Use of botulinum-A toxin for the treatment of refractory overactive bladder symptoms: an initial experience

The TRUST (EvaluaTion of Bladder Function in Relapsing-Remitting MUltiple Sclerosis Patients Treated with Natalizumab) Observational Study

“…Also, the UDI-6 and IIQ-7 scales used in this study have been validated for women, 14 although use of these measures with male patients has been described. 29,30 In conclusion, patients treated with natalizumab experience significantly improved incontinence-related QOL as measured by UDI-6 and IIQ-7 scores. The magnitude of this effect suggests that natalizumab may decrease the impact of incontinence on QOL.…”

Botulinum toxin and neuromodulation for overactive bladder treatment

“…Bir çal›flmada maksimum etkinin enjeksiyondan 7-30 gün sonra görüldü¤ü belirtilmifltir (14) . BoNT uygulanan 35 hastayla yap›lan bir di¤er çal›flmada ifllemden sonra düzelmenin bafllamas› ortalama 5.3 gün (1-14) maksimum düzelme ise 8.3 gün (2-20) olarak belirtilmifltir (19) . Botulinum toksinin detrüsörde yaratt›¤› etki geçici bir etkidir.…”

Botulinum A Toxin Intravesical Injections in the Treatment of Refractory Overactive Bladder in Patients with Parkinson's Disease

“…In neurogenic detrusor overactivity as well as in patients with idiopathic detrusor overactivity, the post-treatment reduction in detrusor pressures during both phasic involuntary contractions and on voiding (Popat et al, 2005;Reitz et al, 2004;Schurch et al, 2005) suggests an effect of BoNT/A on the motor innervation of the detrusor, although the neurological deficit which additionally affects voiding efficiency in the NDO group may partly explain the high rate of posttreatment clean intermittent self-catheterisations (CISC). Patients, however, also report a rapid reduction in their sensations of urgency, which are associated with involuntary detrusor overactivity (Rapp et al, 2004;Schmid et al, 2006). Although the exact nature and cause of urgency remains to be elucidated, abnormal afferent activity is thought to be a significant cause of spinal NDO (Yoshimura, 1999), and much less is known about the role of afferents in IDO.…”