The overactive bladder: current aetiological concepts
The overactive bladder: current aetiological concepts
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膀胱过度活动症：当前病因学概念
DOI：
10.1046/j.1464-410x.83.s2.4.x
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发表时间：
1999
影响因子：
4.5
通讯作者：
J. Bosch
中科院分区：
文献类型：
--
作者：
J. Bosch
介绍与不稳定膀胱相关的神经性因素ICS将膀胱过度活动症定义为客观显示收缩、自发或自发的膀胱过度活动症。我们对排尿反射的许多理解是基于de Groat等人的工作。[3];排尿激发，在膀胱测压图的充盈阶段，当患者试图抑制排尿反射时，是脊髓延髓的。为了减少这种反射的固有不稳定性，该系统由中枢神经调节[1]。这一定义自动排除了将围产期逼尿肌活动与外周抑制和兴奋机制分类的可能性。排尿反射的关键要素是：下尿路充盈为“活动过度”，因为没有客观证据表明患者可能试图抑制与CNS的动静脉连接的尿路;骶髓下部，在动态尿动力学研究的情况下收缩。更复杂的是，由膀胱副交感神经运动核和膀胱过度活动症核组成的骶排尿中枢可能无症状。对于有症状的膀胱过度活动症，控制括约肌功能的过度活动Onuf;以及脑桥排尿中心（PMC）及其m区膀胱必须以低于患者功能性膀胱容量的体积发生，并且应分别在拖曳储存和排尿下发生[4，5]。这种反射的“on-oC”开关被认为位于正常的日常活动环境中。它的存在并不一定意味着神经系统疾病。在PMC中，调节膀胱和括约肌功能之间的协调。放大和精细ICS的第一份报告中有如下陈述：“由于外周抑制和兴奋信号作用于15 cmH 2 O，导致出现超过反射活动调谐的收缩，这清楚地表明当要求患者排尿时，逼尿肌收缩不受抑制”。骶骨排尿中枢大多数情况下，反射是在抑制中调制的。在第四份报告中，这一陈述没有被添加到膀胱过度活动症的定义中（由间脑和大脑皮质功能[3]以保守的方式发表）。大脑皮层在某种意义上是负责的（1981）[2]。15 cmH 2 O阈值的使用仍然很普遍，尽管对于反射的时间没有科学依据。使用单光子发射计算机断层扫描的脑功能扫描具有任意值。事实上，闭合机制非常弱的患者可能会开始漏尿，即使有认知功能受损的老年急迫性尿失禁患者逼尿肌灌注不足，逼尿肌压力升高远低于15 cmH 2 O。在临床上，典型的患者大脑皮层作为一个整体，特别是额叶[6]。皮质介导的“on-oC”膀胱过度活动症的时间被认为存在尿急和/或尿频和/或急迫性尿失禁。这些患者的确切转换机制受损，导致膀胱过度活动症。后者是紧迫感和膀胱过度活动症之间的关系尚未得到充分探讨。至少以单一不稳定压力波为特征，导致不自主排尿[7]。虽然对于尿急和逼尿肌压力升高的关系没有不正常的怀疑，但由于许多神经痛患者，由于收缩力受损，膀胱常常排空不完全。因此，这种临床主诉的尿急并不具有膀胱过度活动症。此外，在正常受试者中，Resnick和Yalla将感觉实体称为逼尿肌反射亢进伴收缩力受损（DHIC）[8]。排尿的紧迫性在排尿开始后几乎立即消失，此时逼尿肌压力脑桥上病变通常与75-100%的患者的逼尿肌反射亢进相关[9];通常仍在增加。在帕金森病中，这在大约25%的患者中是真实的[10]。
Introduction Neurogenic factors associated with the unstable bladder The ICS defines the overactive bladder as one that is objectively shown to contract, spontaneously or on Much of our understanding of the micturition reflex is based on the work by de Groat et al. [3]; the voiding provocation, during the filling phase of a cystometrogram while the patient is attempting to inhibit micturreflex is spinobulbospinal. To decrease the inherent instability of such a reflex, the system is modulated by central ition [1]. This definition automatically precludes the possibility of classifying detrusor activity during ambuand peripheral inhibitory and excitatory mechanisms. Key elements of the voiding reflex are; the lower urinary latory filling as ‘overactivity’, as there is no objective proof of possible attempts by the patient to inhibit the tract, with its aCerent and eCerent connections to the CNS; the lower part of the sacral spinal cord, with the contraction under the circumstances of an ambulatory urodynamic study. To further complicate the issue, the sacral micturition centre consisting of the parasympathetic motor nucleus for the bladder and the nucleus of overactive bladder may be asymptomatic. For the overactive bladder to be symptomatic, the overactive Onuf controlling sphincteric function; and the pontine micturition centre (PMC), with its land m-region conbladder must occur at volumes below the patient’s functional bladder capacity and should occur under trolling storage and micturition, respectively [4,5]. The ‘on-oC’ switch of the reflex is thought to be located in circumstances of normal everyday activity. Its presence does not necessarily imply a neurological disorder. In the PMC, where the coordination between bladder and sphincteric function is regulated. Amplification and finethe first report of the ICS, the following statement was made; ‘the presence of contractions exceeding tuning of reflex activity takes place as a result of peripheral inhibitory and excitatory signals acting on the 15 cmH 2 O clearly indicates an uninhibited detrusor contraction when the patient has been asked to inhibit’. sacral micturition centre. Most of the time the reflex is modulated in an inhibiThis statement was not added to the definition of the overactive bladder in the fourth report (published in tory fashion by diencephalic and cerebral cortical functions [3]. The cerebral cortex in a sense is responsible 1981) [2]. The use of the 15 cmH 2 O threshold is still widespread, although there is no scientific basis for this for the timing of the reflex. Functional brain scanning using single-photon emission computed tomography has arbitrary value. Indeed, patients with a very weak closure mechanism may start leaking urine even when shown that cognitively impaired geriatric patients with urge incontinence suCer from underperfusion of the the detrusor pressure rise is much lower than 15 cmH 2 O. Clinically, the typical patient with an cerebral cortex as a whole, and of the frontal lobes in particular [6]. Cortically mediated timing of the ‘on-oC’ overactive bladder is thought to present with urgency and/or frequency, and/or urge incontinence. The exact switching mechanism in these patients is impaired, leading to an uninhibited overactive bladder. The latter is relationship between the sensation of urgency and overactive bladder has not been fully explored. At least characterized by a single unstable pressure wave leading to involuntary voiding [7]. Although there is no dyssysome doubt exists as to the relation of urgency and detrusor pressure rise, because many patients with nergia, there is often incomplete emptying of the bladder due to impaired contractility. Therefore, this clinical complaints of urgency do not have an overactive bladder. Furthermore, in normal subjects, the sensation entity has been termed detrusor hyper-reflexia with impaired contractility (DHIC) by Resnick and Yalla [8]. of urgency to void almost immediately disappears after the initiation of micturition, when the detrusor pressure Suprapontine lesions in general have been associated with detrusor hyper-reflexia in 75–100% of patients [9]; is usually still increasing. in Parkinson’s disease this was true in about 25% of patients [10].