Injection of Botulinum toxin into the detrusor muscle is a treatment for urinary incontinence secondary to neurogenic detrusor overactivity while injection into the external urethral sphincter is a treatment for detrusor-sphincter dyssynergia and high post void residual urines.
| Author Year; Country Score Research Design Sample Size | Methods | Outcome |
| Fougere et al. 2016 Canada Pre-post N=17 | Population: N=17 (12M, 5F) with chronic traumatic SCI at or above T6 and concomitant autonomic dysreflexia and neurogenic detrusor overactivity Mean (SD) age: 44 (10) Mean (SD) years post injury: 21 (11) AIS-A/B/C = 9/5/3 11 cervical, 6 thoracic
Treatment: One cycle of Botox injection (200U in 20mL 0.9% saline, injected into 20 sites of detrusor muscle), 2wk after baseline measurements & 1mo before post-treatment measurements
Outcome Measures: Urodynamic studies (UDS), 24h ambulatory BP monitoring (ABPM), AD Health-related QoL questionnaire, I-QOL questionnaire | 1. Pre vs. post-botox during UDS (mean±SD): Significantly lower SBP (mmHg) at: First urge to preform CIC (112±17 vs. 114±14), at max volume infused (151±25 vs. 133±17), and at max SBP (153±25 vs. 134±16) Significantly lower ΔSBP* (mmHg) at: First urge to preform CIC (34±20 vs. 15±11), at max volume infused (40±24 vs. 18±12), and at max SBP (42±23 vs. 20±10) Significantly lower ΔHR (bpm) at: First urge to preform CIC (-8±11 vs. -6±10), at max volume infused (-17±12 vs. -9±14), and at max SBP (-16±13 vs. -8±14) 2. Pre vs. post-botox during bladder events (mean±SD, from 24h ABPM): Significantly reduced max SBP (157±21 vs. 139±21) & ΔSBP** during CIC 3. AD eliminated in 10 participants (ΔSBP <20mmHg), attenuated in 7 4. Significantly fewer participants reporting AD symptoms post-botox (15 to 9) 5. Significantly reduced frequency of AD during CIC post-treatment (67% to 25%) 6. Significant improvement in all subsections and in total scores of QoL measures *change in measure vs. supine baseline **change in measure vs. seated baseline CIC = clean intermittent catheterization |
| Chen & Kuo 2012; Taiwan Pre-post N=49 (with AD=34) | Population: 49 patients (31M, 18F) with SCI and detrusor sphincter dyssynergia; Level of SCI: 27 cervical, 22 thoracic; mean age in yrs: 41.6, range 22-74; mean DOI in yrs: 8, range 1-35. Treatment: Patients received two sets of 200 U BoNT-A injections into the detrusor at baseline and 6 months later. Outcome Measures: Improvement in the severity of AD; net change in the grade of incontinence; net changes in the scores of the Urogenital Distress Inventory (UDI-6); Incontinence Impact Questionnaire; quality of life index; urodynamic parameters. | 1. 15 patients did not have AD at baseline or after treatment. 2. AD was completely resolved in 3 patients, and improved in 18; treatment made no difference in 3 patients and AD was exacerbated in 10. 3. No significant differences in any urodynamic variables between patients with and without AD. 4. A significantly greater improvement in the UDI-6 was noted in patients without AD and those in whom AD improved than in those with AD. Occurrence of AD was not significantly associated with persistent urinary incontinence after the BoNT-A injections. 5. No significant difference in the quality of life index between patients with and without AD at the end point. |
| Chen et al. 2008; Taiwan Pre-post N=20 (with AD=4) | Population: 20 suprasacral SCI subjects with detrusor external sphincter dyssynergia (DESD); Mean age 37.9 (15.7); 17 male; 12 cervical, 3 thoracic, 5 lumbar; AIS diagnosis: 11 AIS-A, 2 AIS-B, 4 AIS-C, 3 AIS-D. Treatment: A single dose of 100 IU botulinum toxin A was applied into the external urethral sphincter via cystoscopy. Outcome Measures: maximal detrusor pressure, maximal urethral pressure, maximal detrusor leak point pressure, integrated electromyography (IEMG) of the external urethral sphincter and, maximal pressure on static urethral pressure profilometry, recorded before and 4 weeks after the injection; post-voiding residues, measured 1, 2, 3, and 6 months post-injection. | 1. 4 patients who had AD symptoms before treatment reported decreased frequency and intensity of AD. 2. There was significant reduction in the IEMG (from 16.7(13.6) to 12.5(12.9) uV), as well as static urethral pressure (from 139.4(40.5) to 104.8(30.5) cmH2O) and maximal urethral pressure (from 107.5(69.1) to 80.2(35.7) cmH2O). 3. There was no significant difference in the maximal detrusor pressure or detrusor leak point pressure. 4. Post-voiding residues were significantly reduced at 1st, 2nd, 3rd, and 6th months post-injection. |
Five pre-post studies (n=132) (Dykstra et al. 1988; Schurch et al. 2000; Chen et al. 2008; Kuo 2008; Chen & Kuo 2012) found injection of Botulinum toxin into the detrusor muscle or bladder sphincter to be an effective method for treating urinary incontinence or retention secondary to neurogenic detrusor overactivity and bladder sphincter dyssynergia. In these conditions, injections of the Botulinum toxin either allowed increased urinary bladder capacity (i.e. reduced overactivity of the bladder) or facilitated improved evacuation of urine (reduced bladder sphincter dyssynergia). The duration of effect was reported to last up to 9 months (Schurch et al. 2000). All studies were level 4 and showed positive effects. In fact, following treatment with Botulinum toxin, 3 individuals reported fewer episodes of AD (Kuo 2008), 4 individuals reported decreased frequency and intensity of AD (Chen et al. 2008), 3 individuals who experienced severe AD during bladder emptying reported disappearance of these symptoms altogether (Schurch et al. 2000), 3 individuals reported AD was completely resolved (Chen & Kuo 2012), and 18 individuals experienced improvement in AD symptoms (Chen & Kuo 2012). While the evidence suggests that Botulinum toxin may be a viable treatment for neurogenic detrusor overactivity, the evidence supporting the application of Botulinum toxin specifically for the prevention of AD is inconclusive.
Botulinum toxin injections into the detrusor muscle or external urethral sphincter seem to be a safe and valuable therapeutic option in SCI patients who perform clean intermittent self-catheterization and have incontinence resistant to anticholinergic medications. Its use in the prevention of AD is less well defined.
