Abstract
To assess and compare the effect of botulinum A toxin (BTX-A) injections into the detrusor in idiopathic and neurogenic detrusor overactivity resistant to anticholinergic treatment. In a prospective study, 11 patients with idiopathic and 11 with neurogenic detrusor overactivity resistant to anticholinergic treatment were injected with 300 U of BTX-A (Botox) into the detrusor. Clinical and urodynamic parameters were assessed before and after BTX-A injections. In idiopathic as well as in neurogenic detrusor overactivity, median daytime frequency decreased significantly from 11 to 4 (P = 0.004) and 12 to 5 (P = 0.001), median nocturia from 3 to 1 (P = 0.004) and 3 to 1 (P = 0.001), and median number of used pads from 5 to 0 (P = 0.001) and 5 to 0 (P = 0.002), respectively. There was a significant increase in median maximum cystometric capacity from 220 to 340 ml (P = 0.001) and 190 to 410 ml (to instead of) (P = 0.001), median bladder compliance from 20 to 55 ml/cm H(2)O (P = 0.001) and 23 to 60 ml/cm H(2)O (P = 0.004) and median post void residual from 10 to 140 ml (P = 0.002) and 30 to 240 ml (P = 0.002), respectively. Median maximum detrusor pressure decreased significantly from 45 to 29 cm H(2)O (P = 0.002) and 40 to 24 cm H(2)O (P = 0.002), and median detrusor pressure at maximum flow rate from 30 to 14 ml/sec (P = 0.001) and 38 to 21 ml/sec (P = 0.016), respectively. Due to post void residuals >150 ml following BTX-A injections, de novo clean intermittent self-catheterization was necessary in nine patients (four with idiopathic and five with neurogenic detrusor overactivity) and in one patient (with idiopathic detrusor overactivity) a suprapubic catheter was placed. The effect of BTX-A injections lasted for a median time of 5 months in both idiopathic and neurogenic detrusor overactivity. There was no significant difference in idiopathic compared to neurogenic detrusor overactivity in regard to clinical and urodynamic parameters assessed before and after BTX-A injections. BTX-A injections into the detrusor have a significant and comparable but temporally limited effect in idiopathic and neurogenic detrusor overactivity resistant to anticholinergic treatment.
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