Re: A conditioning stimulus can influence an external urethral sphincter contraction by a magnetic stimulation

The conundrum as to how sacral nerve stimulation (SNS), often known as neuromodulation, can be therapeutic for both the overactive bladder (OAB) and urinary retention (e.g., associated with an overactive sphincter, Fowler’s Syndrome) has not been resolved. On the one hand, SNS appears to suppress detrusor instability in OAB to improve continence, whereas in retention it appears to release excessive detrusor inhibition associated with the overactive sphincter to enable voiding. The study described by Wefer et al. claims to provide a possible method by which the external urethral sphincter can be ‘‘inhibited’’ using appropriately timed stimuli to the pudendal a¡erent nerves. The authors principal aim was to test the response of sub-threshold conditioning pudendal a¡erent electrical stimulation on intra-urethral pressures (representing external urethral sphincter contractions) evoked by supra-threshold lumbar-sacral magnetic stimulation. A secondary aim was to demonstrate the e¡ects of empty and full bladders on these responses. The authors raised the possibility of the technique being ‘a new neuromodulative approach,’ which ‘‘ . has the capacity to inhibit pudendal motoneurones in the spinal cord, which (could) potentially lead to a reduction on the sphincter tone’’ and hence ‘‘ . may prevent secondary inhibitory e¡ects on the detrusor. ’’ In the context of the experiment of Wefer et al., the term ‘inhibition’ may not be correct. Paired pulses applied in the form of a condition-test paradigm to the pudendal a¡erent pathways (i.e., electrical stimulation of the pudendal a¡erents in the dorsal penile nerve given as a conditional stimulation followed by magnetic stimulation of the same pudendal a¡erents at the level of the sacral roots as a test stimulus) give rise to varying temporal summation in the re£ex pathway dependent on the interval between the pulses [Rodi and Vodusek, 1995]. Maximal summation of the sphincter electromyogram (and intra-urethral pressure) usually occurs when the interval is 2^ 4 msec and this is followed by a progressive fall as the interval extends to higher values [Balasubramaniam et al., 2003]. So, the mean reduction in sphincter pressure seen by Wefer et al., when their paired pulses were applied at di¡erent intervals (from 10 to 100 msec with an empty bladder) was very likely due to a fall in temporal summation and not necessarily an active inhibition. A complete explanation for the results of Wefer et al. would have been complicated because they applied the two pulses to two di¡erent sites of the same pathway, one being purely a¡erent (e.g., dorsal penile nerves) and the other being a mixed sensory-motor nerve (e.g., whole sacral nerve roots). An additional problem was that di¡erent levels of stimulation were applied at the two di¡erent sites. Returning to Fowler’s syndrome: The real question is, if the pathology is thought to be local to the sphincter, how does sacral nerve stimulation modulate action on the detrusor centrally rather than have any direct e¡ect on the sphincter abnormality locally [Dasgupta and Fowler, 2003]? It is di⁄cult to see how the so-called ‘‘inhibition’’ of sphincter activity (particulary in normal men) described here byWefer et al. is likely to have a signi¢cant bearing on reducing detrusor inhibition (in a condition which is predominantly a problem associated with women! ). Of course, a supra-spinal mechanism could be involved and this might depend on long-latency re£exes [Fowler et al., 2000]. M.D. Craggs* Institute of Urology & Nephrology University College London United Kingdom