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Commentary on Management of Neurogenic Bladder
oozW3.C7/96/1546-1990~.~
Tm:JOURNAL
Vol. 154,1990, December 1995 Printed in U.S.A.
OF UROLOGY
CopyrightQ 1996 by AMERICAN UROLOGICAL. ASSOCIATION, INC.
This Month in Investigative Urology COMMENTARY ON MANAGEMENT OF NEUROGENIC BLADDER Managing the bladder in the patient with altered innervation either from congenital malformation,trauma,or tumor remains a major challenge. Diversion with tubes or &mies has the advantage of short4miting pathophysiology,but at a significant price: appliance failure, infection, calculi and losa of renal function, even cancer. Treatment without diversion, however, can be complex even though the principles are quite simple: 1)ensure a large compliant, continent reBervoir that 2) is easily and completely emptid on a regular basis. Clean intermittent catheterization (CIC) is, perhaps, the single most significant advancement in the treatment of neurogenic bladder. In combination with medications or intestinocyetoplastvCIC has resulted in satisfactory management in the majoriw of these patients these include recurrent i d d o n , stone formation, and is presently our gold standard.However, long-term consequences of CIC re&, potential for upper tract infection and damage. In addition, the problems relating to intestid mucosa in the Urinary tract are well documented. Clearly, improvementsin the methods of lIlLLnagingthe neurogenic bladder can be made. Intuitively, these would focus on true total rehabilitation or reconstruction of the bladder resulting in a h o d ” bladder with “normal” function. Therefore, the goals of management of the neurogenic bladder patient would be to preserve bladder wall structure (includingepithelium) and function through correctionof the neurologic defect. To this point, such goals have been very elusive because the primary dysfunction seems to be, not only altered innervation, but also altered bladder muscle and extracellular matrix. Probably the only true cure for the neurogenic bladder has been realized through the technique of early intravesical bladder stimulation in children with myelodysplasia, which has occasionally resulted in normal bladder function.1 Unfortunately, the process is time and labor intensive with a very small percentage of the patients treated attaining the desired results. Perhaps this relates, in part,to the fact that change in the structure of the bladder wall can relate to a l t e d innervation such that the primary pathology (altered innervation) almostbecomes secondary to chronic changes in the bladder wall (thismay be a direct result of werstimulation or chronic infection or a combination of both, particularly in the first year of life). Many of these changes could be considered analogous to those noted in the patient with chronic prostatic obstruction which, &r relief of obstruction, do not completely revem. An obvious answer would be early correction of the neurologic defect, a process that has been pursued only by the courageous few such as E d Tanagho. In most centers such a process is left to the neurologic surgeons who occasionally can relieve cord tethering or successfully close a myelomeningocele at birth or effectively remove a tumor with resultant salvage of bladder function. Unfortunately, such therapeutic triumphs are rare. More commonly, the urologist is confronted with a bladder which has significant dysfunction due to altered innervation and has relatively few tools other than intermittent catheterization and/or we correct the primary pathophysiology?”. The bladder augmentation. Yet few of us have directly addressed the question, simple truth is, we have no tools to use because we are ignorant of the anatomy and the physiology and, in general, as surgeons, are not well equipped or ready to alter the neuroanatomy of the bladder. William Bradley is probably one of the crusaders to a d b the treatment of the neurogenic bladder through ’neurologic’ manipulation. It was, in part, through his efforts that a commercially available bladder stimulation device was developed.2 The device did prove to be, occasionally, spectacularly effective. However, it had its spectacular failures as well because it was dependent on field depolarization that resulted, not only in detrusor contraction, but also sphincteric and diaphragmatic contractions that caused pain and dyssynergia. Through this early experience it became evident that selectivenerve root stimulation would be necessary to achieve normal debusor function. Dr.E d Tauagho has clearly championed this concept and found that selective stimulation of ventral roots (S2,3,4) with dorsal rhimtomy can result in effective bladder storage and emptying.3 His techniques have been carried to several centers with encouraging results. The paper by Hohenfellner et al. in this issue of The Journal of Urology is clearly a potential extension of this concept, providing a potential for stimulation in patients who have peripheral nerve damage to the bladder (the myelodysplasia patients). The authors show very strong evidence that bladder smooth muscle can be excited with stimulation of a somatic nerve previously implanted into the bladder wall. Theoretically,extension of this work could lead to reinnervation or selective innervation of a neurogenic bladder which, through appropriate stimulation, could be made to function “normally.” Logically, total bladder reconstruction would depend on innervation and, based on this study, the reconstruction of nerve supply could be possible with nerve transplant and stimulation. Realietieally, we are probably some years from true bladder reconstruction or replacement. It doesn’t take much insight, however, to appreciate the fact that appropriate tissue innervation will be critical in these developments. It is fascinating to this editor that, in this model, the implanted femoral nerve so rapidly (within 4 months) and functionally grows into the recipient bladder tissue such that stimulation of the nerve effectively initiates a detrusor contraction (which was previously reported not to be the case4).Furthermore, it is also remarkable that stimulation of the nerve innervating the striated muscle flap on the bladder wall apparently causes a bladder detrusor depolarization. Both demonstrate apparent intracellular connections which would be critical in synthesizing a functional bladder. Evidence for a phenomenon may be seen dufing fluorourodynamics in the augmented bladder where a detrusor contraction seems to carry over onto the augmented segment and occasionally vice versa. These experiments were performed in a model in which bladder innervation was carefully protected, so application to the true neurogenic bladder situation may not be totally d o g o u s . Obviously, we are in the very early stages of our understanding of bladder anatomy and physiology, but concerted efforts are intemifying and the results should be very exciting indeed. Michael E. Mitchell Division of Pediatric Urology University of Washington Seattle, Washington REFERENCES
1. &plan,
W. E., Richards, J. W. and Richards, I.: Intravesical transurethral bladder stimulation to increase bladder capacity. J. Urol., 142:
600, 1989. 2. Bradley, W. E.. Timm. G . W and Chou, S. N.: A decade of experience with electronic stimulation of the micturition reflex. Urol. Int., 26: 283, 1971.
3. Tanagho, E. A., Schmidt. R. A. and Orvis, B. R.: Neural stimulation for control ofvoiding dysfunction: a preliminary report In 22 patients with serious neuropathic voiding disorders. J. Urol., 142: 340. 1989. 4. Rao, C . R., Bruce. A. W., Lynwood, D. W. and Robertson. D. M.: Heinnervation of the neurogenic blatlder \:lth somatic motor nerves. Invest. Urol., 9 59, 1971. 1990
Tm:JOURNAL
Vol. 154,1990, December 1995 Printed in U.S.A.
OF UROLOGY
CopyrightQ 1996 by AMERICAN UROLOGICAL. ASSOCIATION, INC.
This Month in Investigative Urology COMMENTARY ON MANAGEMENT OF NEUROGENIC BLADDER Managing the bladder in the patient with altered innervation either from congenital malformation,trauma,or tumor remains a major challenge. Diversion with tubes or &mies has the advantage of short4miting pathophysiology,but at a significant price: appliance failure, infection, calculi and losa of renal function, even cancer. Treatment without diversion, however, can be complex even though the principles are quite simple: 1)ensure a large compliant, continent reBervoir that 2) is easily and completely emptid on a regular basis. Clean intermittent catheterization (CIC) is, perhaps, the single most significant advancement in the treatment of neurogenic bladder. In combination with medications or intestinocyetoplastvCIC has resulted in satisfactory management in the majoriw of these patients these include recurrent i d d o n , stone formation, and is presently our gold standard.However, long-term consequences of CIC re&, potential for upper tract infection and damage. In addition, the problems relating to intestid mucosa in the Urinary tract are well documented. Clearly, improvementsin the methods of lIlLLnagingthe neurogenic bladder can be made. Intuitively, these would focus on true total rehabilitation or reconstruction of the bladder resulting in a h o d ” bladder with “normal” function. Therefore, the goals of management of the neurogenic bladder patient would be to preserve bladder wall structure (includingepithelium) and function through correctionof the neurologic defect. To this point, such goals have been very elusive because the primary dysfunction seems to be, not only altered innervation, but also altered bladder muscle and extracellular matrix. Probably the only true cure for the neurogenic bladder has been realized through the technique of early intravesical bladder stimulation in children with myelodysplasia, which has occasionally resulted in normal bladder function.1 Unfortunately, the process is time and labor intensive with a very small percentage of the patients treated attaining the desired results. Perhaps this relates, in part,to the fact that change in the structure of the bladder wall can relate to a l t e d innervation such that the primary pathology (altered innervation) almostbecomes secondary to chronic changes in the bladder wall (thismay be a direct result of werstimulation or chronic infection or a combination of both, particularly in the first year of life). Many of these changes could be considered analogous to those noted in the patient with chronic prostatic obstruction which, &r relief of obstruction, do not completely revem. An obvious answer would be early correction of the neurologic defect, a process that has been pursued only by the courageous few such as E d Tanagho. In most centers such a process is left to the neurologic surgeons who occasionally can relieve cord tethering or successfully close a myelomeningocele at birth or effectively remove a tumor with resultant salvage of bladder function. Unfortunately, such therapeutic triumphs are rare. More commonly, the urologist is confronted with a bladder which has significant dysfunction due to altered innervation and has relatively few tools other than intermittent catheterization and/or we correct the primary pathophysiology?”. The bladder augmentation. Yet few of us have directly addressed the question, simple truth is, we have no tools to use because we are ignorant of the anatomy and the physiology and, in general, as surgeons, are not well equipped or ready to alter the neuroanatomy of the bladder. William Bradley is probably one of the crusaders to a d b the treatment of the neurogenic bladder through ’neurologic’ manipulation. It was, in part, through his efforts that a commercially available bladder stimulation device was developed.2 The device did prove to be, occasionally, spectacularly effective. However, it had its spectacular failures as well because it was dependent on field depolarization that resulted, not only in detrusor contraction, but also sphincteric and diaphragmatic contractions that caused pain and dyssynergia. Through this early experience it became evident that selectivenerve root stimulation would be necessary to achieve normal debusor function. Dr.E d Tauagho has clearly championed this concept and found that selective stimulation of ventral roots (S2,3,4) with dorsal rhimtomy can result in effective bladder storage and emptying.3 His techniques have been carried to several centers with encouraging results. The paper by Hohenfellner et al. in this issue of The Journal of Urology is clearly a potential extension of this concept, providing a potential for stimulation in patients who have peripheral nerve damage to the bladder (the myelodysplasia patients). The authors show very strong evidence that bladder smooth muscle can be excited with stimulation of a somatic nerve previously implanted into the bladder wall. Theoretically,extension of this work could lead to reinnervation or selective innervation of a neurogenic bladder which, through appropriate stimulation, could be made to function “normally.” Logically, total bladder reconstruction would depend on innervation and, based on this study, the reconstruction of nerve supply could be possible with nerve transplant and stimulation. Realietieally, we are probably some years from true bladder reconstruction or replacement. It doesn’t take much insight, however, to appreciate the fact that appropriate tissue innervation will be critical in these developments. It is fascinating to this editor that, in this model, the implanted femoral nerve so rapidly (within 4 months) and functionally grows into the recipient bladder tissue such that stimulation of the nerve effectively initiates a detrusor contraction (which was previously reported not to be the case4).Furthermore, it is also remarkable that stimulation of the nerve innervating the striated muscle flap on the bladder wall apparently causes a bladder detrusor depolarization. Both demonstrate apparent intracellular connections which would be critical in synthesizing a functional bladder. Evidence for a phenomenon may be seen dufing fluorourodynamics in the augmented bladder where a detrusor contraction seems to carry over onto the augmented segment and occasionally vice versa. These experiments were performed in a model in which bladder innervation was carefully protected, so application to the true neurogenic bladder situation may not be totally d o g o u s . Obviously, we are in the very early stages of our understanding of bladder anatomy and physiology, but concerted efforts are intemifying and the results should be very exciting indeed. Michael E. Mitchell Division of Pediatric Urology University of Washington Seattle, Washington REFERENCES
1. &plan,
W. E., Richards, J. W. and Richards, I.: Intravesical transurethral bladder stimulation to increase bladder capacity. J. Urol., 142:
600, 1989. 2. Bradley, W. E.. Timm. G . W and Chou, S. N.: A decade of experience with electronic stimulation of the micturition reflex. Urol. Int., 26: 283, 1971.
3. Tanagho, E. A., Schmidt. R. A. and Orvis, B. R.: Neural stimulation for control ofvoiding dysfunction: a preliminary report In 22 patients with serious neuropathic voiding disorders. J. Urol., 142: 340. 1989. 4. Rao, C . R., Bruce. A. W., Lynwood, D. W. and Robertson. D. M.: Heinnervation of the neurogenic blatlder \:lth somatic motor nerves. Invest. Urol., 9 59, 1971. 1990