Potential impact of epidural stimulation on neurogenic bladder function and the value of urodynamic studies throughout usage

2021 ◽  
Vol 44 (4) ◽  
pp. 515-516
Author(s):  
Lisa Beck ◽  
Daniel Veith ◽  
Margaux Linde ◽  
Megan Gill ◽  
Jonathan Calvert ◽  
...  
2020 ◽  
Vol 29 ◽  
pp. 096368972090246 ◽  
Author(s):  
Guan Qun Zhu ◽  
Seung Hwan Jeon ◽  
Kyu Won Lee ◽  
Hyuk Jin Cho ◽  
U-Syn Ha ◽  
...  

There is still a lack of sufficient research on the mechanism behind neurogenic bladder (NB) treatment. The aim of this study was to explore the effect of overexpressed stromal cell-derived factor-1 (SDF-1) secreted by engineered immortalized mesenchymal stem cells (imMSCs) on the NB. In this study, primary bone marrow mesenchymal stem cells (BM-MSCs) were transfected into immortalized upregulated SDF-1-engineered BM-MSCs (imMSCs/eSDF-1+) or immortalized normal SDF-1-engineered BM-MSCs (imMSCs/eSDF-1−). NB rats induced by bilateral pelvic nerve (PN) transection were treated with imMSCs/eSDF-1+, imMSCs/eSDF-1−, or sham. After a 4-week treatment, the bladder function was assessed by cystometry and voiding pattern analysis. The PN and bladder tissues were evaluated via immunostaining and western blotting analysis. We found that imMSCs/eSDF-1+ expressed higher levels of SDF-1 in vitro and in vivo. The treatment of imMSCs/eSDF-1+ improved NB and evidently stimulated the recovery of bladder wall in NB rats. The recovery of injured nerve was more effective in the NB+imMSCs/eSDF-1+ group than in other groups. High SDF-1 expression improved the levels of vascular endothelial growth factor and basic fibroblast growth factor. Apoptosis was decreased after imMSCs injection, and was detected rarely in the NB+imMSCs/eSDF-1+ group. Injection of imMSCs boosted the expression of neuronal nitric oxide synthase, p-AKT, and p-ERK in the NB+imMSCs/eSDF-1+ group than in other groups. Our findings demonstrated that overexpression of SDF-1 induced additional MSC homing to the injured tissue, which improved the NB by accelerating the restoration of injured nerve in a rat model.


Author(s):  
J. Eric Ahlskog

Urinary problems occur with normal aging. In women they often relate to the changes in female anatomy due to the delivering of babies. With superimposed age-related changes in soft tissues, laxity may result in incontinence (loss of urinary control), especially with coughing, laughing, or straining. In men the opposite symptom tends to occur: urinary hesitancy (inability to evacuate the bladder). This is due to constriction of the bladder outlet by an enlarging prostate; the prostate normally surrounds the urethra, through which urine passes. DLB and PDD are often associated with additional bladder problems. Recall that the autonomic nervous system regulates bladder function and that this system tends to malfunction in Lewy disorders. Hence, reduced bladder control is frequent among those with DLB, PDD, and Parkinson’s disease. This condition is termed neurogenic bladder, which implies that the autonomic nervous system control of bladder reflexes is not working properly. This may manifest as urgency with incontinence or hesitancy. Neurogenic bladder problems require different strategies than those used for treating the simple age-related problems that develop in mid-life and beyond. Moreover, there are certain caveats to treatment once a neurogenic bladder is recognized. The bladder is simply a reservoir that holds urine. It is located in the lower pelvis and is distant from the kidneys. The kidneys essentially filter the circulating blood and make the urine. The urine flows down from the kidneys into the bladder, as shown in Figure 14.1. Normally, as the bladder slowly fills with urine, a reflex is triggered when it is nearly full. This results in conscious awareness of the need to urinate, plus it primes the reflexive tendency of the bladder to contract in order to expel the urinary contents. The bladder is able to contract because of muscles in the bladder walls. Normally, nerves activate these muscles at the appropriate time, which forcefully squeeze the bladder, expelling the urine. Nerve sensors in the bladder wall are activated by bladder filling and transmit this information to the central nervous system, ramping up bladder wall muscle activity.


2013 ◽  
Vol 305 (12) ◽  
pp. F1656-F1662 ◽  
Author(s):  
Rui Xue ◽  
Zhankui Jia ◽  
Xiaomu Kong ◽  
Guofu Pi ◽  
Shengli Ma ◽  
...  

To investigate the expression of four subtypes of PGE2 E-prostanoid (EP) receptors (EP1–EP4) and the effects of EP3/EP4 on bladder dysfunction in a new neurogenic bladder model induced by experimental autoimmune encephalomyelitis (EAE), the mouse model of EAE was induced using a previously established method, and bladder function in mice with different defined levels of neurological impairment was then examined, including micturition frequencies and voiding weight. Bladders were then harvested for analysis of EP receptor expression by Western blot. Activities of agonists/antagonists of EP3 and EP4 receptors as well as PGE2 were also evaluated at different stages of EAE. The results showed that EAE mice developed profound bladder dysfunction characterized by significantly increased micturition and significantly decreased urine output per micturition. EAE-induced upregulation of EP3 and EP4 receptors in the bladder was accompanied by bladder dysfunction. However, EAE had no significant effect on EP1 and EP2 receptors. Moreover, PGE2 and agonists/antagonists of EP3 and EP4 receptors significantly affected bladder dysfunction in EAE mice. Thus, we believe that EAE mice are useful for investigations of the neurogenic bladder. In addition, EP3 and EP4 receptors play a role in EAE-induced bladder dysfunction, providing us with a new target for the treatment of neurogenic bladders.


2012 ◽  
Vol 2012 ◽  
pp. 1-5
Author(s):  
Tatsuro Sasaji ◽  
Noboru Yamada ◽  
Kazuo Iwai

A 76-year-old man presented with a Denis Zone III sacral fracture after a traffic accident. He also developed urinary retention and perineal numbness. The patient was diagnosed with neurogenic bladder dysfunction caused by the sacral fracture. A computed tomogram (CT) revealed that third sacral lamina was fractured and displaced into the spinal canal, but vertebral body did not displace. The fracture lines began at the center of lamina and extended bilateraly. The fracture pattern was unique. The sacrum was osteoporosis, and this fracture may be based on osteoporosis. We performed laminectomy to decompress sacral nerve roots. One month after surgery, the patient was able to urinate. Three months after surgery, his bladder function recovered normally. One year after surgery, he returned to a normal daily life and had no complaints regarding urination. One-year postoperative CT showed the decompressed third sacrum without displacement.


Urology ◽  
1986 ◽  
Vol 27 (4) ◽  
pp. 371-378 ◽  
Author(s):  
Alain B. Rossier ◽  
Bushra A. Fam

1999 ◽  
Vol 162 (3 Part 2) ◽  
pp. 1068-1071 ◽  
Author(s):  
MARTIN KAEFER ◽  
AJAY PABBY ◽  
MARY KELLY ◽  
MARY DARBEY ◽  
STUART B. BAUER

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