Pathophysiology of the underactive bladder

Aizawa, Naoki; Igawa, Yasuhiko

doi:10.4111/icu.2017.58.s2.s82

Cited by 35 publications

(33 citation statements)

References 101 publications

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“… 26 Moreover, in those studies NLRP3 activation directly leads to denervation, 37 an important change that may contribute to the late stage DBD where the bladder is insensate and decompensated, unable to adequately empty. 38 Further studies will explore the role of NLRP3 and NLRP3-mediated denervation in the development of DBD.…”

Section: Discussionmentioning

confidence: 99%

Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria

Inouye¹,

Hughes²,

Jin³

et al. 2018

RRU

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PurposeDiabetes is a grave and progressive condition characterized by debilitating complications. Diabetic bladder dysfunction (DBD) is a very common complication with no specific treatments currently available. Unlike other tissues affected by this disease, the bladder is subjected to two independent insults; 1) polyuria, created by the osmotic effects of glucose in the urine, and 2) hyperglycemia itself. Based on our understanding of inflammation as a major contributor to the underlying organ damage in several other diabetic complications, its presence in the bladder during DBD and the contribution of polyuria and hyperglycemia to its development were assessed.MethodsAwake, restrained cystometry was performed on wild type C57BL/6 mice and diabetic (Akita) mice on a C57BL/6 background at 15 weeks of age. A subgroup of the Akita mice were treated with phlorizin, an inhibitor of sodium-glucose linked transporter types 1 and 2 that prevents glucose reabsorption in the kidney. All groups were assessed for serum glucose, 4-hour voiding totals, and inflammation in the bladder (Evans blue assay).ResultsAkita mice develop cystometrically-defined DBD by 15 weeks of age, as evidenced by an increase in urinary frequency, a decrease in voiding volume, and an increase in post-voiding residual volume. Phlorizin effectively normalized serum glucose in these animals while increasing the urine output. Inflammation in the bladder was present in the diabetic animals at this time point, but not detectable in animals receiving phlorizin.ConclusionInflammation in the bladder of diabetic mice correlates with the development of DBD and is triggered by hyperglycemia, not polyuria.

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Section: Discussionmentioning

confidence: 99%

Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria

Inouye¹,

Hughes²,

Jin³

et al. 2018

RRU

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“…Although the pathophysiology of UAB is not yet clearly defined, the main mechanism is decline in the detrusor contractile function due to myogenic failure, efferent nerve dysfunction, afferent nerve dysfunction, and failure of the central nervous system to coordinate voiding function [5]. Urinary incontinence is caused by a failure of the storage function of the lower urinary tract that is related to abnormal detrusor activity, such as DO or inadequate bladder outlet pressure.…”

Section: Pathophysiologymentioning

confidence: 99%

Management of Urinary Incontinence With Underactive Bladder: A Review

Cho

Kim

2020

Int Neurourol J

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Urinary incontinence is caused by storage function failure, while underactive bladder (UAB) is caused by a decline in detrusor contractility and voiding dysfunction. As the treatment mechanisms for incontinence and UAB are contrary to each other, it is difficult to treat both incontinence and UAB, and the patient’s quality of life can be further degraded. Conventional midurethral sling (MUS), such as transobturator tape or retropubic MUS, introduces a risk of postoperative voiding dysfunction in stress urinary incontinence with UAB. However, there have been several reports about the efficacy and safety of conventional MUS. Adjustable sling procedures, such as transobturator adjustable tape or the Remeex system, have better outcomes than conventional MUS because they control tension both during and after surgery. When voiding dysfunction occurs after incontinence treatment with UAB, voiding symptoms can be improved by various therapeutic modalities. Clean intermittent catheterization is recommended for patients with significant increased postvoid residual volumes or urinary retention. Although pharmacotherapy such as with alpha-blockers or parasympathomimetics can be considered for UAB, there is insufficient evidence of their effect on incontinence with UAB. Future therapies, such as stem cell therapy or gene therapy, may be used to treat incontinence with UAB. The possibility of management urgency urinary incontinence that related to detrusor hyperactivity with impaired contractility using sacral neuromodulation has been suggested. Further research is needed to establish evidence for the efficacy and safety of treatments for incontinence with UAB and improve patient quality of life.

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“…The persistent NOUR elicited by prolonged TNS occurred without invasive techniques such as nerve/muscle damage that have been used to produce animal models of NOUR in previous studies. 8,9 It is also worth noting that maximal voiding pressure was not increased during TNSinduced NOUR nor decreased by SPNS which improved voiding efficiency, indicating that this model of NOUR does not involve functional urethral outlet obstruction. The dysfunctions identified in our model including a reduction in bladder contraction amplitude and duration, reduced voiding efficiency and a large PVR volume resemble the clinical symptoms of NOUR.…”

Section: Discussionmentioning

confidence: 90%

“…Clinically, NOUR without an identifiable cause, that is, no nerve/muscle disease or damage, is classified as idiopathic, which includes many NOUR patients with unidentified functional changes in the central nervous system. Although myogenic/neurogenic animal models can be produced by bladder ischemia or pelvic nerve injury, 8,9 a recent study 10 in cats successfully produced an animal model of NOUR without nerve/muscle injury by prolonged stimulation of somatic afferent axons in the tibial nerve. This cat model of NOUR was used in the current study to determine if stimulation of the superficial peroneal nerve can reverse NOUR elicited by prolonged tibial nerve stimulation (TNS).…”

Section: Introductionmentioning

confidence: 99%

Superficial peroneal neuromodulation of nonobstructive urinary retention in cats

Zhao

Chen

Guo

et al. 2020

Neurourology and Urodynamics

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Aims To determine if superficial peroneal nerve stimulation (SPNS) can improve nonobstructive urinary retention (NOUR). Methods In α‐chloralose anesthetized cats, NOUR was induced by repetitive application (4‐16 times) of 30‐minute tibial nerve stimulation (TNS: 5 Hz frequency, 0.2 ms pulse width) at 4 to 6 times threshold intensity (T) for inducing toe twitches. SPNS (1 Hz, 0.2 ms) at 2 to 4 times threshold intensity (T) for inducing posterior thigh muscle contractions was applied either continuously (SPNSc) during a cystometrogram (CMG) or during voiding (SPNSv) by a surgically implanted cuff electrode or by skin surface electrodes to determine if the stimulation reduced NOUR induced by prolonged TNS. Results During control CMGs, efficient (86.4% ± 5.5%) voiding occurred with a postvoid residual (PVR) volume equal to 14.9% ± 6.2% of control bladder capacity. NOUR elicited by prolonged TNS significantly (P < .05) increased bladder capacity to 168.6% ± 15.5% of control, reduced voiding efficiency to 30.4% ± 4.8%, and increased PVR to 109% ± 9.2% of control. Using the implanted cuff electrode, SPNSc and SPNSv significantly (P < .05) increased voiding efficiency to 66.7% ± 7.4% and 65.0% ± 5.9%, respectively, and reduced PVR to 52.2% ± 11.4% and 64.3% ± 11.6%, respectively. SPNSc but not SPNSv significantly (P < .05) reduced bladder capacity to 133.4% ± 15% of control. Transcutaneous SPNSv but not SPNSc also significantly (P < .05) reversed the TNS‐induced NOUR responses. Conclusions This study shows that SPNS is effective in reversing NOUR induced by prolonged TNS. Transcutaneous SPNS provides the opportunity to develop a noninvasive neuromodulation therapy for NOUR to treat more patients than current sacral neuromodulation therapy.

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Pathophysiology of the underactive bladder

Cited by 35 publications

References 101 publications

Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria

Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria

Management of Urinary Incontinence With Underactive Bladder: A Review

Superficial peroneal neuromodulation of nonobstructive urinary retention in cats

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