In patients with spinal cord injury (SCI), intradetrusor onabotulinumtoxinA injections is a standard treatment for refractory neurogenic detrusor overactivity (NDO). However, treatment effects on supraspinal lower urinary tract control (LUT) are poorly understood. 
Therefore, the aim of this study was to elucidate supraspinal LUT control and effects of intradetrusor onabotulinumtoxinA injections in SCI patients.

In a structural and functional magnetic resonance imaging (MRI) study, we prospectively assessed SCI patients (n=23, mean age 40±12 yrs.) with refractory NDO due to a complete (n=15) or incomplete lesion (n=8). All patients underwent urodynamic evaluation (UDI) and MRI measurements prior and 5-8 weeks after intradetrusor onabotulinumtoxinA injections. MRI measurements consisted of tensor based morphometry (TBM) and functional MRI (fMRI) using 3 different bladder stimulation tasks: repetitive bladder filling of 100mL body warm and cold (4°C) saline, starting with an empty or prefilled bladder (block design). Patients repetitively rated their desire to void during bladder stimulation tasks.

UDI revealed a significant increase in maximum cystometric capacity and decrease in maximum detrusor pressure after treatment (p≤0.005).
For evaluation of the MRI measurement, one SCI patient had to be excluded due to head motions during data acquisition.
Desir to void during bladder stimulation task significantly decreased after treatment (p≤0.002).
TBM elucidated a significant (p=0.05, familywise error-corrected (FWE)) volume decrease in the bilateral orbitofrontal cortex after treatment.
Comparing fMRI measurements pre- vs. posttreatment, one sample t-test showed significant (p=0.05, FWE) supraspinal blood oxygenation level dependent (BOLD) signal changes in areas known to be involved in LUT control at both time points. Paired t-test revealed more activation (p=0.001 uncorrected) in the bilateral frontal operculum, triangle, prefrontal and orbitofrontal cortex, the cingulate cortex, the periaqueductal gray, the basal ganglia, the secondary motor as well as the secondary sensory areas pre- vs. posttreatment.
No correlation between lesion level or completeness of the lesion and BOLD signal intensity could be found.

SCI patients showed significant supraspinal activation in areas known to be involved in LUT control during bladder stimulation tasks. Intradetrusor onabotulinumtoxinA treatment resulted in supraspinal structural changes and BOLD signal decrease.

These findings imply that extra-spinal pathways are involved in LUT control overtaking sensory functions and underlay afferent effects of onabotulinumtoxinA treatment.