Traumatic spinal cord injury (TSCI) causes neurogenic bladder dysfunction, which predisposes to urinary tract infections (UTI) and, ultimately, upper tract damage leading to renal failure. In the present mouse model, UTIs are the main cause of death after TSCI. Neuroprotective effects of low-energy shock wave treatment (SWT) via a toll-like receptor 3 (TLR3) dependent mechanism were described previously. We hypothesised that SWT after TSCI prevents bladder dysfunction by minimising neurodegeneration.
Clip-contusion TSCI was performed in either C57BL/6 wild type (WT) or TLR3 knockout (TLR3-/-) mice (n=20 per group). Randomly assigned treatment groups (n=10 WT and n=10 TLR3-/-) received SWT (500 impulses, 0.1mJ/mm2, 5Hz) 14 days post-operatively. All animals underwent high resolution 3D MRI imaging after 72 days of follow-up. Mortality was recorded, spinal cord scar size and residual urine volumes were measured using OsiriX software.
MRI measurements showed statistically significant reduced residual urine volumes (0.25+/- 0.05mm3 vs. 0.82+/-0.08mm3, p<0.05) and less spinal cord scarring (0.85+/-0.05mm2 vs. 2.6+/-0.3mm2) in treated WT animals. Overall survival was higher in treated WT animals compared to the untreated control group (9 vs. 7, n.s.). Shock wave effects were abolished in TLR3 knockout groups (residual urine volume: 0.9+/-0.2 vs. 0.65+/-0.35, n.s.; spinal cord scar size: 1.7+/-0.2mm2 vs. 1.4+/-0.03mm2, n.s.).
SWT prevents damage to bladder function after TSCI in a mouse model. This may indicate a possible novel strategy of treating neurogenic bladder dysfunction after acute spinal injury.