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Experience with Measurement of Bladder Electrical Activity
0022-5347/78/1201-0082$02.00/0 Vol. 120, July Printed in U.SA.
THE JOURNAL OF UROWGY
Copyright © 1978 by The Williams & Wilkins Co.
Urological Neurology and U rodynamics EXPERIENCE WITH MEASUREMENT OF BLADDER ELECTRICAL ACTIVITY JOHN B. NANNINGA
AND
PAUL KAPLAN
From the Department of Urology, Northwestern U niuersity Medical School and the Rehabilitation Institute of Chicago, Chicago, Illinois
ABSTRACT
A series of patients is presented in whom the recording of bladder electrical activity was performed. There was a significant difference in frequency of the spike activity between patients with upper and lower motor neuron injury. This technique would seem to offer greater clinical application in areas of bladder dysfunction and evaluation of drugs on the bladder. men may pick up acitvity from the rectus muscles in the 0.5 to 1 mV. range that, incidentally, was not synchronous with bladder muscle. In the control patients 2 electrodes were placed in the bladder by cystoscopy to identify bladder electrical activity when the electrodes were definitely in bladder muscle. Subsequently, we found that by inserting the electrodes through the. catheter cystoscopy was no longer necessary. The bladder was filled with sterile saline at a rate of about 1 ml. per second to the point at which a bladder contraction occurred or, in the case of the areflexic bladder, the bladder was filled to about 400 ml. No attempt was made to fill beyond this point because of the danger of perforation. Previous cystometric studies had documented those patients in whom there was no bladder reflex at higher volumes. The electrical activity was recorded on a TECA TE4 electromyograph with tape storage and direct write-out. Analysis consisted of counting 10 consecutive spikes at various bladder volumes. The bladder pressure was recorded through the catheter on the electronic recording apparatus, The sudden disappearance of the electrical activity from the oscilloscope indicated that the electrode had disengaged during filling, thus requiring reinsertion of the needle and wire into bladder muscle.
There has been renewed interest in the study of electrical activity of the bladder. Previous studies by Boyce demonstrated the presence of slow waves that were thought to coincide with bladder muscle activity. 1 At about the same time Franksson and Petersen reported on their findings of a higher frequency activity in the bladder. 2 In the last few years other investigators have used more sophisticated recording equipment and have documented evidence for a high frequency activity. 3 ' 4 We have studied this electrical activity in the bladder of normal subjects and in patients with a specific neurological disorder to see if changes in the bladder electrical activity correlated with the neurological lesion. 5 Our findings in normal subjects and in patients with upper and lower motor neuron injuries are reported. The evidence gained would seem to be of value in better understanding bladder function and treatment. METHODS
Patients selected for study had suffered a spinal injury or other destructive lesions to a specific area of the spinal cord. We classified the patients as to whether the bladder reflex was present (upper motor neuron) or the sacral cord had been iajured, resulting in an areflexic bladder (lower motor neuron). Three neurologically normal patients underwent study in conjunction with evaluation for urinary infection. Urine specimens from these patients were sterile at the time of the examination. Another patient was evaluated at the time of an open operation for a bladder tumor. The process of recording involved the placement of a tefloncoated stainless steel wire (0.10 mm. in diameter), bared at the tip and mounted on a 22 gauge needle, which was attached to a ureteral catheter (5F), into bladder muscle. The electrode was inserted into a Foley catheter with an open tip. The catheter with the electrode inside then was passed into the bladder and the balloon was inflated. The ureteral catheter with the needle and wire was then advanced beyond the tip of the catheter into bladder muscle. After insertional activity was noted on an oscilloscope several minutes were allowed to pass for stabilization. The reference electrode was placed over the hip (below the iliac crest), which eliminated artifact from the rectus muscles. This recording technique was described by Franksson and Petersen. 2 Early in our studies we found that placement of the reference electrode anteriorly on the abdo-
RESULTS
The recorded activity consisted of spikes of 10 to 50 µ, V. at a frequency of about 5 to 150 spikes per second (Hz.). No attempt was made to study the slow wave activity (0.1 to 1 Hz.). The type of activity is shown in figures 1 and 2. The findings for 3 normal patients were mean amplitude 26.7 µ,V. ± 3.5 and mean frequency 122.8 Hz. ± 14.4. These values approximate those reported by Jones and associates. 6 Activity also was recorded from the bladder of a patient undergoing segmental resection of a bladder tumor. These recordings demonstrated activity associated with stretch that was similar to that seen in the intact bladder distended with fluid. Recordings from the dome and lateral walls were essentially the same. Trigonal recording was inconclusive because of difficulty in producing stretch in that area. It also was noted that recording from the mucosa produced inferior recordings - accurate measurement required the needle to be in contact with muscle. In 12 patients with upper motor neuron injury and reflex bladder the amplitude of the spikes was 22.9 µ,V. ± 5 and the frequency was 136 Hz. ± 29 at the time of contraction. A
Accepted for publication August 12, 1977. Read at annual meeting of American Urological Association, Chicago, Illinois, April 24-28, 1977. 82
FIG. 1. A, top line represents bladder activity and bottom line represents perineal muscle electromyographic activity. Bladder is electrically quiet in this patient. Calibration-top line vertical 10 µ, V. and bottom line 100 µ, V. per division. Speed-10 msec. per division. p.V. -microvolts. B, top tracing demonstrates low amplitude bladder activity during early filling phase in patient with upper motor neuron injury and reflex bladder. Note brief burst of activity in sphincter region (lower tracing). Calibration as in part A of figure.
FIG. 2. Bladder filling in patient with upper motor neuron injury. Spiking activity in top tracing, from bladder, is in 25 to 40 µ, V. range. Increase in sphincter activity is noted in lower tracing. Scale-vertical (top) 25 µ,V. per division and vertical (bottom) 100 µ,V. per division. Speed 100 msec. per division.
sample of this activity is shown in figure 3. After 0.6 mg. atropine was given intramuscularly the mean amplitude decreased from 22.9 to 19.8 µ.V. The frequency decreased from 136 to 111 Hz.
In 14 patients with lower motor neuron injury the mean amplitude was 12.7 µ,V. ± 3.0 and the mean frequency was 19.4 Hz. ± 3.4. These values are significantly different from those of the upper motor neuron group (p < 0.01). A clinical
84
NANNINGA AND KAPLAN
Fm. 3. Spiking activity during bladder contraction is shown on top tracing. Scale-vertical 10 µ,V. per division and speed 10 msec. per division.
application is demonstrated in a patient with a sacral cord lesion who had been on catheter drainage because of a small bladder capacity and incontinence. Figure 4 illustrates the cystometric and electrical findings. It can be seen that there is little activity in the muscle and that the bladder is most likely scarred and contracted. Attempts at bladder training were futile.
80
cm H20
3Hz 60
DISCUSSION
There has been controversy concerning just what constitutes bladder electrical activity. 3• 4 Spiking electrical activity has been documented from smooth muscle cells of the rabbit bladder and guinea pig bladder muscle. 7 • 8 Surface recording from the rabbit and canine bladders also has demonstrated spikes. 9• 10 Also, there is evidence, based on sacral ventral root stimulation and analysis of the electrical activity, that some or all of the slow wave activity is artifact. 4 However, there is ample evidence that at least some smooth muscles, particularly those of the intestines, do generate slow wave activity.11 We chose to concentrate on the faster component of the frequency spectrum and our studies would seem to indicate that the fast wave activity does correlate with the neurological lesion (upper versus lower motor neuron). Furthermore, we believe that the fast wave activity is from the bladder and not skeletal muscle. We base this belief on the electrical activity recorded from the surgically exposed bladder when the patient had been given succinylcholine and on the reported inability of the bladder electrodes to record abdominal muscle activity. 12 In the patients in whom we used monopolar recording the placement of the reference electrode over the hip eliminated artifact from the rectus muscles. When the electrode is placed more anteriorly over the abdomen much higher voltage activity in the 0.5 to 1.0 mV. range was obtained, which was not synchronous with bladder activity. It is possible that the electrical activity recorded in our study represents postganglionic nerve activity rather than smooth muscle electromyographic activity. DeGroat and Saum have reported the recording of postganglionic nerve activity from the cat bladder at a frequency of about 100 spikes per second (isovolumetric contraction). 13 We attempted to resolve this by administering atropine and did document some reduction in frequency and amplitude, which suggests that
40
20
OL--------------50 75 25 volume (ml) Fm. 4. Increase in bladder pressure is not accompanied by any increase in bladder electrical activity. Patient had small capacity bladder that failed to empty completely. Contracted, fibrosed bladder would seem to be explanation.
the activity is smooth muscle in origin, but all activity was obviously not eliminated. Possibly other neurotransmitters contribute to generating the electrical activity. 14 Also, Carpenter has presented evidence that muscarinic receptors in close proximity to the neuroeffector junction are atropine resistant. 15 Craggs and Stephenson were more successful in isolating a spectrum of activity (10 to 40 Hz.), which was atropine sensitive, thus supporting this electrical activity as being true electromyographic in origin. 4 We believe that the spiking activity greater than 40 Hz. should not necessarily be excluded from bladder activity since this may represent activity other than muscarinic in type. The clinical use of the recording of bladder electromyographic activity remains to be defined fully. It is useful in
85 patients in °v1hom the bladder may have been damaged and the status of the muscle is in doubt. It also should be helpful in identifying certain functional voiding disturbances. Evaluation of drugs acting on the bladder would seem to be another use ofrecording bladder electrical activity. REFERENCES
1. Boyce, W. H.: Bladder electromyography: a new approach to the
2.
3. 4. 5. 6. 7. 8.
9.
diagnosis of urinary bladder dysfunction. J. Urol., 67: 650, 1952. Franksson, C. and Petersen, I.: Electromyographic recording from the normal human urinary bladder, internal urethral sphincter and ureter. Acta Physiol. Scand., 106: 150, 1953. LaJoie, W. J., Cosgrove, M. D., Jones, W. G. and Kaplan, P. E.: Electromyography of the human urinary bladder. Electromyogr. Clin. Neurophysiol., 15: 191, 1975. Craggs, M. D. and Stephenson, J. D.: The real bladder electromyogram. Brit. J. Urol., 48: 443, 1976. Kaplan, P. E., Nanninga, J. D. and Lal, S.: Electromyography and cystometry of the neurogenic bladder. Electromyogr. Clin. Neurophysiol., 16: 463, 1976. Jones, W. G., LaJoie, W. J. and Cosgrove, M. D.: Electromyography in pathologic bladder. Urology, 4: 186, 1974. Ursillo, R. C.: Electrical activity of the isolated nerve-urinary bladder strip preparation of the rabbit. Amer. J. Physiol., 201: 408, 1961. Creed, K. E.: Membrane properties of the smooth muscle membrane of the guinea-pig urinary bladder. Pfluegers Arch., 326: 115, 1971. Burnstock, G. and Prosser, C. L.: Conduction in smooth muscles: comparative electrical properties. Amer. J. Physiol., 199: 553, 1960.
10. Fredericks C. M., Anderson, G. F. Rasmussen, E. A. and Pierce, J. IV!.: Electrophysiology of the canine urinary bladder. Invest. Urol., 7: 33, 1969. 11. Prosser, C. L.: Smooth muscle. Ann. Rev. Physiol., 36: 503, 1974. 12. LaJoie, W. J., Cosgrove, M. D. and Jones, W. G.: Electromyographic evaluation of human detrusor muscle activity in relation to abdominal muscle activity. Arch. Phys. Med. Rehabil., 57: 382, 1976. 13. DeGroat, W. C. and Saum, W. R.: Synaptic transmission in parasympathetic ganglia in the urinary bladder of the cat. J. Physiol., 256: 137, 1976. 14. Burnstock, G., Dumsday, B. and Smythe, A.: Atropine resistant excitation of the urinary bladder: the possibility of transmission via nerves releasing a purine nucleotide. Brit. J. Pharmacol., 44: 451, 1972. 15. Carpenter, F. G.: Atropine resistance and rnuscarinic receptors in the rat urinary bladder. Brit. J. Pharmacol., 59: 43, 1977. 1
1
EDITORIAL COMMENT The difficulties with interpretation of electromyographic activity obtained by insertion of electromyogram electrodes into the detrusor muscle include the uncertainty of whether the recorded muscle activity is from the reference electrode or the detrusor muscle and the nagging doubt that because of the size of individual smooth muscle cells (less than 5 µ,. in diameter) and their population geometry individual cellular activity would sum to produce a potential recordable by use of macroelectrodes used in clinical electromyogram work. Nevertheless, the method does offer the possibility of delineating end organic neuropathic disease and the ability to distinguish between a neuropathy and myopathy of the detrusor muscle. W.E.B.
THE JOURNAL OF UROWGY
Copyright © 1978 by The Williams & Wilkins Co.
Urological Neurology and U rodynamics EXPERIENCE WITH MEASUREMENT OF BLADDER ELECTRICAL ACTIVITY JOHN B. NANNINGA
AND
PAUL KAPLAN
From the Department of Urology, Northwestern U niuersity Medical School and the Rehabilitation Institute of Chicago, Chicago, Illinois
ABSTRACT
A series of patients is presented in whom the recording of bladder electrical activity was performed. There was a significant difference in frequency of the spike activity between patients with upper and lower motor neuron injury. This technique would seem to offer greater clinical application in areas of bladder dysfunction and evaluation of drugs on the bladder. men may pick up acitvity from the rectus muscles in the 0.5 to 1 mV. range that, incidentally, was not synchronous with bladder muscle. In the control patients 2 electrodes were placed in the bladder by cystoscopy to identify bladder electrical activity when the electrodes were definitely in bladder muscle. Subsequently, we found that by inserting the electrodes through the. catheter cystoscopy was no longer necessary. The bladder was filled with sterile saline at a rate of about 1 ml. per second to the point at which a bladder contraction occurred or, in the case of the areflexic bladder, the bladder was filled to about 400 ml. No attempt was made to fill beyond this point because of the danger of perforation. Previous cystometric studies had documented those patients in whom there was no bladder reflex at higher volumes. The electrical activity was recorded on a TECA TE4 electromyograph with tape storage and direct write-out. Analysis consisted of counting 10 consecutive spikes at various bladder volumes. The bladder pressure was recorded through the catheter on the electronic recording apparatus, The sudden disappearance of the electrical activity from the oscilloscope indicated that the electrode had disengaged during filling, thus requiring reinsertion of the needle and wire into bladder muscle.
There has been renewed interest in the study of electrical activity of the bladder. Previous studies by Boyce demonstrated the presence of slow waves that were thought to coincide with bladder muscle activity. 1 At about the same time Franksson and Petersen reported on their findings of a higher frequency activity in the bladder. 2 In the last few years other investigators have used more sophisticated recording equipment and have documented evidence for a high frequency activity. 3 ' 4 We have studied this electrical activity in the bladder of normal subjects and in patients with a specific neurological disorder to see if changes in the bladder electrical activity correlated with the neurological lesion. 5 Our findings in normal subjects and in patients with upper and lower motor neuron injuries are reported. The evidence gained would seem to be of value in better understanding bladder function and treatment. METHODS
Patients selected for study had suffered a spinal injury or other destructive lesions to a specific area of the spinal cord. We classified the patients as to whether the bladder reflex was present (upper motor neuron) or the sacral cord had been iajured, resulting in an areflexic bladder (lower motor neuron). Three neurologically normal patients underwent study in conjunction with evaluation for urinary infection. Urine specimens from these patients were sterile at the time of the examination. Another patient was evaluated at the time of an open operation for a bladder tumor. The process of recording involved the placement of a tefloncoated stainless steel wire (0.10 mm. in diameter), bared at the tip and mounted on a 22 gauge needle, which was attached to a ureteral catheter (5F), into bladder muscle. The electrode was inserted into a Foley catheter with an open tip. The catheter with the electrode inside then was passed into the bladder and the balloon was inflated. The ureteral catheter with the needle and wire was then advanced beyond the tip of the catheter into bladder muscle. After insertional activity was noted on an oscilloscope several minutes were allowed to pass for stabilization. The reference electrode was placed over the hip (below the iliac crest), which eliminated artifact from the rectus muscles. This recording technique was described by Franksson and Petersen. 2 Early in our studies we found that placement of the reference electrode anteriorly on the abdo-
RESULTS
The recorded activity consisted of spikes of 10 to 50 µ, V. at a frequency of about 5 to 150 spikes per second (Hz.). No attempt was made to study the slow wave activity (0.1 to 1 Hz.). The type of activity is shown in figures 1 and 2. The findings for 3 normal patients were mean amplitude 26.7 µ,V. ± 3.5 and mean frequency 122.8 Hz. ± 14.4. These values approximate those reported by Jones and associates. 6 Activity also was recorded from the bladder of a patient undergoing segmental resection of a bladder tumor. These recordings demonstrated activity associated with stretch that was similar to that seen in the intact bladder distended with fluid. Recordings from the dome and lateral walls were essentially the same. Trigonal recording was inconclusive because of difficulty in producing stretch in that area. It also was noted that recording from the mucosa produced inferior recordings - accurate measurement required the needle to be in contact with muscle. In 12 patients with upper motor neuron injury and reflex bladder the amplitude of the spikes was 22.9 µ,V. ± 5 and the frequency was 136 Hz. ± 29 at the time of contraction. A
Accepted for publication August 12, 1977. Read at annual meeting of American Urological Association, Chicago, Illinois, April 24-28, 1977. 82
FIG. 1. A, top line represents bladder activity and bottom line represents perineal muscle electromyographic activity. Bladder is electrically quiet in this patient. Calibration-top line vertical 10 µ, V. and bottom line 100 µ, V. per division. Speed-10 msec. per division. p.V. -microvolts. B, top tracing demonstrates low amplitude bladder activity during early filling phase in patient with upper motor neuron injury and reflex bladder. Note brief burst of activity in sphincter region (lower tracing). Calibration as in part A of figure.
FIG. 2. Bladder filling in patient with upper motor neuron injury. Spiking activity in top tracing, from bladder, is in 25 to 40 µ, V. range. Increase in sphincter activity is noted in lower tracing. Scale-vertical (top) 25 µ,V. per division and vertical (bottom) 100 µ,V. per division. Speed 100 msec. per division.
sample of this activity is shown in figure 3. After 0.6 mg. atropine was given intramuscularly the mean amplitude decreased from 22.9 to 19.8 µ.V. The frequency decreased from 136 to 111 Hz.
In 14 patients with lower motor neuron injury the mean amplitude was 12.7 µ,V. ± 3.0 and the mean frequency was 19.4 Hz. ± 3.4. These values are significantly different from those of the upper motor neuron group (p < 0.01). A clinical
84
NANNINGA AND KAPLAN
Fm. 3. Spiking activity during bladder contraction is shown on top tracing. Scale-vertical 10 µ,V. per division and speed 10 msec. per division.
application is demonstrated in a patient with a sacral cord lesion who had been on catheter drainage because of a small bladder capacity and incontinence. Figure 4 illustrates the cystometric and electrical findings. It can be seen that there is little activity in the muscle and that the bladder is most likely scarred and contracted. Attempts at bladder training were futile.
80
cm H20
3Hz 60
DISCUSSION
There has been controversy concerning just what constitutes bladder electrical activity. 3• 4 Spiking electrical activity has been documented from smooth muscle cells of the rabbit bladder and guinea pig bladder muscle. 7 • 8 Surface recording from the rabbit and canine bladders also has demonstrated spikes. 9• 10 Also, there is evidence, based on sacral ventral root stimulation and analysis of the electrical activity, that some or all of the slow wave activity is artifact. 4 However, there is ample evidence that at least some smooth muscles, particularly those of the intestines, do generate slow wave activity.11 We chose to concentrate on the faster component of the frequency spectrum and our studies would seem to indicate that the fast wave activity does correlate with the neurological lesion (upper versus lower motor neuron). Furthermore, we believe that the fast wave activity is from the bladder and not skeletal muscle. We base this belief on the electrical activity recorded from the surgically exposed bladder when the patient had been given succinylcholine and on the reported inability of the bladder electrodes to record abdominal muscle activity. 12 In the patients in whom we used monopolar recording the placement of the reference electrode over the hip eliminated artifact from the rectus muscles. When the electrode is placed more anteriorly over the abdomen much higher voltage activity in the 0.5 to 1.0 mV. range was obtained, which was not synchronous with bladder activity. It is possible that the electrical activity recorded in our study represents postganglionic nerve activity rather than smooth muscle electromyographic activity. DeGroat and Saum have reported the recording of postganglionic nerve activity from the cat bladder at a frequency of about 100 spikes per second (isovolumetric contraction). 13 We attempted to resolve this by administering atropine and did document some reduction in frequency and amplitude, which suggests that
40
20
OL--------------50 75 25 volume (ml) Fm. 4. Increase in bladder pressure is not accompanied by any increase in bladder electrical activity. Patient had small capacity bladder that failed to empty completely. Contracted, fibrosed bladder would seem to be explanation.
the activity is smooth muscle in origin, but all activity was obviously not eliminated. Possibly other neurotransmitters contribute to generating the electrical activity. 14 Also, Carpenter has presented evidence that muscarinic receptors in close proximity to the neuroeffector junction are atropine resistant. 15 Craggs and Stephenson were more successful in isolating a spectrum of activity (10 to 40 Hz.), which was atropine sensitive, thus supporting this electrical activity as being true electromyographic in origin. 4 We believe that the spiking activity greater than 40 Hz. should not necessarily be excluded from bladder activity since this may represent activity other than muscarinic in type. The clinical use of the recording of bladder electromyographic activity remains to be defined fully. It is useful in
85 patients in °v1hom the bladder may have been damaged and the status of the muscle is in doubt. It also should be helpful in identifying certain functional voiding disturbances. Evaluation of drugs acting on the bladder would seem to be another use ofrecording bladder electrical activity. REFERENCES
1. Boyce, W. H.: Bladder electromyography: a new approach to the
2.
3. 4. 5. 6. 7. 8.
9.
diagnosis of urinary bladder dysfunction. J. Urol., 67: 650, 1952. Franksson, C. and Petersen, I.: Electromyographic recording from the normal human urinary bladder, internal urethral sphincter and ureter. Acta Physiol. Scand., 106: 150, 1953. LaJoie, W. J., Cosgrove, M. D., Jones, W. G. and Kaplan, P. E.: Electromyography of the human urinary bladder. Electromyogr. Clin. Neurophysiol., 15: 191, 1975. Craggs, M. D. and Stephenson, J. D.: The real bladder electromyogram. Brit. J. Urol., 48: 443, 1976. Kaplan, P. E., Nanninga, J. D. and Lal, S.: Electromyography and cystometry of the neurogenic bladder. Electromyogr. Clin. Neurophysiol., 16: 463, 1976. Jones, W. G., LaJoie, W. J. and Cosgrove, M. D.: Electromyography in pathologic bladder. Urology, 4: 186, 1974. Ursillo, R. C.: Electrical activity of the isolated nerve-urinary bladder strip preparation of the rabbit. Amer. J. Physiol., 201: 408, 1961. Creed, K. E.: Membrane properties of the smooth muscle membrane of the guinea-pig urinary bladder. Pfluegers Arch., 326: 115, 1971. Burnstock, G. and Prosser, C. L.: Conduction in smooth muscles: comparative electrical properties. Amer. J. Physiol., 199: 553, 1960.
10. Fredericks C. M., Anderson, G. F. Rasmussen, E. A. and Pierce, J. IV!.: Electrophysiology of the canine urinary bladder. Invest. Urol., 7: 33, 1969. 11. Prosser, C. L.: Smooth muscle. Ann. Rev. Physiol., 36: 503, 1974. 12. LaJoie, W. J., Cosgrove, M. D. and Jones, W. G.: Electromyographic evaluation of human detrusor muscle activity in relation to abdominal muscle activity. Arch. Phys. Med. Rehabil., 57: 382, 1976. 13. DeGroat, W. C. and Saum, W. R.: Synaptic transmission in parasympathetic ganglia in the urinary bladder of the cat. J. Physiol., 256: 137, 1976. 14. Burnstock, G., Dumsday, B. and Smythe, A.: Atropine resistant excitation of the urinary bladder: the possibility of transmission via nerves releasing a purine nucleotide. Brit. J. Pharmacol., 44: 451, 1972. 15. Carpenter, F. G.: Atropine resistance and rnuscarinic receptors in the rat urinary bladder. Brit. J. Pharmacol., 59: 43, 1977. 1
1
EDITORIAL COMMENT The difficulties with interpretation of electromyographic activity obtained by insertion of electromyogram electrodes into the detrusor muscle include the uncertainty of whether the recorded muscle activity is from the reference electrode or the detrusor muscle and the nagging doubt that because of the size of individual smooth muscle cells (less than 5 µ,. in diameter) and their population geometry individual cellular activity would sum to produce a potential recordable by use of macroelectrodes used in clinical electromyogram work. Nevertheless, the method does offer the possibility of delineating end organic neuropathic disease and the ability to distinguish between a neuropathy and myopathy of the detrusor muscle. W.E.B.