The nature of detrusor bladder neck dyssynergia in non-neurogenic bladder dysfunction
The nature of detrusor bladder neck dyssynergia in non-neurogenic bladder dysfunction
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DOI：
10.1016/s0165-1838(97)00078-7
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发表时间：
1997-10-13
期刊：
影响因子：
--
通讯作者：
Ito, H
中科院分区：
文献类型：
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作者：
Yamanishi, T;Yasuda, K;Ito, H
关于膀胱颈挛缩的病理学或性质有两种主要观点。一种是器质性纤维化，另一种是交感神经功能增强，或逼尿肌膀胱颈协同失调。使用微尖换能器导管以尿动力学方式报告了神经源性膀胱中存在主动逼尿肌膀胱颈协同失调。然而，尚未证实逼尿肌膀胱颈协同失调是否是无神经源性膀胱患者膀胱颈挛缩的原因。本研究旨在通过视频尿动力学研究确定非神经源性膀胱受试者的膀胱颈挛缩是否与逼尿肌膀胱颈协同失调具有相同的性质。该研究包括 32 名 16-84 岁的男性受试者（平均 52.3）：17 名膀胱颈挛缩受试者，包括 7 名与最小并发症相关的受试者（4 名患有良性前列腺增生，3 名患有不完全神经病变）和 15 名非膀胱颈挛缩受试者（10 名健康志愿者、2 名慢性前列腺炎、3 名前列腺痛）。使用 5 微尖传感器导管测量排尿期间膀胱内、膀胱颈、尿道外括约肌和球状尿道的压力。使用图像增强器对换能器进行正确定位。排尿性膀胱尿道造影发现膀胱出口梗阻位于膀胱颈（直径小于0.75 cm），定义为膀胱颈挛缩。逼尿肌膀胱颈协同失调定义为逼尿肌收缩期间膀胱颈水平的压力高于膀胱内的压力。对通过上述方法判断为逼尿肌膀胱颈协同失调的受试者口服α受体阻滞剂盐酸特拉唑嗪（0.5mg，b.i.d，两周），以确认逼尿肌膀胱颈协同失调是否确实是由于交感神经功能增强所致。 7 例膀胱颈挛缩患者中发现逼尿肌膀胱颈协同失调：6 例膀胱颈挛缩患者并发症最少，只有 1 例膀胱颈挛缩患者无并发症（p < 0.01）。在排尿开始和结束时发现逼尿肌膀胱颈协同失调，但在最大流量时未发现。六例患有逼尿肌膀胱颈协同失调的患者，在服用特拉唑嗪后症状消失。总之，逼尿肌膀胱颈协同失调不被认为是非神经源性膀胱膀胱颈挛缩排尿功能障碍的主要因素。在交感神经过度活跃或α受体数量增加的情况下，会出现逼尿肌膀胱颈协同失调，主要见于受困的良性前列腺增生和神经系统疾病患者。 (C) 1997 Elsevier Science B.V.
There have been two major opinions on the pathology or nature of the bladder neck contracture. One is an organic fibrosis, and the other is an accentuated sympathetic nervous function, or detrusor bladder neck dyssynergia. The existence of active detrusor bladder neck dyssynergia in neurogenic bladder was reported in a urodynamical manner using microtip transducer catheters. However, it has not been confirmed whether or not detrusor bladder neck dyssynergia is responsible for bladder neck contracture in patient without neurogenic bladder. The present study was designed to determine by means of video urodynamic study whether or not bladder neck contracture would be of the same nature as detrusor bladder neck dyssynergia in non-neurogenic bladder subjects. The study included 32 male subjects of 16-84 years old (average 52.3): 17 bladder neck contracture subjects including 7 subjects associated with minimum complications (4 with trapped benign prostatic hyperplasia and 3 with incomplete neurological lesion) and 15 non-bladder neck contracture subjects (10 healthy volunteers, 2 chronic prostatitis, 3 prostatodynia). A 5-microtip transducer catheter was used to measure the pressure in the bladder and at the bladder neck, the external urethral sphincter and the bulbous urethra during voiding. Proper localization of the transducers was done with an image intensifier. Bladder outlet obstruction localized at the bladder neck (diameters smaller than 0.75 cm) on voiding cystourethrogram was defined as bladder neck contracture. Detrusor bladder neck dyssynergia was defined where pressures were higher at the level of bladder neck than in the bladder during detrusor contraction. An alpha-blocker, terazosin hydrochloride (0.5 mg, b.i.d., two weeks), was orally administered to subjects judged to have detrusor bladder neck dyssynergia by the above methods for the purpose of confirming whether detrusor bladder neck dyssynergia was really due to accentuated sympathetic nervous function. Detrusor bladder neck dyssynergia was found in seven cases with bladder neck contracture: 6 cases with bladder neck contracture with minimum complications and only 1 case with bladder neck contracture without complications (p < 0.01). Detrusor bladder neck dyssynergia was found at the beginning and ending of micturition, but not at maximum flow. In six cases with detrusor bladder neck dyssynergia, the condition disappeared after terazosin. In conclusion, detrusor bladder neck dyssynergia was not thought to be a major factor of voiding dysfunction in bladder neck contracture in non-neurogenic bladder. In the presence of sympathetic hyperactivity or in cases with increased number of alphareceptors, detrusor bladder neck dyssynergia occurs, being predominantly noted in trapped benign prostatic hyperplasia and neurological disorder patients. (C) 1997 Elsevier Science B.V.