Abstract
Tibial nerve stimulation (TNS) is a form of peripheral neuromodulation which has been found effective in treating overactive bladder symptoms, with lesser side effects than first line pharmacotherapy. Despite its widespread clinical use, the underlying mechanism of action is not fully understood. Our aim was to study its effect on the bladder neurophysiology and the trigger mechanism of voiding in the overactive detrusor, simulated by acetic acid (AA) instillation. In urethane anaesthetized male Wistar rats, the tibial nerve was stimulated for 30 min at 5 Hz, pulse width 200 µs and amplitude approximately three times the threshold to induce a slight toe movement. The pressure at which a voiding contraction was triggered (pthres) did not change significantly between the pre- and post-TNS measurements in AA induced detrusor overactivity. It was found that TNS significantly reversed the effects of AA irritation by increasing the bladder compliance and the bladder volume at pthres, as well as suppressed the threshold afferent nerve activity. The slope of the linear relationship between pressure and the afferent activity increased after AA instillation and decreased significantly after stimulation. In addition to its well-known central inhibitory mechanisms, this study has demonstrated that TNS improves bladder storage capacity by delaying the onset of voiding, via an inhibitory effect on the bladder afferent signaling at the peripheral level.
Highlights
A voiding reflex is initiated by bladder afferent nerve fibers which run through the major pelvic ganglion via the pelvic nerve to the L4–S3 level of the spinal cord
Irritation of the bladder with acetic acid (AA) induced an increase in the threshold afferent activity, which was significantly reversed in the poststimulation AA measurements
The maximum pressure just before the high frequency oscillations (HFO) was found comparable between the three groups, whereas the corresponding afferent nerve activity increased on AA instillation and decreased poststimulation
Summary
A voiding reflex is initiated by bladder afferent nerve fibers which run through the major pelvic ganglion via the pelvic nerve to the L4–S3 level of the spinal cord. Bladder efferent fibers originate at the same level, travel via the spinal nerve, synapse in the major pelvic ganglion and innervate the bladder smooth muscle (Pascual et al 1989; Keast et al 1989). It is generally believed that superseding a threshold of afferent nerve activity triggers efferent firing to the bladder wall i.e. initiates a voiding contraction (van Asselt et al 1999). In pathological conditions such as detrusor overactivity this afferent–efferent mechanism is disturbed (de Groat 1997).
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