Diagnostic Value of Intravesical Lidocaine for Overactive Bladder

Yokoyama, Osamu; Komatsu, Kazuto; Kodama, K.; Yotsuyanagi, Satoshi; Niikura, Susumu; Namiki, Mikio

doi:10.1097/00005392-200008000-00016

Cited by 20 publications

(23 citation statements)

References 23 publications

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“…It seems that GP electrovibration stimulates mechanoreceptors within it and the impulses pass along the pudendal nerve to the spinal cord which eventually sends impulses to the CMs, SVs and VA affecting their contraction. It may be useful to denote that lidocaine does not block the muscle activity but rather the sensory fibres (C and A α‐fibres) which are responsible for pain and reflex activity (Yokoyami et al. , 2000; Silva et al.…”

Section: Discussionmentioning

confidence: 99%

Electromyographic study of ejaculatory mechanism

2009

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Cavernosus muscle (CM), seminal vesicle (SV) and vasal ampullary (VA) contractions at ejaculation are said to be reflex mechanisms (ejaculatory reflex), which have been scarcely dealt with in the literature. We investigated the hypothesis that contraction of the CMs, SVs and VA at ejaculation is a reflex action. The electromyographic (EMG) activity of CM, SV and VA during ejaculation was recorded in 28 healthy men. The test was repeated after separate anaesthetization of the glans penis (GP), CMs, SVs, and VA in the pre-ejaculatory period. Latent ejaculatory time (LET) was calculated. CMs showed no EMG activity until rigid erection phase was reached. SVs and VA exhibited resting EMG activity which increased gradually with different stages of erection. At ejaculation, CMs, SVs and VA showed two to four intermittent contractions. The mean LET was 1.3 +/- 0.2 sec. GP anaesthetization led to the disappearance of CM, SV and VA EMG activity at ejaculation, while bland gel did not affect EMG activity. CMs, SVs and VA when anaesthetized in the pre-ejaculatory period exhibited no EMG activity at ejaculation, while saline did not affect EMG activity. Increased EMG activity of CM, SV and VA apparently denotes increase in their contractile activity. CM, SV and VA contraction on GP stimulation and ejaculation are assumed to be reflex actions and are mediated through the 'glans-cavernosovesicular reflex' (GCVR) which presumably represents the ejaculatory reflex. Changes in LET or evoked response would indicate a defect in the reflex pathway. The GCVR might act as an investigative tool in diagnosing erectile dysfunction, provided further studies are performed in this respect.

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Section: Discussionmentioning

confidence: 99%

Electromyographic study of ejaculatory mechanism

2009

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“…4). 40 Furthermore, among patients with overactive bladder caused by brain lesions, spinal lesions, or BPH, as well as those with idiopathic overactive bladder, the percentage increase in bladder capacity was the smallest (29%) in those with overactive bladder due to BPH. Intravesical administration of lidocaine increased bladder capacity more effectively in patients with spinal lesions or cord injuries than in those with other lesions 40,41 .…”

Section: Detrusor Overactivity and Bladder Sensationsmentioning

confidence: 92%

Urethral Sensations are Related to the Development of Detrusor Overactivity

Yokoyama

Miwa

Oyama

et al. 2011

LUTS

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Urgency is the core symptom of the overactive bladder symptom complex, but the underlying mechanisms are not fully understood. Clinical findings have led to the assumption that bladder outlet obstruction (BOO) caused by benign prostatic enlargement (BPE) induces storage symptoms and detrusor overactivity. Presumably, BOO by BPE accounts for urgency; however, urgency is not always caused by BOO. Sensory nerves in the wall of the urethra fire in response to urethral fluid flow, and this activity initiates bladder contractions in the quiescent bladder and augments ongoing contractions in the active bladder. In humans, prostatic urethral anesthesia results in significant increases in bladder capacity among BPH patients without neurological diseases, therefore sensory stimuli from an anatomically altered prostatic urethra has the possibility to induce urgency and detrusor overactivity. Studies in animals demonstrate the basis for an excitatory urethra to bladder reflex. Urethral stimulation by prostaglandin E2 induces an excitatory effect on micturition reflex by activation of C-fiber afferent nerves. α1A -adrenoceptor blocker has an inhibitory effect on the micturition reflex, suggesting excitatory urethra to bladder reflex is mediated by α1A -adrenoceptor. Even if there is no obstruction, increase in urethral sensory due to BPE may induce the development of the detrusor overactivity.

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“…[8][9][10][11] Other studies have confirmed the effectiveness and tolerability of intravesical RTX in neurologically normal and abnormal subjects, 12,13 and recent clinical evidence has suggested that IDO may be triggered by C-fiber afferent input. 5,[14][15][16] Several other reports have confirmed the positive effects of intravesical capsaicin for the treatment of hypersensitive disorders as well as for DO. 9,12,17,18 Based on this scientific and clinical background we studied the efficacy and safety of intravesical instillation of RTX in a randomized, double-blind, placebo-controlled study of women with urgency incontinence secondary to IDO.…”

Section: Introductionmentioning

confidence: 82%