Urodynamics remain the gold standard for objectively evaluating bothersome lower urinary tract symptoms (LUTS) and offer indirect insight into the autonomic innervation of the lower urinary tract (LUT). Disruptions to the autonomic nervous system (ANS), particularly sympathetic and parasympathetic denervation, are frequently encountered in urological and neurological practice due to their common manifestation as LUTS. This narrative review synthesises current evidence on urodynamic features observed during bladder filling and voiding and their relationship to autonomic innervation in health and disease, drawing on established principles of LUT neural physiology. It contrasts normal urodynamic patterns with characteristic findings reported in neurological disorders associated with ANS disruption, such as multiple system atrophy, Parkinson's disease, diabetic and amyloid neuropathies, and spinal cord injury, to infer autonomic pathway integrity. These findings include changes in cystometric capacity, bladder compliance, filling sensations, and bladder neck appearance, the presence of detrusor overactivity or incontinence, and voiding phase abnormalities, including detrusor underactivity and bladder outflow obstruction. Together, these findings may provide insight into autonomic regulation across both health and disease. Urodynamics do not directly measure neural activity, and interpretation may be influenced by overlapping somatic effects, variable diagnostic thresholds, and non-neurogenic or co-existing pathology, but they remain an indispensable clinical tool for understanding LUT function and ANS involvement.

Neurogenic bladder (NB) is a devastating complication following sacral spinal cord injury (SSCI), often leading to urinary incontinence, recurrent infections, and progressive renal dysfunction, which severely impair patients' quality of life and survival. Current therapeutic options remain largely palliative and fail to reverse the underlying neurogenic pathology. This study employed mild photothermal therapy (MPTT) to treat SSCI-induced NB in rats and systematically investigated its efficacy and mechanisms. Results showed that MPTT effectively improved bladder morphology and urodynamic parameters, with more significant effects observed in early intervention. Mechanistically, MPTT inhibited bladder fibrosis, alleviated chronic inflammation, restored the balance between cell proliferation and apoptosis, promoted functional angiogenesis, and repaired structural damage and function of bladder nerve fibers. MPTT ameliorates SSCI-NB function through multi-target effects, and its time-dependent therapeutic efficacy suggests the necessity of early and repeated interventions, providing experimental and theoretical evidence for new NB treatment strategies.