Detrusor contractility and overactive bladder in patients with cerebrovascular accident


Osamu Natsume md, Department of Urology, Nara Medical University, Shijo-cho 840, Kashihara City, Nara 634-8522, Japan. Email:


Objectives:  A retrospective analysis of urodynamic studies was conducted to investigate detrusor contractility following cerebrovascular accident.

Methods:  Fifty-seven patients (34 men and 23 women) who were rehabilitated following cerebrovascular accident were included in the analysis. Subjects with maximum contractile power values less than 10 W/m2 in men and 8 W/m2 in women, in the absence of bladder outlet obstruction, were defined as having detrusor underactivity.

Results:  A significantly lower maximum value of detrusor contractile power and a larger residual urine volume, particularly more prevalent in women than in men, appeared unexpectedly after cerebrovascular accident. Patients with underactivity had significantly lower maximum and average flow rates, lower contractile power, and an increased postvoid residual relative to their normal counterparts. The prevalence of underactivity was 35% in the men and 43% in the women. Furthermore, 67% of the men and 80% of the women with underactivity had overactive bladder symptoms. On the other hand, detrusor underactivity was observed in 8 (35%) of 23 overactive bladder patients in the men and 8 (42%) of 19 in the women.

Conclusions:  Post-cerebrovascular accident patients presented various patterns of detrusor contractility. Specific attention to the possible occurrence of detrusor underactivity in these patients is essential for the successful management of overactive bladder syndrome.


Voiding disorders in patients with cerebrovascular accident (CVA) have an impact on their well-being1 and social participation. These disorders are of concern for stroke care. Overactive bladder (OAB), which is a symptom syndrome defined by the International Continence Society (ICS)2 as urinary urgency with or without urge incontinence, usually with urinary frequency and nocturia, is a common voiding disturbance following CVA. Antimuscarinic drugs in clinical practice are the mainstay for the relief of OAB symptoms at present. Nevertheless, there have been many patients refractory to antimuscarinic treatment and the limited efficacy and side-effects of these drugs make alternative treatment approaches desirable.3 Therefore, patients with reduced detrusor contractility, namely, detrusor underactivity (DUA), which is defined as a contraction of reduced strength or duration resulting in prolonged or incomplete bladder emptying within a normal time span,2 should be managed carefully.4 However, there is little available data referring to the relationship between post-CVA detrusor contractility and voiding efficiency, although there are a variety of reports using filling cystometry in patients with CVA.5,6 This study was conducted to investigate the relationship between post-CVA detrusor contractility, OAB, and bladder emptying. This relationship could contribute to more successful management of voiding disturbance following CVA. Particular emphasis has been placed on the predisposition to DUA, which is a pathology that interferes with the pharmacological management of OAB even among post-CVA patients with OAB symptoms, particularly in women.


Between August 2001 and April 2006, a total of 103 consecutive patients complaining of post-CVA voiding manifestations 1 month to less than 1 year since the onset of CVA were identified. Eighteen patients who experienced difficulty undergoing urodynamic examination or who were unwilling to consent to it were excluded. Subjects underwent a pressure flow study (PFS) to estimate their detrusor contractility. A total of 57 subjects, consisting of 34 men and 23 women aged 37–81 years (mean 64.8 years), were enrolled for further analysis. In the men, subjects who met the criteria for obstruction grade 0 or 1 on the Schäfer nomogram were available for this analysis. In the women, subjects without a Qmax less than 10 mL/s in pressure flow studies combined with a detrusor pressure recorded at the maximum flow rate (PdetQmax) more than 20 cmH2O were analyzed. These criteria are consistent with a definition of female bladder outlet obstruction proposed by Grout and coworkers, where obstructive bladder outlet is defined by a Qmax less than 12 mL/s in repeated free-flow studies with a PdetQmax more than 20 cmH2O, and with the fact that a Qmax obtained by pressure flow studies with a urethral catheter in place is significantly lower than one obtained by free-flow studies.7 Endoscopic examinations or voiding cystourethrography results were reviewed for patients with low flow and high PdetQmax, because a PFS alone may fail to diagnose bladder outlet obstruction.7 All patients were given sufficient information and consent was obtained. Patients with other neurological disorders, such as diabetes mellitus, spinal cord injury, or disease, uterine myoma, or any previous intrapelvic surgery that might affect their detrusor motor function were excluded. Prior to urodynamic examination, the administration of antimuscarinic drugs that could potentially affect detrusor function was discontinued for approximately 7 days. All patients underwent urinalysis and any patient with urinary tract infection received the appropriate treatment. Filling cystometry followed by PFS was conducted with a 6Fr. dual lumen urethral catheter line (PORGÈS Co., Ltd, Japan) and an 8 Fr. rectal pressure line in place using the 3-channel subtracted urodynamic system Libra Plus Medical Measurement Systems software (Netherlands). The methods and definitions corresponded to those of the ICS.2 The postvoid residual (PVR) after each PFS was estimated by catheterizing the patient through the urethral catheter. Voided volume (VV), total bladder capacity (TBC), PVR as a percentage of TBC (%PVR), maximum (Qmax), and average (Qave) flow rate, and PdetQmax were measured. The detrusor contractile power (activity) or detrusor contractility was estimated using the maximum value of the approximation of power per detrusor muscle surface area (WFmax).8 Urethral resistance was calculated as PdetQmax divided by the square of Qmax.9

There is no cut-off value using PFS parameters for DUA. In this study, the %PVR correlated negatively with WFmax in both the men and women (Fig. 1a,b), where bladder emptying was noticeably reduced in the range of WFmax less than 10 W/m2 in the men and 8–10 W/m2 in the women. Therefore, herein, DUA was defined as follows using the parameter WFmax. Subjects were considered to have DUA if their WFmax values were less than 10 W/m2 in the men and less than 8 W/m2 in the women. Subjects with WFmax values of 10 W/m2 or more in the men and 8 W/m2 or more in the women were considered to have normal detrusor contractility, and these served as controls to compare with patients with DUA.

Figure 1.

Relation between WFmax and %PVR in all male (a) and female patients (b).

The included patients were segregated into OAB or non-OAB groups according to the presence or absence of OAB symptoms. When we were unable to confirm the presence of urgency owing to aphasia or cognitive impairment, despite complications with noticeable urinary frequency or incontinence, the patient was classified into an ‘unknown group’. History taking alone seemed unreliable, particularly in patients with aphasia or cognitive impairment. Therefore, to increase reliability, information about the patients regarding episodes of urgency or urge incontinence was obtained by utilizing frequency charts recorded with the aid of the nursing staff or their respective care-givers. Using the motor domain of the functional independence measure (FIM) scale,10 the poststroke severity in the activities of daily living (ADL) was assessed at the time of urodynamic examination in all patients.

Student's t-test was used to compare the differences in patient characteristics and the examined continuous variables between the two groups. A χ2 test was performed to compare the differences in the categorical variables, and Fisher's exact test was used only for small sample sizes. A linear or binomial regression model was used to describe the correlation between two numerical variables using Pearson's correlation coefficients. P-values less than 0.05 were considered significant.


Table 1 summarizes the overall backgrounds of the patients. There were no significant differences between males and females with respect to the patients' backgrounds, including age, affected period from the occurrence of CVA, original disease, the prevalence of OAB, hemiplegia site, and FIM motor domain scores.

Table 1.  Clinical characteristics of the subject population
  1. CVA, Cerebrovascular accident; FIM, Functional independence measure; OAB, Overactive bladder.

No. of patients3423 
Age (years)63.6 (37–81)66.4 (51–77)0.257
Affected periods (days)126 (42–266)110 (34–212)0.253
FIM-motor domain scores57 (31–90)50 (18–85)0.103
Cause of CVA
 Cerebral infarction197 
 Intracranial hemorrhage1512
 Subarachnoid hemorrhage04 
Site of hemiparalysis/–paresis
 Not paralytic11 
No. pts. with or without OAB
 With OAB2316 
 Without OAB1060.809

Table 2 lists the overall findings of urodynamic variables and detrusor function in men and women. There was no difference in the prevalence of DUA in the men (35%) and the women (43%). However, the WFmax value was significantly lower in the women (8.1 W/m2) than in the men (12.4 W/m2) despite similar results for TBC, VV, Qmax, Qave, and urethral resistance.

Table 2.  Overall findings of variables obtained by a pressure flow study in men and women
VariablesMen (n = 34)Women (n = 23)P-value
  1. Data are presented as the means, with ranges in parentheses. †One male patient who was unknown in respect to the presence of overactive bladder was excluded. PdetQmax, detrusor pressure recorded at the maximum flow rate; PVR, Postvoid residual urine volume; Qave, Average flow rate; Qmax, Maximum flow rate; Wfmax, Maximum value of the approximation of power per detrusor muscle surface area.

Total bladder capacity (ml)229 (73–514)249 (100–519)0.545
Voided volume (ml)197 (57–506)189 (64–468)0.785
Qmax (ml/s)13.9 (6–28)13.9 (6–31)0.977
Qave (ml/s)7.6 (3–14)6.9 (3–15)0.411
WFmax (W/m2)12.4 (3.5–27.0)8.1 (2.9–18.7)0.002
Detrusor compliance (ml/cmH2O)40 (2.8–100)56 (6.5–162)0.071
PVR (ml)32 (0–380)59 (0–330)0.186
%PVR (%)10.0 (0–87)21.8 (0–79)0.042
PdetQmax (cmH2O)32.4 (15–48)21.5 (4–38)<0.0001
Urethral resistance0.22 (0.04–0.72)0.17 (0.03–0.41)0.203
No. of patients with detrusor underactivity (%)12 (35)10 (43)0.534
No. of patients with overactive bladder (%)23 (70)17 (74)0.731
No. of patients with detrusor overactivity (%)14 (41)7 (30)0.410

Twelve male patients (35%) were grouped as having DUA, and 8 (67%) of those showed concurrent OAB symptoms (Table 3). Similarly, 10 female patients (43%) were grouped as having DUA, and 8 (80%) of those showed concurrent OAB symptoms. On the other hand, there were 8 (35%) male patients with DUA of 23 OAB patients and 8 (42%) of 19 in the women. The group with DUA had a significant decrease in Qmax, Qave, and WFmax and an increase in PVR and %PVR despite a TBC similar to the group with normal detrusor contractility in both the men and the women, although the age of this group was significantly higher and the affected periods shorter in the group with DUA in the men. There was no difference in detrusor compliance between the groups in both the men and the women. Detrusor overactivity was positive in 21 (37%) overall, in 18 (45%) of the 40 OAB patients, and in 33% of male patients and 20% of female patients with DUA. Whether detrusor overactivity was present or not did not affect the measured values of WFmax in either men or women.

Table 3.  Comparison of data between the groups divided according to detrusor contractility in men and women
 Men (n = 34)Women (n = 23)
Underactive (n = 12)Normal (n = 22)P-valueUnderactive (n = 10)Normal (n = 13)P-value
  • One was excluded due to an unknown presence of overactive bladder (OAB).

  • ‡Fisher's exact test. Data are presented as the means, with ranges in parentheses. FIM, Functional independence measure; OAB, Overactive bladder; PdetQmax, detrusor pressure recorded at the maximum flow rate; PVR, Postvoid residual urine volume; Qave, Average flow rate; Qmax, Maximum flow rate; Wfmax, Maximum value of the approximation of power per detrusor muscle surface area.

Age (years)69.3 (56–81)60.6 (37–79)0.01069.2 (54–72)64.2 (51–77)0.117
Affected days (days)95 (42–129)144 (61–266)0.009108 (34–202)111 (49–212)0.880
Motor domain score of FIM60 (31–83)56 (39–90)0.53248 (18–73)52 (29–85)0.566
Frequency of delivery2.3 (2–3)2.2 (1–4)0.693
Total bladder capacity (mL)242 (88–494)222 (73–514)0.634246 (100–519)251 (106–489)0.924
Voided volume (mL)158 (57–316)219 (73–514)0.094146 (64–468)223 (101–404)0.094
Qmax (mL/s)11.0 (6–17)15.5 (9–28)0.0069.4 (6–16)17.3 (10–31)0.0009
Qave (mL/s)5.8 (3–8)8.5 (5–14)0.0044.5 (3–7)8.8 (5–15)0.0011
WFmax (W/m2)7.8 (3.5–9.8)14.9 (10.5–27)<0.00014.6 (2.9–7.3)10.7 (8.0–18.7)<0.0001
Detrusor compliance (ml/cmH2O)49 (6.1–100)35 (2.8–81)0.15246.2 (10.1–120)62.6 (6.5–162)0.323
PVR (ml)85 (0–380)4 (0–29)0.0014100 (6–330)28 (0–112)0.022
%PVR (%)25.8 (0–87)1.5 (0–7)<0.000139 (4.4–79.3)9 (0–34.4)0.0008
PdetQmax (cmH2O)26.7 (15–40)35.5 (19–48)0.00516.2 (4–31)25.5 (15–38)0.0095
Urethral resistance0.29 (0.07–0.72)0.18 (0.04–0.44)0.0450.23 (0.03–0.41)0.12 (0.03–0.38)0.036
No. of patients with OAB (%)8 (67)15 (71)>0.99998 (80)9 (69)0.660
No. of patients with DO (%)4 (33)9 (41)0.7272 (20)5 (38)0.405

Figure 2 shows representative examples of WF values plotted as a function of the instantaneous bladder volume obtained in patients with and without OAB. As Griffiths and coworkers described,8 an ideal curve was seen following an increasing detrusor pressure with a sudden strong desire to void at the end of filling cystometry in patients with a WFmax of more than 8–10 W/m2 (Fig. 2a,b). On the other hand, a non-ideal contraction pattern with fluctuation and prematurely fading contraction (Fig. 2c,d) was likely to be seen in patients with a WFmax of less than approximately 8–10 W/m2.

Figure 2.

Representative examples of WF values plotted as a function of the instantaneous bladder volume of a detrusor overactivity-positive, 71-year-old female patient without an overactive bladder (a) and a detrusor overactivity-positive, 59-year-old female patient with an overactive bladder (b) where WFmax values of more than 10 W/m2 are recorded and ideal curves are seen overall. Representative examples of WF in a detrusor overactivity-positive, 60-year-old male patient with an overactive bladder (c) and a detrusor overactivity-positive, 51-year-old female patient with an overactive bladder (d) are shown. Detrusor contractile power plotted as a function of the instantaneous bladder volume with fluctuation and a fading contraction pattern during voiding are seen overall. Particularly in case (d), 79 mL of postvoid residual urine remains, regardless of a maximum flow rate of 16 mL/s.


This study found that the concurrence of DUA in patients with OAB, which is a symptom-defined condition characterized by urinary urgency and a major component of voiding disturbance following CVA, was likely to be prevalent in both men and women. The implication of this finding is that caution regarding the possible concurrence of DUA is needed in the management of decreased bladder emptying in patients with CVA. In particular, female patients may suffer from a greater decrease in bladder emptying than male patients. This condition is not so surprising considering that normal voiding detrusor pressure is generally significantly lower in women than in men.11

Herein, the following question is raised: ‘could a decreased WFmax be merely a consequence of advanced age or a reduced initial bladder volume?’ Regarding this issue, some studies noted that WFmax is volume-independent12 and has good reproducibility.13 Also, in this study, there was no difference in TBC between the groups with underactive and normal detrusor contractility in both men and women. It is conceivable, however, that detrusor underactivity could have been, in part, present prior to the onset of CVA because bladder function appears to deteriorate throughout adult life.14,15

DUA is less understood than OAB, and various factors including aging itself may potentially contribute to its etiology.16 As a possible etiology, the voiding reflex pathway after CVA may be modulated by a variety of transmitter mechanisms in the suprapontine area.17 It is also conceivable that a mechanism that promotes complete bladder emptying acts ineffectively, being linked to less sustained detrusor contractile power and fading contraction.3,8,18 Yokoyama et al. showed that bladder activity following ischemic brain damage might be modified via the alteration of a central control mechanism that is known to influence the voiding reflex.19 Interestingly, Matsuura et al. referred to the possible involvement of some cortical areas in bladder perception following intravesical cold water stimulation.20 They observed in a PET study that brain areas were activated predominantly on the left side, and they considered that two functionally separate pathways may be involved in bladder perception. Petersen et al. showed a positive cooling reflex in some OAB patients with a suprapontine pathology.21 The present study also confirmed a positive ice water test in 13 (68%) of 19 OAB patients who underwent the test (data not shown).

Generally, age-related changes in detrusor contractility might potentially affect the predisposition to DUA of patients suffering from CVA. Van Mastrigt found that normal contractility values for women decreased almost linearly with age from 30 W/m2 at early ages to 12 W/m2 at an age of 70 years, whereas this trend was considerably less pronounced in men.15 However, this finding was contradicted by a finding of no age-associated changes of detrusor contractility by Madersbacher et al.22 Furthermore, other factors such as a lack of estrogen and pelvic floor dysfunction including urogenital prolapse might affect detrusor contractility in women. Stern et al. suggested the potential influence of estrogen on bladder emptying in postmenopausal women in a retrospective, case-controlled study using oral estrogen replacement therapy.23 Elbadawi et al. observed widespread degeneration of muscle cells and axons in the aging detrusor,24 and Zhu et al. suggested that estrogen deficiency might contribute to these changes in impaired contractility.25,26

To date, there have been no standard criteria using urodynamic parameters for DUA. Van Mastrigt et al. indicated that the preoperative prediction of a significant residual urine volume after transurethral prostatectomy was possible using a discrimination value of 9.9 W/m2 for WFmax.13 In addition, Griffiths et al. in an assessment of detrusor contraction in healthy premenopausal women found that WF values ranged from 5 to 10 W/m2 in non-ideal voidings where detrusor contraction was less well sustained.8 These discriminating values would back up the present observation that urodynamic values of WFmax less than 10 W/m2 in men and less than 8 W/m2 in women, in the absence of bladder outlet obstruction, might be appropriate to characterize DUA. Moreover, the present analysis demonstrated that significant differences in Qmax, Qave, and voiding efficiency, as well as the values of WFmax, were found despite a similar TBC between the groups with normal and underactive detrusor contractility. These findings satisfy the conditions for DUA affected by an inadequate contractile strength or duration to affect complete bladder emptying, as indicated by ICS and previous investigators.11

Although the efficacy of antimuscarinic drugs against OAB symptoms (which mainly reduce detrusor pressure during the bladder storage phase and enable an increase of bladder capacity)3,27 is well documented, it remains unclear whether these pharmacological agents currently used for the treatment of OAB are equally effective and safe when DUA is also present.16 It is very interesting to note that all patients with OAB symptoms who were diagnosed with detrusor hyperactivity with an impaired contractile function were women whose WFmax values were markedly low, ranging from 2.9 to 5.3 W/m2 with a mean value of 4.1 W/m2. This dysfunction is defined as a PVR of 100 mL or greater or as a %PVR of 50% or greater.4 A combination of lowered Qmax and Qave, regardless of well stored bladder volume may be useful as first line discriminating indicators in the screening for DUA.

In CVA, various voiding manifestations including urinary retention are often observed.28 For example, a problematic symptom such as severe hesitancy on initiation resulting in failing to pass urine due to the diminishing desire to void, which we ordinarily describe as ‘misfiring in voiding’, was also observed in the present patient population. Brittain et al. reported that the impact on ADL was not related to stroke per se but to the severity of urinary symptoms.29 In particular, OAB might exacerbate symptoms due to bladder outlet obstruction or vice versa30,31 and have a profound impact on ADL.

In conclusion, pressure flow study found that the rate of DUA was unexpectedly prevalent among stroke patients. Individual variation in detrusor contractility after CVA was seen, and concurrent OAB symptoms frequently appeared in patients with DUA. Because DUA and OAB are generally pathologies that could mutually interfere with each other during their treatment, careful attention to detrusor contractility to improve OAB symptoms is essential for successful urological management following CVA. New targets for treatment of impaired bladder sensation may provide more successful therapeutic alternatives to OAB after CVA in the future. It is hoped that further clinical investigations will lead to a better understanding of the pathophysiology of post-CVA OAB and to a treatment approach that takes into consideration the characteristics of the causative disease.