Detrusor Acontractility after Acute Spinal Cord Injury—Myth or Reality?

Bywater, Mirjam; Tornic, Jure; Mehnert, Ulrich; Kessler, Thomas M.

doi:10.1016/j.juro.2018.01.046

Cited by 41 publications

(28 citation statements)

References 29 publications

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“…3 -40 days after SCI) 36,37 . Early treatment to avoid higher intravesical pressure with lower bladder compliance followed by vesicoureteral reflux associated with DO has been suggested to keep patients' renal and bladder function serving as a 'low pressure tank' without waiting for the irreversible complications of SCI 36,37 .…”

Section: Loss Of Pdgfrα + Cells Caused By Sci Were Due To Apoptotic Changes In Detrusormentioning

confidence: 99%

Phenotypic Changes of Detrusor PDGFR Alpha Positive Cells in Spinal Cord Injury-Induced Detrusor Overactivity

Lee

Park

Choi

et al. 2021

Preprint

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Volume accommodation occurs via a novel mechanism involving interstitial cells in detrusor muscles. The interstitial cells in the bladder are PDGFRα+ , and they restrain the excitability of smooth muscle at low levels and prevent the development of transient contractions (TCs). A common clinical manifestation of spinal cord injury (SCI)-induced bladder dysfunction is detrusor overactivity (DO). Although a myogenic origin of DO after SCI has been suggested, a mechanism for development of SCI-induced DO has not been determined. In this study we hypothesized that SCI-induced DO is related to loss of function in the regulatory mechanism provided by PDGFRα+ cells. Our results showed that transcriptional expression of Pdgfra and Kcnn3 was decreased after SCI. Proteins encoded by these genes also decreased after SCI, and a reduction in PDGFRα+ cell density was also documented. Loss of PDGFRα + cells was due to apoptosis. TCs in ex vivo bladders during filling increased dramatically after SCI, and this was related to the loss of regulation provided by SK channels, as we observed decreased sensitivity to apamin. These findings show that damage to the mechanism restraining muscle contraction during bladder filling that is provided by PDGFRα + cells is causative in the development of DO after SCI.

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Section: Loss Of Pdgfrα + Cells Caused By Sci Were Due To Apoptotic Changes In Detrusormentioning

confidence: 99%

Phenotypic Changes of Detrusor PDGFR Alpha Positive Cells in Spinal Cord Injury-Induced Detrusor Overactivity

Lee

Park

Choi

et al. 2021

Preprint

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“…10,11 However, Bywater et al demonstrated that a significant portion of early SCI patients had abnormal urodynamic parameters before 40 days post injury, and they advocated earlier targeted therapies to preserve upper and lower urinary tract function. 12 Children may experience a shorter duration of spinal shock as compared to adults, causing some experts to allow for evaluation earlier than 3 months. 11 Balancing against that recommendation, an early assessment may demonstrate poor parameters before bladder function has fully recovered, thus necessitating repeat invasive testing.…”

Section: Evaluation Of Neurogenic Bladdermentioning

confidence: 99%

Medical Management of Neurogenic Bladder for Children and Adults: A Review

Lucas

2019

Topics in Spinal Cord Injury Rehabilitation

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Neurogenic bladder is a chronic condition affecting patients of all ages with significant medical and quality of life implications. Goals of treatment consist of protection of the upper urinary tract and promotion of reliable urinary continence. Successful management involves medications and most often bladder drainage via clean intermittent catheterization. This article reviews current literature on medical management to achieve goals of treatment.

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“…Urodynamic evaluation is the cornerstone in the evaluation of lower urinary tract dysfunction in SCI patients, but its technique and timing are essential [6,12,14] . Several urological authorities and guidelines recommend performing the first study 3 to 6 months after the injury [8,12,14] , as recent evidence has shown that adverse urodynamic parameters can appear as early as 40 days after SCI [15] . However, in our practice, the first UDS is performed at the first sign of change in the urinary tract.…”

Section: Urodynamic Studymentioning

confidence: 99%

Evaluation, treatment, and surveillance of neurogenic detrusor overactivity in spinal cord injury patients

Alsulihem¹,

Corcos²

2019

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Neurogenic detrusor overactivity is a common urodynamic finding in patients with supra-sacral spinal cord injury. Early evaluation, stepped management, and close follow-up reduce the risk of upper urinary tract deterioration, renal failure and incontinence. In this article, we aim to outline the modern pathway of the management of this complex disease. Evaluation of patients with history, physical examination, renal function assessment, cystoscopy, and urodynamic study are essential. Management of neurogenic detrusor overactivity with adequate bladder drainage, medical therapy, intradetrusor botulinum injections, and surgery can be offered in a stepwise manner. Follow-up after specific interventions should be done in a timely fashion to detect treatment response and to avoid complications of poorly managed neurogenic detrusor overactivity.

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Detrusor Acontractility after Acute Spinal Cord Injury—Myth or Reality?

Cited by 41 publications

References 29 publications

Phenotypic Changes of Detrusor PDGFR Alpha Positive Cells in Spinal Cord Injury-Induced Detrusor Overactivity

Phenotypic Changes of Detrusor PDGFR Alpha Positive Cells in Spinal Cord Injury-Induced Detrusor Overactivity

Medical Management of Neurogenic Bladder for Children and Adults: A Review

Evaluation, treatment, and surveillance of neurogenic detrusor overactivity in spinal cord injury patients

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