The cerebro-pelvic axis: a unified framework linking higher brain function, pelvic floor control, and lower urinary tract dysfunction

Clinical practice often treats higher brain disorders (e.g., Alzheimer's disease and prolonged disorders of consciousness) and pelvic floor dysfunction (e.g., stress urinary incontinence and overactive bladder) as unrelated problems, despite frequent co-occurrence and overlapping vulnerability contexts (e.g., aging, frailty, medications). Here, “axis” denotes a control-architecture mapping and phenotyping heuristic for LUT control and pelvic-floor outlet coordination, rather than a claim of new anatomy or shared etiology. Accordingly, we use a hypothesis-generating control-loop framing that links descending executive control with ascending interoceptive signaling to account for this clinicobiological mismatch. Within this framework, two provisional working failure-mode categories: top-down disintegration, in which impaired supraspinal control weakens volitional inhibition and shifts continence toward reflex-dominant regulation; and bottom-up disturbance, in which persistent peripheral salience-like signals may up-weight interoceptive processing and contribute to maladaptive central network adaptations. These categories are LUT-focused working categories and are not intended as a comprehensive taxonomy of all LUT phenotypes. We further introduce Coordinated Axis Neuromodulation (CAN) as a hypothesis-driven intervention concept that temporally couples cortical, spinal, and peripheral stimulation and may facilitate control-loop–level rebalancing compared with single-node modulation; this proposal requires direct empirical validation. This framework yields testable predictions, including directionally specific coupling between cortical biomarkers (e.g., executive/salience network metrics) and peripheral readouts (e.g., pelvic-floor EMG timing indices and/or diary-defined urgency/UUI burden; urodynamics as supportive phenotyping/secondary mechanistic data when included), and differential response profiles of CAN protocols across failure-mode–stratified cohorts. We outline a validation route spanning synchronized neurophysiology–pelvic physiology paradigms (e.g., EMG timing and diary endpoints; urodynamics as supportive phenotyping/secondary mechanistic data when included), proof-of-mechanism studies, and safety-monitored, mechanism-oriented RCTs designed to falsify or refine the CPA/CAN hypothesis.