Danilov V V, Danilova T I, Danilov V V
Urologiia. 2010 Jul-Aug(4):15-20.
The analysis of 58 cases of overactive bladder has shown that detrusor activity is not linked with clinical symptoms but is caused by supra segmentary lesion of the nervous system. The clinical picture of overactive bladder fits the proposed neurophysiological model where ischemic damage of the association neuron located in the lumbar spinal marrow triggers miction disorders leading to preganglionary detrusor denervation. Combined therapy with alpha1-adrenoblocker and M-cholinolytic is pathogenetically sound. Trospium chloride (spasmex) was used for long-term treatment of the patients as it produces minimal number of side effects and enables dose and schedule variation.
对58例膀胱过度活动症患者的分析表明，逼尿肌活动与临床症状无关，而是由神经系统的节段上病变引起的。膀胱过度活动症的临床表现符合所提出的神经生理模型，即位于腰髓的联络神经元的缺血性损伤引发排尿障碍，导致节前逼尿肌去神经支配。α1肾上腺素阻滞剂和M胆碱能阻滞剂联合治疗在发病机制上是合理的。氯化托哌铵（斯帕美克斯）用于患者的长期治疗，因为它产生的副作用最少，并且能够改变剂量和用药时间表。
