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Can neurologic examination predict type of detrusor sphincter-dyssynergia in patients with spinal cord injury?
ADULT UROLOGY
CAN NEUROLOGIC EXAMINATION PREDICT TYPE OF DETRUSOR SPHINCTER-DYSSYNERGIA IN PATIENTS WITH SPINAL CORD INJURY? BRIGITTE SCHURCH, DANIEL M. SCHMID, GILLES KARSENTY,
AND
ANDRE REITZ
ABSTRACT Objectives. To assess the correlations in males with spinal cord injury (SCI) between the neurologic status and type of detrusor-sphincter dyssynergia (DSD) observed during urodynamic examinations and to evaluate the change in the DSD pattern over time. Methods. A total of 105 male patients with chronic SCI were neurologically examined according to the American Spinal Cord Injury Association protocol and underwent video-urodynamic examinations. DSD observed during urodynamic studies was classified according to the Blaivas classification. To assess the stability of the DSD over time, patients who had been recently injured were clinically and urodynamically controlled after 1 year and thereafter. Results. A statistically significant positive correlation was found between the DSD type and completeness or incompleteness of the SCI lesion. Patients with an incomplete sensory and motor SCI lesion presented with DSD type 1 compared with patients with complete sensory and motor SCI lesion, who had DSD type 2 to type 3. A correlation was also found between the American Spinal Cord Injury Association scores and the DSD type. No correlation was found between the DSD type and lesion level. At medium to long-term follow-up, a significant change was found in the DSD type. Conclusions. The neurologic status and DSD type after SCI showed significant correlations. Therefore, neurologic examination and determination of the DSD type might be helpful to complete the neurourologic diagnosis and to assist in confirming completeness of the lesion after acute injury. Because DSD seems to become aggravated with time, regular urodynamic follow-up examinations are mandatory in patients with DSD to adjust their treatment, if necessary. UROLOGY 65: 243–246, 2005. © 2005 Elsevier Inc.
D
etrusor-sphincter dyssynergia (DSD) is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral sphincter and/or periurethral striated muscle.1 Previous data have suggested that this is a condition found exclusively in patients with a neurologic lesion of the suprasacral spinal cord.2 DSD adversely influences the achievement of balanced bladder function after suprasacral spinal cord injury (SCI). Classically, this syndrome has been regarded as functional subvesical obstruction that From the Department of Neuro-Urology, Swiss Paraplegic Center, Balgrist University Hospital; and Department of Urology, University Hospital, Zurich, Switzerland Reprint requests: Brigitte Schurch, M.D., Department of Neuro-Urology, Swiss Paraplegic Center, Balgrist University Hospital, Forchstrasse 340, Zurich 8008, Switzerland. E-mail: [email protected] Submitted: July 3, 2004, accepted (with revisions): September 15, 2004 © 2005 ELSEVIER INC. ALL RIGHTS RESERVED
leads to vesical hypertonicity, high-pressure contractile activity, vesicoureteral reflux, and, ultimately, renal damage and destruction. Detrusor-sphincter dyssynergia has been well described and classified.2,3 However, controversies remain concerning the correlation between the clinical neurologic level and severity of the spinal cord lesion (complete, incomplete) and the type of DSD. We first assessed the correlations between the neurologic status and type of DSD observed during urodynamic examinations and second evaluated the possible change in the DSD pattern over time in male patients with SCI. MATERIAL AND METHODS A total of 105 patients with a spinal cord lesion, who were admitted for rehabilitation to our institution, were studied. All patients were assessed neurologically on the day of admission according to the American Spinal Cord Injury Association protocol.4 Only patients with American Spinal Cord Injury 0090-4295/05/$30.00 doi:10.1016/j.urology.2004.09.024 243
Association impairment grade A to D were included. Accordingly, the spinal cord lesion was classified as complete or incomplete. Incomplete was defined as the presence of any sensory or motor function in the lowest sacral segments. Additionally, the bulbocavernous reflex and the voluntary contraction of the external anal sphincter were clinically tested in all patients. First, urodynamic examination was performed at least once during hospitalization. To assess the changes in bladder function over time, the patients were scheduled for urodynamic re-examination after discharge from the hospital and at least 1 year after the first urodynamic examination. Bladder function was always correlated with the neurologic status and was assessed on the same day as the urodynamic examination. Drugs that could interfere with the urethrovesical function were discontinued at least 48 hours before examination. The urodynamic examinations were performed and neurogenic bladder dysfunction was defined according to the recommendations of the International Continence Society.5 The urodynamic examination consisted of video-cysto-urethromanometry performed in patients lying supine. Two multiple microtip-transducer catheters were used for urethrovesical and anorectal pressure recordings, respectively,6,7 and proper localization of the transducers within bladder and external urethral sphincter in relation to the anatomic landmarks of the pelvis was confirmed using fluoroscopy. In all patients, the bladder was filled with a constant slow filling rate of 5 mL/min. For practical reasons, DSD is mostly separated into two types (intermittent and continuous); however, in this study DSD was classified in three types according to Blaivas et al.2 According to this classification, type 1 DSD is characterized by a crescendo increase of the sphincter activity that reaches its maximum at the peak of the detrusor contraction. As the detrusor pressure begins to decline, sudden complete external sphincter relaxation occurs. Voiding occurs only during the down slope of the detrusor pressure as the sphincter relaxes. Type 2 DSD is characterized by clonic contractions of the external urethral sphincter interspersed throughout the detrusor contraction. These patients usually void with an interrupted spurting stream. In type 3 DSD, the external urethral sphincter contraction persists throughout the entire detrusor contraction. These patients void with an obstructive stream or cannot void at all. The statistical analysis was performed using a Statistical Analysis Systems software package. Fisher’s exact test (level of statistical significance at P ⬍0.05) was used to evaluate the statistical significance between the completeness of the spinal cord lesion and the type of DSD. The Spearman correlation coefficient (level of statistical significance at P ⬍0.03) was used to evaluate the correlation between the level of the lesion and the type of DSD. The sign rank test was used to assess the change in the type of DSD over time (level of statistical significance at P ⬍0.05). The chi-square test was used to evaluate the correlation between the voluntary contraction of the external urethral sphincter and the DSD type (level of statistical significance at P ⬍0.05).
RESULTS A total of 105 male patients could be analyzed. All but 10 had a traumatic spinal cord lesion. All 10 patients with a nontraumatic spinal cord lesion presented with a spinal injury as a consequence of vascular damage. The mean age at injury was 39.2 years (range 15 to 76 years). Of the 105 patients, 41 had tetraplegia (19 complete and 22 incomplete) and 64 had paraplegia (16 complete and 48 incom244
FIGURE 1. Proportion of detrusor-sphincter-dyssynergia (DSD) types according to Blaivas classification at first urodynamic examination (n ⫽ 105).
plete); 81 were in the early (less than 12 months) and 24 in the chronic (more than 1 year) postinjury phase. The mean time between the SCI and the first urodynamic examination was 100 days (SD 79.1) in the patients injured for less than 1 year and 3278.5 days (SD 3059.8) for the patients injured for longer than 1 year. At the first urodynamic examination, all but 2 patients had neurogenic detrusor overactivity with concomitant DSD. In the latter 2 patients, the bladder was considered to still be in spinal shock, with the detrusor areflexive. DSD was classified as type 1 in 15 patients (14.6%), type 2 in 80 patients (77.6%), and type 3 in 8 patients (7.8%). Of the 105 patients, 38 (36.2%) emptied their bladder by clean intermittent catheterization, 36 (34.3%) by suprapubic taping, and 19 (18%) by combining different voiding maneuvers (voluntary voiding plus clean intermittent catheterization or Crédé or tapping; tapping or Crédé plus clean intermittent catheterization; or tapping plus Crédé). Only 2 patients (2%) were able to completely empty their bladder through voluntary voiding. Ten acute-injured patients (9.5%) still had an indwelling transurethral (n ⫽ 2) or suprapubic (n ⫽ 8) catheter. In all subjects, we found a positive correlation between the severity of the spinal cord lesion and the type of DSD (Fisher’s exact test, P ⬍0.01). Patients with an incomplete sensory and motor neurologic deficit presented with type 1 DSD compared with patients with complete sensory and/or motor neurologic deficits who had type 2 or 3 DSD (Fig. 1). A statistically significant correlation was also found between the ability to voluntarily contract the external urethral sphincter and the DSD type. Patients with preserved voluntary contraction of the external urethral sphincter had a less severe DSD type compared with patients who had lost this ability (chi-square test, P ⬍0.01; Fig. 2). In contrast, we found no correlation between the level of the lesion (eg, tetraplegia versus paraplegia) and UROLOGY 65 (2), 2005
(from DSD type 1 to DSD type 2 or DSD type 2 to DSD type 3). Only 8.3% improved in DSD (from DSD type 2 to DSD type 1 or DSD type 3 to DSD type 2 or 1). COMMENT
FIGURE 2. Preserved or absent ability to voluntarily contract external anal sphincter in patients with different detrusor-sphincter-dyssynergia (DSD) types (n ⫽ 105).
FIGURE 3. Proportion of detrusor-sphincter-dyssynergia (DSD) types according to Blaivas classification at 1 year of follow-up (n ⫽ 66).
the DSD type (Spearman correlation coefficient, P ⬎0.03). Of the 81 patients injured for less than 1 year, 66 could be neurologically and urodynamically re-examined. The mean time between the first and second examinations was 535.4 days (SD 410). During the second urodynamic examination, all but 2 patients still had DSD. As in the first examination, a positive correlation was found between the severity of the spinal cord lesion and the DSD type (Fig. 3). At this time, no statistically significant change was found in the DSD type (sign rank test, P ⬎0.05). All 66 patients were neurologically and urodynamically re-examined a third time. The mean time between the first and third urodynamic examination was 1518.6 days (SD 1423). At the third examination, a statistically significant change was found in the DSD distribution compared with the first urodynamic examination (sign rank test, P ⬍0.05), despite no change found at the neurologic evaluation. Of the 66 patients, 65.5% remained in the same category as initially and 26.6% changed UROLOGY 65 (2), 2005
Previous data reported by Blaivas et al.,2 Yalla et al.,3 and Tanagho8 have demonstrated that micturition is normally 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 a neurologic lesion of suprasacral cord, this orderly sequence is usually lost and bladder-external sphincter dyssynergia ensues.2,3,8 All of our patients with a suprasacral cord lesion and outside of spinal shock had DSD. The DSD type correlated well with the neurologic deficit. Patients with complete sensory and/or motor deficit had either type 2 or 3 DSD compared with patients with incomplete sensory and motor deficits, who had type 1 DSD. Thus, both the sensory ascending tract and motor descending tract are important for synergic voiding. This finding correlates well with the anatomicphysiologic description of the central control of micturition. Apparently, lumbosacral afferents project into the mesencephalic periaqueductal gray matter.9 From there, efferent nerve fibers activate neurons located in the pontine micturition center (based in the medial part of the dorsolateral pontine tegmentum), which project to the sacral intermediolateral cell column and to the sacral intermediomedial cell column or dorsal gray commissure.10 The increase in bladder pressure resulting from this reflex loop is caused by monosynaptic and excitatory projection to the bladder motoneurons.11 The relaxation of the external urethral sphincter during micturition is caused by excitatory projection of the pontine micturition center to GABA-ergic interneurons in the dorsal gray commissure in the spinal cord.12 The preservation of part of the descending tract in patients with minor DSD was corroborated clinically because most of these patients preserved the ability to voluntarily contract their external urethral sphincter. However, even if some supraspinal control persisted, it was still not sufficient to ensure full sphincter synergia during involuntary bladder contractions. It might be that, in sensory-motor incomplete SCI, both spinal (C fibers mediated) and supraspinal (A delta-fibers mediated) reflex pathways coexist, resulting in the development of automatic micturition with partial synergic voiding. In contrast, as soon as the descending supraspinal tracts are fully destroyed the detrusor-to-detrusor reflexes are me245
diated only by the spinal central pathways, independently of some preservation of the sensory ascending pathways. Detrusor-sphincter-dyssynergia was originally understood as a manifestation of the improper execution and coordination of the somatic guarding reflex by the external urethral sphincter, resulting from a loss of input from the pontine micturition center.13 After SCI, reorganization of the spinal reflexes occurs and the normal spinal-bulbar-spinal micturition reflex is replaced by a spinal detrusorto-detrusor reflex.14 However, nothing is known about how this new reflex loop interacts with external urethral sphincter motor neurones. In spinal cord-transected cats, a reorganization of the synaptic input to sphincter motor neurons was found, and it was speculated that these synaptic alterations are involved in the development of DSD.15 Our results have shown that the DSD type is correlated with the neurologic deficit, such that the DSD type might be suspected by the neurologic evaluation findings. This is an important point, because patients with type 2 and 3 DSD are considered to have a greater risk of urologic complications. In these patients, bladder outflow obstruction is continuous throughout the detrusor contraction. Voiding either does not occur or the flow rate is markedly impaired. Detrusor trabeculations, reflux, or secondary ureterovesical obstruction should logically occur earlier and be more severe, even though this has not yet been proved. Recently, Weld et al.16 studied the clinical significance of the DSD type in a population of 269 patients with post-traumatic SCI and found that the presence of DSD was associated with complete injuries, elevated bladder pressures, and upper urinary tract complications. Also, these associations were more prominent with continuous than with intermittent DSD.16 Considering the possible upper urinary tract damage, it was concluded that the presence of continuous DSD may require earlier urodynamic follow-up. From our results, it seems that DSD tended to worsen over time. This finding is at variance with the report of Yalla et al.,3 who stated that DSD abates with time. Weld et al.16 found that the proportion of patients with type 1 DSD decreased, and that of patients with type 2 DSD increased, with time. This may be interpreted as an aggravation of the DSD in the patients affected, which is consistent with our findings. CONCLUSIONS Neurologic status and DSD type after SCI show statistically significant correlations and, therefore,
246
neurologic examination and determination of DSD type may be helpful to complete neurourologic diagnosis and to assist in confirming completeness of the lesion after acute injury. Because DSD seems to become worse with time, regular urodynamic follow-up examinations are mandatory in patients with DSD to adjust treatment, if necessary. REFERENCES 1. Abrams P, Cardozo L, Fall M, et al: The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 21: 167–178, 2002. 2. Blaivas JG, Sinha HP, Zayed AA, et al: Detrusor-external sphincter dyssynergia: a detailed electromyographic study. J Urol 125: 545–548, 1981. 3. Yalla SV, Blunt KJ, Fam BA, et al: Detrusor-urethral sphincter dyssynergia. J Urol 118: 1026 –1029, 1977. 4. Ditunno JF Jr: American spinal injury standards for neurological and functional classification of spinal cord injury: past, present and future. 1992 Heiner Sell Lecture of the American Spinal Injury Association. J Am Paraplegia Soc 17: 7–11, 1994. 5. Stohrer M, Goepel M, Kondo A, et al, for the International Continence Society Standardization Committee: The standardization of terminology in neurogenic lower urinary tract dysfunction: with suggestions for diagnostic procedures. Neurourol Urodyn 18: 139 –158, 1999. 6. Rossier AB, and Fam BA: 5-Microtransducer catheter in evaluation of neurogenic bladder function. Urology 27: 371– 378, 1986. 7. Schurch B, Yasuda K, and Rossier AB: Detrusor bladder neck dyssynergia revisited. J Urol 152(6 Pt 1): 2066 –2070, 1994. 8. Tanagho EA: Interpretation of the physiology of micturition, in Hinman F Jr (Ed): Hydrodynamics in Micturition. Springfield, Illinois, Thomas C Charles, 1971, pp 18 – 40. 9. Blok BF, and Holstege G: Direct projections from the periaqueductal gray to the pontine micturition center (M-region): an anterograde and retrograde tracing study in the cat. Neurosci Lett 166: 93–96, 1994. 10. Holstege G, Griffiths D, de Wall H, et al: Anatomical and physiological observations on supraspinal control of bladder and urethral sphincter muscles in the cat. J Comp Neurol 250: 449 – 461, 1986. 11. Blok BF, and Holstege G: The central nervous system control of micturition in cats and humans. Behav Brain Res 92: 119 –125, 1998. 12. Griffiths DJ, McCracken PN, Harrison GM, et al: Cerebral aetiology of urinary urge incontinence in elderly people. Age Ageing 23: 246 –250, 1994. 13. Park JM, Bloom DA, and McGuire EJ: The guarding reflex revisited. Br J Urol 80: 940 –945, 1997. 14. Morrison J: Reflex control of the lower urinary tract, in Torrens M, and Morrison J (Eds): The Physiology of the Lower Urinary Tract. Berlin, Springer-Verlag, 1987, pp 193–235. 15. Beattie MS, Leedy MG, and Bresnahan JC: Evidence for alterations of synaptic inputs to sacral spinal reflex circuits after spinal cord transection in the cat. Exp Neurol 123: 35– 50, 1993. 16. Weld KJ, Graney MJ, and Dmochowski RR: Clinical significance of detrusor sphincter dyssynergia type in patients with post-traumatic spinal cord injury. Urology 56: 565–568, 2000.
UROLOGY 65 (2), 2005
CAN NEUROLOGIC EXAMINATION PREDICT TYPE OF DETRUSOR SPHINCTER-DYSSYNERGIA IN PATIENTS WITH SPINAL CORD INJURY? BRIGITTE SCHURCH, DANIEL M. SCHMID, GILLES KARSENTY,
AND
ANDRE REITZ
ABSTRACT Objectives. To assess the correlations in males with spinal cord injury (SCI) between the neurologic status and type of detrusor-sphincter dyssynergia (DSD) observed during urodynamic examinations and to evaluate the change in the DSD pattern over time. Methods. A total of 105 male patients with chronic SCI were neurologically examined according to the American Spinal Cord Injury Association protocol and underwent video-urodynamic examinations. DSD observed during urodynamic studies was classified according to the Blaivas classification. To assess the stability of the DSD over time, patients who had been recently injured were clinically and urodynamically controlled after 1 year and thereafter. Results. A statistically significant positive correlation was found between the DSD type and completeness or incompleteness of the SCI lesion. Patients with an incomplete sensory and motor SCI lesion presented with DSD type 1 compared with patients with complete sensory and motor SCI lesion, who had DSD type 2 to type 3. A correlation was also found between the American Spinal Cord Injury Association scores and the DSD type. No correlation was found between the DSD type and lesion level. At medium to long-term follow-up, a significant change was found in the DSD type. Conclusions. The neurologic status and DSD type after SCI showed significant correlations. Therefore, neurologic examination and determination of the DSD type might be helpful to complete the neurourologic diagnosis and to assist in confirming completeness of the lesion after acute injury. Because DSD seems to become aggravated with time, regular urodynamic follow-up examinations are mandatory in patients with DSD to adjust their treatment, if necessary. UROLOGY 65: 243–246, 2005. © 2005 Elsevier Inc.
D
etrusor-sphincter dyssynergia (DSD) is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral sphincter and/or periurethral striated muscle.1 Previous data have suggested that this is a condition found exclusively in patients with a neurologic lesion of the suprasacral spinal cord.2 DSD adversely influences the achievement of balanced bladder function after suprasacral spinal cord injury (SCI). Classically, this syndrome has been regarded as functional subvesical obstruction that From the Department of Neuro-Urology, Swiss Paraplegic Center, Balgrist University Hospital; and Department of Urology, University Hospital, Zurich, Switzerland Reprint requests: Brigitte Schurch, M.D., Department of Neuro-Urology, Swiss Paraplegic Center, Balgrist University Hospital, Forchstrasse 340, Zurich 8008, Switzerland. E-mail: [email protected] Submitted: July 3, 2004, accepted (with revisions): September 15, 2004 © 2005 ELSEVIER INC. ALL RIGHTS RESERVED
leads to vesical hypertonicity, high-pressure contractile activity, vesicoureteral reflux, and, ultimately, renal damage and destruction. Detrusor-sphincter dyssynergia has been well described and classified.2,3 However, controversies remain concerning the correlation between the clinical neurologic level and severity of the spinal cord lesion (complete, incomplete) and the type of DSD. We first assessed the correlations between the neurologic status and type of DSD observed during urodynamic examinations and second evaluated the possible change in the DSD pattern over time in male patients with SCI. MATERIAL AND METHODS A total of 105 patients with a spinal cord lesion, who were admitted for rehabilitation to our institution, were studied. All patients were assessed neurologically on the day of admission according to the American Spinal Cord Injury Association protocol.4 Only patients with American Spinal Cord Injury 0090-4295/05/$30.00 doi:10.1016/j.urology.2004.09.024 243
Association impairment grade A to D were included. Accordingly, the spinal cord lesion was classified as complete or incomplete. Incomplete was defined as the presence of any sensory or motor function in the lowest sacral segments. Additionally, the bulbocavernous reflex and the voluntary contraction of the external anal sphincter were clinically tested in all patients. First, urodynamic examination was performed at least once during hospitalization. To assess the changes in bladder function over time, the patients were scheduled for urodynamic re-examination after discharge from the hospital and at least 1 year after the first urodynamic examination. Bladder function was always correlated with the neurologic status and was assessed on the same day as the urodynamic examination. Drugs that could interfere with the urethrovesical function were discontinued at least 48 hours before examination. The urodynamic examinations were performed and neurogenic bladder dysfunction was defined according to the recommendations of the International Continence Society.5 The urodynamic examination consisted of video-cysto-urethromanometry performed in patients lying supine. Two multiple microtip-transducer catheters were used for urethrovesical and anorectal pressure recordings, respectively,6,7 and proper localization of the transducers within bladder and external urethral sphincter in relation to the anatomic landmarks of the pelvis was confirmed using fluoroscopy. In all patients, the bladder was filled with a constant slow filling rate of 5 mL/min. For practical reasons, DSD is mostly separated into two types (intermittent and continuous); however, in this study DSD was classified in three types according to Blaivas et al.2 According to this classification, type 1 DSD is characterized by a crescendo increase of the sphincter activity that reaches its maximum at the peak of the detrusor contraction. As the detrusor pressure begins to decline, sudden complete external sphincter relaxation occurs. Voiding occurs only during the down slope of the detrusor pressure as the sphincter relaxes. Type 2 DSD is characterized by clonic contractions of the external urethral sphincter interspersed throughout the detrusor contraction. These patients usually void with an interrupted spurting stream. In type 3 DSD, the external urethral sphincter contraction persists throughout the entire detrusor contraction. These patients void with an obstructive stream or cannot void at all. The statistical analysis was performed using a Statistical Analysis Systems software package. Fisher’s exact test (level of statistical significance at P ⬍0.05) was used to evaluate the statistical significance between the completeness of the spinal cord lesion and the type of DSD. The Spearman correlation coefficient (level of statistical significance at P ⬍0.03) was used to evaluate the correlation between the level of the lesion and the type of DSD. The sign rank test was used to assess the change in the type of DSD over time (level of statistical significance at P ⬍0.05). The chi-square test was used to evaluate the correlation between the voluntary contraction of the external urethral sphincter and the DSD type (level of statistical significance at P ⬍0.05).
RESULTS A total of 105 male patients could be analyzed. All but 10 had a traumatic spinal cord lesion. All 10 patients with a nontraumatic spinal cord lesion presented with a spinal injury as a consequence of vascular damage. The mean age at injury was 39.2 years (range 15 to 76 years). Of the 105 patients, 41 had tetraplegia (19 complete and 22 incomplete) and 64 had paraplegia (16 complete and 48 incom244
FIGURE 1. Proportion of detrusor-sphincter-dyssynergia (DSD) types according to Blaivas classification at first urodynamic examination (n ⫽ 105).
plete); 81 were in the early (less than 12 months) and 24 in the chronic (more than 1 year) postinjury phase. The mean time between the SCI and the first urodynamic examination was 100 days (SD 79.1) in the patients injured for less than 1 year and 3278.5 days (SD 3059.8) for the patients injured for longer than 1 year. At the first urodynamic examination, all but 2 patients had neurogenic detrusor overactivity with concomitant DSD. In the latter 2 patients, the bladder was considered to still be in spinal shock, with the detrusor areflexive. DSD was classified as type 1 in 15 patients (14.6%), type 2 in 80 patients (77.6%), and type 3 in 8 patients (7.8%). Of the 105 patients, 38 (36.2%) emptied their bladder by clean intermittent catheterization, 36 (34.3%) by suprapubic taping, and 19 (18%) by combining different voiding maneuvers (voluntary voiding plus clean intermittent catheterization or Crédé or tapping; tapping or Crédé plus clean intermittent catheterization; or tapping plus Crédé). Only 2 patients (2%) were able to completely empty their bladder through voluntary voiding. Ten acute-injured patients (9.5%) still had an indwelling transurethral (n ⫽ 2) or suprapubic (n ⫽ 8) catheter. In all subjects, we found a positive correlation between the severity of the spinal cord lesion and the type of DSD (Fisher’s exact test, P ⬍0.01). Patients with an incomplete sensory and motor neurologic deficit presented with type 1 DSD compared with patients with complete sensory and/or motor neurologic deficits who had type 2 or 3 DSD (Fig. 1). A statistically significant correlation was also found between the ability to voluntarily contract the external urethral sphincter and the DSD type. Patients with preserved voluntary contraction of the external urethral sphincter had a less severe DSD type compared with patients who had lost this ability (chi-square test, P ⬍0.01; Fig. 2). In contrast, we found no correlation between the level of the lesion (eg, tetraplegia versus paraplegia) and UROLOGY 65 (2), 2005
(from DSD type 1 to DSD type 2 or DSD type 2 to DSD type 3). Only 8.3% improved in DSD (from DSD type 2 to DSD type 1 or DSD type 3 to DSD type 2 or 1). COMMENT
FIGURE 2. Preserved or absent ability to voluntarily contract external anal sphincter in patients with different detrusor-sphincter-dyssynergia (DSD) types (n ⫽ 105).
FIGURE 3. Proportion of detrusor-sphincter-dyssynergia (DSD) types according to Blaivas classification at 1 year of follow-up (n ⫽ 66).
the DSD type (Spearman correlation coefficient, P ⬎0.03). Of the 81 patients injured for less than 1 year, 66 could be neurologically and urodynamically re-examined. The mean time between the first and second examinations was 535.4 days (SD 410). During the second urodynamic examination, all but 2 patients still had DSD. As in the first examination, a positive correlation was found between the severity of the spinal cord lesion and the DSD type (Fig. 3). At this time, no statistically significant change was found in the DSD type (sign rank test, P ⬎0.05). All 66 patients were neurologically and urodynamically re-examined a third time. The mean time between the first and third urodynamic examination was 1518.6 days (SD 1423). At the third examination, a statistically significant change was found in the DSD distribution compared with the first urodynamic examination (sign rank test, P ⬍0.05), despite no change found at the neurologic evaluation. Of the 66 patients, 65.5% remained in the same category as initially and 26.6% changed UROLOGY 65 (2), 2005
Previous data reported by Blaivas et al.,2 Yalla et al.,3 and Tanagho8 have demonstrated that micturition is normally 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 a neurologic lesion of suprasacral cord, this orderly sequence is usually lost and bladder-external sphincter dyssynergia ensues.2,3,8 All of our patients with a suprasacral cord lesion and outside of spinal shock had DSD. The DSD type correlated well with the neurologic deficit. Patients with complete sensory and/or motor deficit had either type 2 or 3 DSD compared with patients with incomplete sensory and motor deficits, who had type 1 DSD. Thus, both the sensory ascending tract and motor descending tract are important for synergic voiding. This finding correlates well with the anatomicphysiologic description of the central control of micturition. Apparently, lumbosacral afferents project into the mesencephalic periaqueductal gray matter.9 From there, efferent nerve fibers activate neurons located in the pontine micturition center (based in the medial part of the dorsolateral pontine tegmentum), which project to the sacral intermediolateral cell column and to the sacral intermediomedial cell column or dorsal gray commissure.10 The increase in bladder pressure resulting from this reflex loop is caused by monosynaptic and excitatory projection to the bladder motoneurons.11 The relaxation of the external urethral sphincter during micturition is caused by excitatory projection of the pontine micturition center to GABA-ergic interneurons in the dorsal gray commissure in the spinal cord.12 The preservation of part of the descending tract in patients with minor DSD was corroborated clinically because most of these patients preserved the ability to voluntarily contract their external urethral sphincter. However, even if some supraspinal control persisted, it was still not sufficient to ensure full sphincter synergia during involuntary bladder contractions. It might be that, in sensory-motor incomplete SCI, both spinal (C fibers mediated) and supraspinal (A delta-fibers mediated) reflex pathways coexist, resulting in the development of automatic micturition with partial synergic voiding. In contrast, as soon as the descending supraspinal tracts are fully destroyed the detrusor-to-detrusor reflexes are me245
diated only by the spinal central pathways, independently of some preservation of the sensory ascending pathways. Detrusor-sphincter-dyssynergia was originally understood as a manifestation of the improper execution and coordination of the somatic guarding reflex by the external urethral sphincter, resulting from a loss of input from the pontine micturition center.13 After SCI, reorganization of the spinal reflexes occurs and the normal spinal-bulbar-spinal micturition reflex is replaced by a spinal detrusorto-detrusor reflex.14 However, nothing is known about how this new reflex loop interacts with external urethral sphincter motor neurones. In spinal cord-transected cats, a reorganization of the synaptic input to sphincter motor neurons was found, and it was speculated that these synaptic alterations are involved in the development of DSD.15 Our results have shown that the DSD type is correlated with the neurologic deficit, such that the DSD type might be suspected by the neurologic evaluation findings. This is an important point, because patients with type 2 and 3 DSD are considered to have a greater risk of urologic complications. In these patients, bladder outflow obstruction is continuous throughout the detrusor contraction. Voiding either does not occur or the flow rate is markedly impaired. Detrusor trabeculations, reflux, or secondary ureterovesical obstruction should logically occur earlier and be more severe, even though this has not yet been proved. Recently, Weld et al.16 studied the clinical significance of the DSD type in a population of 269 patients with post-traumatic SCI and found that the presence of DSD was associated with complete injuries, elevated bladder pressures, and upper urinary tract complications. Also, these associations were more prominent with continuous than with intermittent DSD.16 Considering the possible upper urinary tract damage, it was concluded that the presence of continuous DSD may require earlier urodynamic follow-up. From our results, it seems that DSD tended to worsen over time. This finding is at variance with the report of Yalla et al.,3 who stated that DSD abates with time. Weld et al.16 found that the proportion of patients with type 1 DSD decreased, and that of patients with type 2 DSD increased, with time. This may be interpreted as an aggravation of the DSD in the patients affected, which is consistent with our findings. CONCLUSIONS Neurologic status and DSD type after SCI show statistically significant correlations and, therefore,
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neurologic examination and determination of DSD type may be helpful to complete neurourologic diagnosis and to assist in confirming completeness of the lesion after acute injury. Because DSD seems to become worse with time, regular urodynamic follow-up examinations are mandatory in patients with DSD to adjust treatment, if necessary. REFERENCES 1. Abrams P, Cardozo L, Fall M, et al: The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 21: 167–178, 2002. 2. Blaivas JG, Sinha HP, Zayed AA, et al: Detrusor-external sphincter dyssynergia: a detailed electromyographic study. J Urol 125: 545–548, 1981. 3. Yalla SV, Blunt KJ, Fam BA, et al: Detrusor-urethral sphincter dyssynergia. J Urol 118: 1026 –1029, 1977. 4. Ditunno JF Jr: American spinal injury standards for neurological and functional classification of spinal cord injury: past, present and future. 1992 Heiner Sell Lecture of the American Spinal Injury Association. J Am Paraplegia Soc 17: 7–11, 1994. 5. Stohrer M, Goepel M, Kondo A, et al, for the International Continence Society Standardization Committee: The standardization of terminology in neurogenic lower urinary tract dysfunction: with suggestions for diagnostic procedures. Neurourol Urodyn 18: 139 –158, 1999. 6. Rossier AB, and Fam BA: 5-Microtransducer catheter in evaluation of neurogenic bladder function. Urology 27: 371– 378, 1986. 7. Schurch B, Yasuda K, and Rossier AB: Detrusor bladder neck dyssynergia revisited. J Urol 152(6 Pt 1): 2066 –2070, 1994. 8. Tanagho EA: Interpretation of the physiology of micturition, in Hinman F Jr (Ed): Hydrodynamics in Micturition. Springfield, Illinois, Thomas C Charles, 1971, pp 18 – 40. 9. Blok BF, and Holstege G: Direct projections from the periaqueductal gray to the pontine micturition center (M-region): an anterograde and retrograde tracing study in the cat. Neurosci Lett 166: 93–96, 1994. 10. Holstege G, Griffiths D, de Wall H, et al: Anatomical and physiological observations on supraspinal control of bladder and urethral sphincter muscles in the cat. J Comp Neurol 250: 449 – 461, 1986. 11. Blok BF, and Holstege G: The central nervous system control of micturition in cats and humans. Behav Brain Res 92: 119 –125, 1998. 12. Griffiths DJ, McCracken PN, Harrison GM, et al: Cerebral aetiology of urinary urge incontinence in elderly people. Age Ageing 23: 246 –250, 1994. 13. Park JM, Bloom DA, and McGuire EJ: The guarding reflex revisited. Br J Urol 80: 940 –945, 1997. 14. Morrison J: Reflex control of the lower urinary tract, in Torrens M, and Morrison J (Eds): The Physiology of the Lower Urinary Tract. Berlin, Springer-Verlag, 1987, pp 193–235. 15. Beattie MS, Leedy MG, and Bresnahan JC: Evidence for alterations of synaptic inputs to sacral spinal reflex circuits after spinal cord transection in the cat. Exp Neurol 123: 35– 50, 1993. 16. Weld KJ, Graney MJ, and Dmochowski RR: Clinical significance of detrusor sphincter dyssynergia type in patients with post-traumatic spinal cord injury. Urology 56: 565–568, 2000.
UROLOGY 65 (2), 2005