Does repetitive transcranial magnetic stimulation induce long-lasting neuroplastic changes to improve detrusor muscle function in stroke survivors with neurogenic overactive bladder?

Abstract

Neurogenic overactive bladder (OAB) is purported to result from damage to the central inhibitory pathways in the brain and spinal cord or peripheral afferent terminal sensitization in the bladder, which unmasks the primitive voiding reflex. Excitation of the pontine micturition center activates descending neural pathways to the spinal cord, resulting in sequential detrusor contraction and urethral relaxation. Damage to the central nervous system mechanism may disrupt normal micturition control, leading to involuntary micturition with concomitant detrusor overactivity.Low-frequency repetitive transcranial magnetic stimulation (rTMS), causing long-term depression of neuronal synaptic transmission, results in presynaptic neuron stimulation within several milliseconds after postsynaptic neuron stimulation. Low-frequency rTMS of the primary motor cortex may induce cortical inhibition via suppression of neural overactivity in descending projections, thereby reversing lower urinary tract symptoms by increasing pelvic floor tonicity and enhancing bladder capacity and bladder filling. Given the role of low-frequency rTMS in improving detrusor overactivity, we hypothesized that low-frequency active rTMS would inhibit cortical excitability and induce long-lasting neuroplastic changes to improve detrusor muscle function in stroke survivors with neurogenic OAB.