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Conditional neuromodulation of neurogenic detrusor overactivity using transrectal stimulation in patients with spinal cord injury: A proof of principle study. Knight SL, Edirisinghe N, Leaker B, Susser J, Craggs MD, Neurourol Urodyn. 2017 Jun 30

The authors report on a proof of concept study of a novel device to control neurogenic detrusor overactivity using conditional neuromodulation. Transrectal stimulation was delivered through an electrostimulator in response to simultaneously recorded external anal sphincter (EAS) contraction as a marker of neurogenic detrusor overactivity. The effect of conditional neuromodulation on bladder capacity and maximum detrusor pressure was investigated in addition to the reliability of dyssynergic sphincter contraction as a marker for NDO. Eight of 12 spinal cord injury (SCI)patients (4 classified as ASIA and 4 classified as ASIB) completed the study The EMG threshold to conditional stimulation was determined by calculating the value of the processed EMG signal at the time that Pdet exceeded 15cmH2O for each of the baseline fills. The minimum of the three values was used to reduce the incidence of false negatives. Conditional neuromodulation through the novel device induced a statistical increase in bladder capacity and reduction in maximum detrusor pressure in 6 out of the 8 patients. EMG recording of the EAS was a reliable surrogate for detection of NDO. The authors have to be congratulated for the work done. Non invasive conditional neuromodulation is an attractive option to treat NDO in SCI patients. In 2005, we conducted a retrospective study aiming at evaluating in patients with SCI and detrusor sphincter dyssynergia whether the onset of external urethral sphincter (EUS) contractions precedes or follows the onset of bladder contractions and to address the issue of potential therapeutic approaches based on the understanding of DSD. Video-urodynamic recordings of patients with SCI that demonstrated both untreated neurogenic overactive bladder and DSD were performed from January 2002 to December 2003. Because multiple transducers catheters have been shown to properly diagnose DSD, a two-channel microtip pressure transducer catheter was inserted into the urethra to measure the bladder and urethral pressures. The pressure transducers were positioned in the bladder and EUS, and the anatomic landmarks using fluoroscopy and the obtained pressure values ensured correct position. Delay A was defined as the period between the onset of an EUS pressure increase and the onset of a bladder pressure increase and delay B as the period between the onset of a urethral sphincter pressure increase and the moment at which the bladder pressure increase reached 10 cm H2O greater than the baseline value. Twenty patients with traumatic SCI matched all inclusion criteria. Delay A was positive (EUS contracted first) in 16 (80%) of 20 patients. The mean time for delay A was 2.2 s. Delay B was positive in all 20 patients (100%). The mean time for delay B was 7.6 s. One hypothesis of the mechanism of DSD after SCI is that afferent input from the bladder, conveyed by C-fibers to the intact sacral spinal cord below the lesion, stimulates parasympathetic motor neurons and concomitantly stimulates, instead of inhibits, motor neurons of Onuf's nucleus, by way of new interneurons and/or new synaptic connections and/or changes in neurotransmitters in a reorganized detrusor to the EUS spinal polysynaptic reflex. Theoretically, the EUS should be activated before bladder contractions for at least two reasons. First, because nerve conduction velocity, which has been shown to be preserved after a spinal cord lesion, is greater in efferent somatic alpha-motor neurons (70-40 m/s) than in efferent preganglionic parasympathetic motor neurons (10 m/s). Second, because the latency and electromechanical coupling time within bladder smooth muscle are likely to be much longer than in the EUS. The latency between Onuf's nucleus stimulation and EUS activation has been evaluated by lumbar magnetic stimulation and varies from 8 ms to 20-60 ms according to the recording method (EUS needle electromyography or EUS pressure, respectively. The exact neuromuscular transmission duration in detrusor smooth muscle remains unknown because, to date, a reliable method to record detrusor electromyography in humans is not available. However, the latency between activation of the parasympathetic sacral center and bladder