical experience with the Mentor bladder stimulator. III. Patients with urinary vesical hypotonia, ibid. 113:335 (1975). HALVERSTADT, D. P., and PARRY, W. L.: Electronic stimulation of the human bladder: 9 years later, ibid. 113: 341 (1975). GRIMES, J. H., NASHOLD, B. S., and CURRIE, D. P.: Chronic electrical stimulation of the paraplegic bladder, ibid. 109:242 (1973). GRIMES, J. H., NASHOLD, B. S., and ANDERSON, E. E.: Clinical application of electronic bladder stimulation in paraplegics, ibid. 113:338 (1975). EMMETT, J. L.: Transurethral resection in treatment of true and pseudo cord bladder, ibid. 53: 4 (1945). GIBBON, N. 0. K., Ross, J. C., and DAMANSKI, M. : Bladder neck resection in the paraplegic: report of over 100 cases, Paraplegia 2: 264 (1965). BUNCE, P. L.: Transurethral resection and Y-Vplasty for neurogenic bladder, in Boyarsky, S., Ed., ibid. ,3 pp. 196- 199. TSUJI, I., NAKAJIMA, F., NISHIDA, T., and ABE, N.: Neurogenic bladder in spinal cord injury: management of patients in Hokkaido, Japan, Urol. Clin. North Am. 1: 139 (1974). Congenital JOHNSTON, J. H., and FARKAS, A.: neuropathic bladder: practicalities and possibilities of conservational management, Urology 5: 719 (1975). SCOTT, F. B., BRADLEY, W. H., and TIMM, G. W.: Treatment of urinary incontinence by an implantable prosthetic urinary sphincter, J. Urol. 112: 75 (1974). ALLEN, T. D.: Neurogenic bladder of paraplegic patient: management with radical Y-V-plasty, Urology 5: 216 (1975). KLEEMAN, F. J. : The physiology of the internal urinary sphincter, J. Urol. 104: 549 (1970). KRANE, R. J., and OLSSON, C. A.: Phenoxybenzamine in neurogenic bladder dysfunction. I. A theory of micturition, ibid. 110:650 (1973). IDEM: Phenoxybenzamine in neurogenic bladder dysfunction. II. Clinical considerations, ibid. 110: 653 (1973). STOCKAMP, K. : Treatment with phenoxybenzamine of upper urinary tract complications caused by intravesical obstruction, ibid. 113: 128 (1975). STOCKAMP, K., and SCHREITER, F.: Alpha adrenolytic treatment of the congenital neuropathic bladder, Urol. Int. 30: 33 (1975).

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The bladder function in spinal injury, Br. J. Surg. 23: 734 (1936). BAUMRAUCKER, G. 0.: Management of the paralyzed bladder, Arch. Surg. 56: 484 (1948). Ross, J. C., GIBBON, N. 0. K., and DAMANSKI, M.: Division of the external urethral sphincter in the treatment of the paraplegic bladder: a preliminary report on a new procedure, Br. J. Urol. 30: 294 (1958). IDEM: Division of the external sphincter in the treatment of the neurogenic bladder: a ten year review, ibid. 30: 294 (1958). GIBBON, N. 0. K.: Division of the external sphincter, ibid. 45: 110 (1973). CURRIE, R. J., BILBISI, A. A., SCHIEBLER, J. C., and BUNTS, R. C.: External sphincterotomy in paraplegics: technique and results, J. Urol. 103: 64 (1970). SCHELLHAMMER, P. F., HACKLER, R. H., and BUNTS, R. C.: External sphincterotomy: an evaluation of 150 patients with neurogenic bladder, ibid. 110: 199 (1973). IDEM: External sphincterotomy: rationale for the procedure and experience with 150 patients, Paraplegia 12: 5 (1974). MALAMENT, M.: External sphincterotomy in neurogenic bladder dysfunction, J. Urol. 108: 554 (1972). KOONTZ, W. W., JR., SMITH, M. V. J., and CURRIE, . External sphincterotomy in boys with meninior&elocele, ibid. 108:649 (1972). HERR, H. W., ENGLEMAN, E. R., and MARTIN, D. C.: External sphincterotomy in traumatic and nontraumatic neurogenic bladder dysfunction, ibid. 113: 32 (1975). ROSSIER, A. B., and OTT, R.: Urinary manometry in spinal cord injury: a followup study. Value of cystosphincterometrography as an indication for sphincterotomy, Br. J. Urol. 46: 439 (1974). ABEL, B. J., Ross, J. C., GIBBON, N. 0. K., and JAMESON, R. M.: Urethral pressure measurement after division of the external sphincter, Paraplegia 13: 37 (1975). Transurethral sphincterotomy: relaKIVIAT, M.: tionship of site of incision to postoperative potency and delayed hemorrhage, J. Urol. 114: 399 (1975). MADESBACHER, H., and SCOTT, F. B.: Twelve o’clock sphincterotomy: technique, indications, results, Urol. Int. 30: 75 (1975). SCHELLHAMMER, P. F. : Personal communication, 1976. SCHOENFELD, L., CARRION, H. M., and POLITANO, V. A.: Erectile impotence: complication of external sphincterotomy, Urology 4: 681 (1974). COMARR, A. E.: Sexual concepts in traumatic cord and cauda equina lesions, J. Urol. 106: 375 (1971). STARK, G.: Pudendal neurectomy in management of neurogenic bladder in myelomeningocele, Arch. Dis. Child. 44: 698 (1969). MULHOLLAND, S. G., YALLA, S. V., RAEZER, D. M., and DUCKETT, J. W., JR.: Primary external urethral sphincter hyperkinesia in a boy, Urology 4: 577 (1974). Ross, J. C., and DAMANSKI, M.: Pudendal neurectomy in the treatment of the bladder in spinal injury, J. Urol. 25: 45 (1953).

79. BORS, E., and COMARR, A. E.: Effect of pudendal nerve operation on the neurogenic bladder, ibid. 72: 666 (1954). 80. KLEEMAN, F. J., and CHUTE, R.: A plan for the evaluation of patients with bladder dysfunction and the use of pudendal neurectomy in selected cases, ibid. 97:1029 (1967). 81. ENCEL, R. M. E., and SCHIRMER, H. K. A.: Pudendal neurectomy in neurogenic bladder, ibid. 112: 57 (1974). 82. FRANZ, D. N.: Drugs for Parkinson’s disease: centrally acting muscle relaxants, in Goodman, L. S., and Gilman, A., Eds., ibid.,25 pp. 221-244. 83. ABEL, B. J., JAMESON, R. M., GIBBON, N. 0. K., and KRISHNAN, K. R.: The neuropathic urethra, Lancet 2: 1229 (1974). 84. DONKER, P. J., IVANOVICI, F., and NOACH, E. L.: Analyses of the urethral pressure profile by means of electromyography and the administration of drugs, Br. J. Urol. 44: 180 (1972). 85. GUTTMAN, L.: Spinal cord injuries: discussion on the treatment and prognosis of traumatic paraplegia, Proc. Roy. Sot. Med. 40: 219 (1949). 86. GUTTMAN, L., and FRANKEL, H. L.: The value of intermittent catheterization in the early management of traumatic paraplegia and tetraplegia, Paraplegia 4: 63 (1966). 87. COMARR, A. E. : Intermittent catheterization for the traumatic cord bladder patient, J. Ural. 108: 79 (1972). 88. FRANKEL, H. L.: Intermittent catheterization, Urol. Clin. North Am. 1: 115 (1974). 89. LAPIDES, J., DIOKNO, A. C., LOWE, B. S., and KALISH, M. D.: Follow-up on unsterile, intermittent self-catheterization, J. Urol. 111: 184 (1974). 90. WEIN, A. J., RAEZER, D. M., BENSON, G. S., and MURPHY, J. J.: At-home intermittent self catheterization in the treatment of patients with neuromuscular bladder dysfunction, Proc. Kimbrough Ural. Sem. 8: 41 (1974). 91. RABINOVITCH, H. H.: Bladder evacuation in child with meningomyelocele, Urology 3: 425 (1974). 92. LYON, R. P., SCOTT, M. P., and MARSHALL, S.: Intermittent catheterization rather than urinary diversion in children with myelomeningocele, J. Urol. 113: 409 (1975). 93. HERR, H. W.: Intermittent catheterization in neurogenic bladder dysfunction, ibid. 113: 477 (1975). 94. INNES, I. R., and NICKERSON, M.: Atropine, scopalamine, and related antimuscarinic drugs, in Goodman, L. S., and Gilman, A., Eds., ibid.,25 pp. 514-532. 95. DIOKNO, A. C., HYNDMAN, C. W., HARDY, D. A., and LAPIDES, J.: Comparison of action of imipramine (Tofranil) and propantheline (Probanthine) on detrusor contraction, J. Urol. 107: 42 (1972). 96. HEOCK, E.: Discussion, Acta Neurol. Stand. [Sup~1.1 42: 180 (1966). 97. COLE, A. T., and FRIED, F. A.: Favorable experiences with imipramine in the treatment of neurogenic bladder, J. Urol. 107: 44 (1972). 98. RAEZER, D. M., BENSON, G. S., WEIN, A. J., and DUCKETT, J. W., JR.: The functional approach to the management of the pediatric neuropathic bladder - a clinical study. Submitted for publication.

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R. E. G.: Imipramine hydrochloride and enuresis, Am. J. Psychiat. 117:551 (1960). 100. MILLER, P., CHAMPELLI, J., and DINELLO, F.: A double blind study of imipramine in the treatment of enuretic schoolchildren, Am. J. Dis. Child. 115: 17 (1968). 101. BYCK, R.: Drugs and the treatment of psychiatric disorders, in Goodman, L. S., and Gihnan, A., Eds., ibid. ,25 pp. 152-200. 102. MAHONEY, D. T., LAFERTE, R. O., and MAHONEY, J. E.: Observations on sphincter augmenting effect of imipramine in children with urinary incontinence, Urology 1: 317 (1973). 103. BENSON, G. S., SARSHIK, S. A., RAEZER, D. M., and WEIS, A. J.: Comparative effects and mechanisms of action of atropine, propantheline, flavoxate, and imipramine on bladder muscle contractility. Submitted for publication. 104. INNES, I. R., and NICKERSON, M.: Norepinephrine, epinephrine, and the sympathomimetic amines, in Goodman, L. S., and Gilman, A., Eds., ibid. ,25 pp. 477-513. 105. DIOKNO, A. C., and TAUB, M.: Ephedrine in treatment of urinary incontinence, Urology 5: 624 (1975). 106. KOHLER, R. P., and MORALES, P. A.: Cystometric evaluation of flavoxate hydrochloride in normal and neurogenic bladder, J. Urol. 100:729 (1968). 107. BHADLEY, D. U., and CAZORT, R. J.: Relief of bladder spasm by flavoxate: a comparative study, J, Clin. Pharmacol. 10: 65 (1970). 108. LISH, P. M., LABUDDE, J. A., PETERS, E. L., and anROBBINS, S. I.: Oxybutynin - a musculotropic tispasmodic drug with moderate anticholinergic action, Arch. Int. Pharmacodyn. 156:467 (1965). a 109. DIOKR’O, A. C., and LAPIDES, J.: Oxybutynin: new drug with analgesic and anticholinergic properties, J. Urol. 108: 307 (1972). 110. KIESSWETTER, H., and SCHOBER, W.: Lioresal in the treatment of neurogenic bladder dysfunction, Urol. Int. 30: 63 (1975). 111. MISAK, S. J., BUNTS, R. C., ULMER, J. L., and EAGLES, W. M.: Nerve interruption procedures in the urologic management of paraplegic patients, J. Urol. 88: 392 (1962). 112. MEIROWSKY, A. M., SCHEIBERT, C. D., and HINCHEB, T. R. : Studies on the reflex arc in paraplegia, I. J. Neurosurg. 7: 33 (1950). 113. HEIMBURGER, R. F., FREEMAN, L. W., and WILDE, N. J.: Sacral nerve innervation of the human bladder, ibid. 5: 154 (1948). 114. ROCKSWOLD, G. L., BRADLEY, W. E., and CHOU, S. N. : Differential sacral rhizotomy in the treatment of neurogenic bladder dysfunction, ibid. 38: 748 (1973). 115. TORRENS, W. J., and GRIFFITH, H. B.: The control 99. MACLEA~V,

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of the uninhibited bladder by selective sacral neurectomy, Br. J. Urol. 46: 639 (1974). 116. SCOTT, F. B., BRADLEY, W. E., and TIMM, G. W.: Treatment of urinary incontinence by an implantable prosthetic sphincter, J. Urol. 112: 75 (1974). 117. HALD, T., BYSTROhl, J,, and ALFTHAN, 0.: Treatment of urinary incontinence by the Scott-BradleyTimm artificial sphincter, Urol. Res. 3: 133 (1975). 118. CALDWELL, K. P. S.: The electrical control of sphincter incompetence, Lancet 2: 174 (1963). 119. MERRILL, D. C., CONWAY, C. C., and DEWOLF, W.: Urinary incontinence: treatment with electrical stimulation of the pelvic floor, Urology 5: 67 (1975). 120. TARABULCY, E., MORALES, P. A., and SULLIVAN, J. F.: Vesicoureteral reflux in paraplegics: results of various forms of management, Paraplegia 10: 44 (1972). 121. REECE, R. W., and HACKLER, R. H.: Vesicoureteroplasty in the paraplegic: long-term followup in 77 patients, J. Urol. 113: 474 (1975). 122. WOODRUFF, M. W., and OBERHEIM, W. S.: Urinary diversion in the treatment of neurogenic bladder, Urol. Clin. North Am. 1: 99 (1974). 123. KOZIOL, I., and HACKLER, R. H.: Cutaneous ureteroileostomy in spinal cord-injured patient: a 15-year experience, J. Urol. 114: 709 (1975). 124. BRICKER, E. M.: Bladder substitution after pelvic evisceration, Surg. Clin. North .4m. 30: 1511 (1950). 125. MURPHY, J. J., and SCHOENBERG, H. W.: Survey of long term results of urinary diversion, Br. J. Urol. 39: 700 (1967). 126. SCHMIDT, J. D., HAWTREY, C. E., FLOCKS, R. H., and CULP, D. A.: Complications, results and problems of ileal conduit diversion, J. Ural. 109: 210 (1973). 127. GREGORY, J. G., GURSAHANI, M., and SCHOENFive-year radiographic review of ileal BERG, H. W.: conduits, ibid. 112:327 (1974). 128. MOGG, R. A.: Treatment of neurogenic urinary incontinence using colonic conduit, Br. J, Urol. 37: 681 (1965). 129. IDEM: Urinary diversion using the colonic conduit, ibid. 39: 687 (1967). 130. KELALIS, P. P.: Urinary diversion in children by the sigmoid conduit, J. Ural. 112: 666 (1974). 131. MORALES, P., and GOLIMBU, M. : Colonic urinary diversion: 10 years of experience, ibid. 113:302 (1975). 132. SKINNER, D. G., GOTTESMAN, J. E., and RICHIE, J, P.: The isolated sigmoid segment: its value in temporary urinary diversion and reconstruction, ihid. 113:614 (1975). 133. SCHWARZ, G. R., and JEFFS, R. D.: Ileal conduit diversion in children: computer analysis of followup from 2 to 16 years, ibid. 114: 285 (1975).

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