Clinical and neurophysiologic effects of botulinum toxin A on neurogenic and idiopathic detrusor overactivity

Introduction & Objectives: Recently it has been suggested that botulinum toxin type A (BoNT/A) injected into the detrusor muscle improves overactive bladder symptoms in patients with Parkinsons’s disease (PD). Recent experimental observations indicate that BoNT/A produces complex effects on the bladder activity acting on efferent as well as afferent pathways. In humans, in a study investigating the effects of bladder filling on the H-reflex size, bladder filling suppressed the H-reflex whereas in patients with spinal cord injury (SCI) it did not. Testing H- reflex size during bladder filling on urodynamic studies therefore allows the investigation of bladder afferents on spinal excitability. Aim of the present study was to investigate in patients with neurogenic and idiopathic detrusor overactivity (IDO) the clinical effect and the mechanism of action of BoNT/A injected into the detrusor muscle. Materials & Methods: Sixteen patients with neurogenic detrusor overactivity (8 with PD and 8 with SCI) and 8 patients with IDO participated in the study. All the patients underwent urodynamics and the H- reflex study from soleus muscle before and 4 weeks after intra-detrusor BoNT/A injection. Results: Confirming previous studies, at the baseline experimental session (pre- BoNT/A) in patients with PD and in those with IDO, the H- reflex from soleus muscle was significantly inhibited at maximal bladder capacity (MCC), whereas it remained unchanged in patients with SCI. Four weeks after BoNT/A injection, in patients with PD in those with IDO the H- reflex was not inhibited at MCC. Conversely in patients with SCI the H reflex decreased at MCC, even though not significantly (Table 1 ). Conclusions: The lack of H- reflex inhibition at MCC in patients with PD and IDO suggests that, besides the known effect on efferent pathways, BoNT/A treatment improves bladder function by acting also on afferent fibers. The changes in the H- reflex at MCC after BoNT/A in patients with SCI suggest that BoNT/A likely modulates C-fibers neurotransmission