0022-5347 /81 /1254-0545$02.00/0 Vol. 125,
THE ,JOtiRNAL OF UROLOGY
Copy,·ight © 1981 by The Williams & Wilkins Co.
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DETRUSOR-EXTERNAL SPHINCTER DYSSYNERGIA: A DETAILED ELECTROMYOGRAPHIC STUDY J. G. BLAIVAS, H. P. SINHA, A. A. H. ZA YED
AND
K. B. LABIB
From the Departments of Urology, and Physical Medicine and Rehabilitation, Tufts University School of Medicine and Tufts New England Medical Center, Boston, Massachusetts
ABSTRACT
We reviewed 54 cases of detrusor-external sphincter dyssynergia following complete urodynamic evaluations. All patients had well defined neurologic lesions of the suprasacral spinal cord. On the basis of urodynamic findings 3 types of dyssynergia were encountered: type 1 (30 per cent) was characterized by a crescendo increase in electromyographic activity that reached a maximum at the peak of the detrusor contraction, type 2 (15 per cent) consisted of clonic sphincter contractions interspersed throughout the detrusor contraction and type 3 (55 per cent) was characterized by a sustained sphincter contraction that coincided with the detrusor contraction. There was no correlation between the clinical neurologic level and the type of dyssynergia. Detrusor-external urethral sphincter dyssynergia is characterized by an involuntary contraction of the external urethral sphincter during an involuntary bladder contraction. Previous data from this laboratory have suggested that this is a condition found exclusively in patients with neurologic lesions of the suprasacral spinal cord. 1 In several recent reports the clinical aspects of this disorder have been summarized 2 - 4 but the electromyographic findings have not been described in detail. MATERIALS AND METHODS
We reviewed 54 patients with detrusor-external sphincter dyssynergia. Each patient underwent a thorough urodynamic evaluation according to methods we have described previously." Bladder, urethral and rectal pressures were monitored during bladder filling with meglumine diatrizoate. Simultaneous fluoroscopy and sphincter electromyography were done. The fluoroscopic and urodynamic data were mixed electronically and displayed on a television monitor. Selected portions of the study were videotaped simultaneously. Electromyography was performed by an experienced electromyographer using coaxial needle electrodes placed percutaneously into the external urethral sphincter." Individual motor unit action potentials were visualized directly on an electromyographic oscilloscope screen. In addition, they were converted to audio signals that were monitored via a loudspeaker. Signal averaging of the individual motor unit action potentials was displayed on a strip chart recorder with the other urodynamic data.
diately after the onset of the detrusor contraction. We acknowledge the possibility that there is a variable delay between the onset of the detrusor contraction and the increase in detrusor pressure. In 6 patients (11 per cent) there was a high level of electromyographic activity that did not change during the detrusor contraction and in 1 patient the dyssynergic increase in sphincter activity immediately preceded the detrusor contraction. The patients were divided into 3 groups on the basis of the temporal relationship between electromyographic activity and detrusor contractions (fig. 1). Type 1 dyssynergia was characterized by a crescendo increase in electromyographic activity that reached its maximum at the peak of the detrusor contraction (fig. 2, A). As the detrusor pressure began its decline there was sudden complete external sphincter relaxation. Voiding occurred only during the downslope of the detrusor pressure curve as the sphincter relaxed (fig. 2, B). Sixteen patients (30 per cent) had type 1 dyssynergia (table 2). Type 2 dyssynergia was characterized by clonic contractions of the external urethral sphincter interspersed throughout the detrusor contraction. These patients usually voided with an interrupted spurting stream (fig. 3). Eight patients (15 per cent) had type 2 dyssynergia (table 3). In type 3 dyssynergia the external urethral sphincter contraction persisted throughout the entire detrusor contraction. These patients voided with an obstructive flow or did not void at all (fig. 4). There were 30 patients (55 per cent) with type 3 dyssynergia (table 4). DISCUSSION
RESULTS
The 54 patients involved 33 male and 21 female subjects, ranging in age from 4 to 61 years, with an average of 26 years. All patients had overt neurologic lesions affecting the suprasacral spinal cord. The neurologic diagnosis and spinal cord level are listed in table 1. In all patients the individual electromyographic motor action potentials were of normal configuration, with an amplitude from 50 to 900 m. volts. Spontaneous potentials (positive sharp waves and fibrillation) were not observed and <15 per cent of the motor units were polyphasic. In 40 patients (87 per cent) the onset of the dyssynergic sphincter contraction was coincident with or occurred immeAccepted for publication September 19, 1980. Supported by a grant from the National Multiple Sclerosis Founda-
tion.
Previous data from our laboratory" and reported by Tanagho 7 have demonstrated that micturition normally is preceded by relaxation of the external urethral sphincter followed within 1 to 15 seconds by a detrusor contraction. This sequence remains intact in patients with cranial neurologic lesions above the level of the pontine mesencephalic micturition center. However, in patients with neurologic lesions of the suprasacral spinal cord this orderly sequence usually is lost and bladder-external sphincter dyssynergia ensues. 1- 4 Moreover, this series demonstrates that in the vast majority of these patients (96 per cent) the dyssynergic sphincter contraction occurs simultaneously with or immediately after the onset of the detrusor contraction. Similarly, in a study of >200 spinal cord injury patients Yalla and associates never observed a pre-voiding decrease in urethral pressure." These data suggest that when the integrity of the pontine mesencephalic micturition pathways is lost reflex mic-
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BLAIVAS AND ASSOCIATES
Type I
Type 3
Type 2
Fm. 1. Dyssynergia. Type 1, crescendo increase in electromyographic activity that suddenly relaxes at peak of detrusor contraction. Type 2, clonic sphincter contractions interspersed throughout detrusor contraction. Type 3, sustained sphincter contraction that persists throughout bladder contraction. 1. Neurologic diagnosis and clinical neurologic level for patients with detrusor-external sphincter dyssynergia
TABLE
No. Pts. Neurologic diagnosis: Traumatic myelopathy Multiple sclerosis Myelodysplasia Spinal cord tumor Pernicious anemia Transverse myelitis Syringomyelia Total Spinal cord level: Cervical Thoracic Lumbar Sacral Indeterminate (multiple sclerosis) Total
TABLE 2.
31 14 5
1 54
21 13 4
2 14 54
Neurologic diagnosis and clinical neurologic level of patients with type 1 dyssynergia No. Pts. N eurologic diagnosis: Traumatic myelopathy Multiple sclerosis Syringomyelia Total Spinal cord level: Cervical Thoracic Indeterminate Total
Fm. 2. Type 1 dyssynergia. A, there is marked increase in electromyographic activity during upswing of detrusor contraction. Posterior urethra is dilated and completely obstructed by external sphincter. B, at peak of detrusor contraction there is sudden complete external sphincter relaxation (electromyographic silence) and voiding ensues. Membranous urethra is now open. R, rectal pressure. EMG, integrated external sphincter electromyogram. B, intravesical pressure.
turition is initiated by an involuntary detrusor contraction rather than relaxation of the external urethral sphincter as normally is the case. In these circumstances there is a probable sequence of events. Bladder distension causes an afferent discharge along the pelvic nerve. This afferent impulse causes increasing external sphincter contraction (via the pudendal efferents). At a certain critical bladder pressure (or wall tension) a reflex detrusor contraction occurs. This further increase in detrusor pressure causes a
12 3
1 16 10 3 3 16
further increased firing of pelvic nerve afferents, which in turn stimulates the external sphincter to contract more vigorously. This event is in contrast to the normal situation, wherein bladder distension results in increasing pelvic and hypogastric discharges that are modulated by a supraspinal pathway (probably the pontine mesencephalic micturition center) 8 • 9 in such a way that external sphincter relaxation precedes the detrusor contraction. This theoretical neurophysiologic model is based on the assumption that the initial increase in bladder pressure is coincident with the onset of the detrusor contraction and that the onset of external sphincter contraction is coincident with the increase in electromyographic activity. These assumptions have been neither proved nor refuted but ultimately the validity of our hypothesis depends upon documenting the precise temporal relationships between detrusor and sphincter activity. In our series once an involuntary detrusor contraction occurred 1 of 3 external sphincter responses was noted: in type 1 dyssynergia external sphincter contraction occurred only during the ascending limb of the detrusor contraction (30 per cent), in
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DETRUSOR-EXTERNAL SPHINCTER DYSSYNERGIA
FIG. 4. Type 3 dyssynergia. Dyssynergic sphincter contraction persists throughout detrusor contraction. Note bladder diverticula. b, intravesical pressure. u, intraurethral pressure in bulbar urethra. r, rectal pressure. emg, integrated external urethral sphincter electromyogram.
B
TABLE 4.
Neurologic diagnosis and clinical neurologic level of patients with type 3 dyssynergia No. Pts.
N eurologic diagnosis: Traumatic myelopathy Multiple sclerosis Myelodysplasia Transverse myelitis
Total Spinal cord level: Cervical Thoracic Lumbar Sacral Indeterminate Total
FIG. 3. Type 2 dyssynergia. Intermittent sphincter contractions interspersed throughout detrusor contraction. A, obstruction at membranous urethra by dyssynergic sphincter contraction. B, with sphincter relaxation voiding ensues. U, intraurethral pressure in bulbar urethra. R, rectal pressure. EMG, integrated external urethral sphincter electromyogram. B, intravesical pressure.
TABLE
3. Neurologic diagnosis and clinical neurologic level of
patients with type 2 dyssynergia No. Pts. N eurologic diagnosis: Traumatic myelopathy Multiple sclerosis Pernicious anemia Spinal cord tumor Total Spinal cord level: Cervical Thoracic Indeterminate Total
3 3 l
1 8
2 3 3 8
type 2 clonic sphincter contractions were interspersed throughout the detrusor contraction (15 per cent) and in type 3 sphincter contraction occurred throughout the detrusor contraction (56 per cent).
16
8 5 1 30 9
7 4
2 8 30
This classification of detrusor-sphincter dyssynergia differs from the one proposed by Y alla and associates. 2 In their system grade O is normal micturition. Grade l dyssynergia is characterized by high voiding pressures with a normal urinary flow rate and inconsistent external urethral sphincter contractions during voiding. Grade 2 dyssynergia corresponds to our types 1 and 2, and grade 3 corresponds to our type 3. In their series patients with incomplete neurologic lesions usually had grade 1 or 2 dyssynergia, whereas, patients with complete lesions usually had grade 2 or 3. In our series there was no correlation between either the clinical neurologic level or the severity of the lesion (complete or incomplete) and the type of dyssynergia. However, this may be owing to the fact that it often is difficult to assess the precise neuroanatomic boundaries of the lesion in any individual patient. Teleologically, it would appear that patients with type 3 dyssynergia should be at the greatest risk for urologic complications because in these patients bladder outflow obstruction is continuous throughout the detrusor contraction. Voiding either does not occur or the flow rate is impaired markedly. Detrusor trabeculations, vesicoureteral reflux or secondary ureterovesical obstruction should occur earlier and be more severe. In patients with type 1 dyssynergia voiding occurs only at the peak of the detrusor contraction, when the external sphincter suddenly relaxes. These patients void more efficiently than type 3 patients and should have lower post-void residual urine volumes. It remains to be shown in type 1 patients whether the decrease in detrusor pressure during voiding is owing to relief of the functional obstruction or to cessation of the detrusor contrac-
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BLAIVAS AND ASSOCIATES
tion. Type 2 patients are in a clinical spectrum between types 1 and 2. More clinical data are needed before these teleologic considerations can be accepted as fact. Moreover, longitudinal studies should be done to see whether the type of dyssynergia changes in time. REFERENCES 1. Blaivas, J. G., Sinha, H. P., Zayed, A. A. H. and Labib, K. B.: Detrusor-external sphincter dyssynergia. J. Urol., 125: 542, 1981. 2. Yalla, S. V., Blunt, K. J., Fam, B. A., Constantinople, N. L. and Gittes, R. F.: Detrusor-urethral sphincter dyssynergia. J. Urol., 118: 1026, 1977. 3. McGuire, E. J. and Brady, S.: Detrusor-sphincter dyssynergia. J.
Urol., 121: 774, 1979. 4. Andersen, J. T. and Bradley, W. E.: The syndrome of detrusorsphincter dyssynergia. J. Urol., 116: 493, 1976. 5. Blaivas, J. G. and Fisher, D. M.: Combined radiographic and urodynamic monitoring: advances in technique. J. Urol., in press. 6. Blaivas, J. G., Labib, K. B., Bauer, S. B. and Retik, A. B.: A new approach to electromyography of the external urethral sphincter. J. Urol., 117: 773, 1977. 7. Tanagho, E. A.: Interpretation of the physiology of micturition. In: Hydrodynamics of Micturition. Edited by F. Hinman, Jr. Springfield, Illinois: Charles C Thomas, Publisher, pp. 18-40, 1971. 8. DeGroat, W. C.: Nervous control of the urinary bladder of the cat. Brain Res., 87: 201, 1975. 9. Bradley, W. E., Timm, G. W. and Scott, F. B.: Innervation of the detrusor muscle and urethra. Urol. Clin. N. Amer., 1: 3, 1974.