The unstable bladder: towards a common mechanism

Brading, Alison F.; Turner, William H.

doi:10.1111/j.1464-410x.1994.tb07447.x

Cited by 205 publications

(110 citation statements)

References 37 publications

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“…Unstable contractions may be due to abnormal muscle properties ("the myogenic hypothesis") (Brading and Turner, 1994). Alternatively, the contractions may follow abnormal activation of the micturition reflex ("neurogenic hypothesis") (de Groat, 1997).…”

Section: Detrusor Denervation In Spinal Cord Injurymentioning

confidence: 99%

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Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

Drake

Hedlund

Mills

et al. 2000

Laboratory Investigation

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SUMMARY:The bladder receives an extensive nerve supply that is predominantly cholinergic, but several putative transmitters are present, some of which are colocalized. Previous studies have shown increased levels of sensory nerves, reduced inhibitory transmitters, and structural and functional changes in the excitatory input in unstable bladder conditions. The present study compared the end-organ nerve supply to the bladder in spinal cord injury (SCI) with uninjured controls. Acetylcholinesterase histochemistry and double-label immunofluorescence were used to investigate neurotransmitter content, with confocal laser scanning microscopy to assess colocalization. Organ bath studies provided functional correlates for the structural changes in the excitatory innervation. Control samples had dense innervation of the detrusor containing a diverse range of transmitters. Hyperreflexic SCI samples showed patchy denervation, and areflexic SCI samples were diffusely denervated. Vasoactive intestinal polypeptide-, neuropeptide Y-, neuronal nitric oxide synthase-, and galanin-immunoreactive nerve fibers were reduced from frequent or moderately frequent to infrequent or very infrequent in SCI. Calcitonin gene-related peptide-immunoreactive fibers were infrequent in controls and SCI samples. Patterns of colocalization were unchanged, but significantly fewer fibers expressed more than one transmitter. The subepithelial plexus was markedly reduced and several of the smaller coarse nerve trunks showed no immunoreactivity to the transmitters assessed. There was no reduction in sensitivity to electrical field stimulation of intrinsic nerves in SCI, but the maximum force generated by each milligram of bladder tissue and the peak force as a proportion of the maximum carbachol contraction were significantly reduced and the responses were protracted. There was no significant functional atropine-resistant neuromuscular transmission in controls or SCI. The reported findings have clinical implications in the management of chronic SCI and development of new treatments.

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Section: Detrusor Denervation In Spinal Cord Injurymentioning

confidence: 99%

“…Since the clinical manifestations of detrusor hyperreflexia are similar to those of idiopathic and obstructive DI, there may be common pathophysiology (Brading and Turner, 1994). Nevertheless, the different nomenclature for the clinical conditions has been proposed by the Standardization Committee of the International Continence Society (Abrams et al, 1986).…”

mentioning

confidence: 99%

Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

Drake

Hedlund

Mills

et al. 2000

Laboratory Investigation

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“…17 ± 20 The second possible mechanism is of myogenic origin, 21 the denervated muscles were changed to the increased collagen ®bers and hypertrophy of smooth muscles ®bers. 22,23 The third possible mechanism is of neurogenic origin. Levin et al 24 stated that hypertrophy of the detrusor muscle could induce a hyperactivity of nerve and muscle cell, Neal et al 25 and Norlen 26 asserted that low compliance was induced by autonomous contraction of newly produced cholinergic nerve ®bers due to prolonged injury of parasympathetic nerves.…”

Section: Discussionmentioning

confidence: 99%

Significance of low compliance bladder in cauda equina injury

Shin

Kim

et al. 2002

Spinal Cord

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Study design: Prospective investigation using serial urodynamic studies. Objective: To evaluate type of neurogenic bladder and to observe changes of autonomous detrusor contraction (ADC) after the normalization of the compliance and capacity of the bladder in cauda equina injury. Setting: Spinal Cord Injury Unit, Yonsei Rehabilitation Hospital, Seoul, Korea. Methods: Urodynamic studies were performed in 50 patients with complete cauda equina injury from trauma with an infusion ratio of 30 ml/min. Findings of urodynamic studies and clinical features of patients with low compliance were compared with those of the normal compliant patients. Fourteen patients with low compliance received oral administration of oxybutynin and propiverine and intravesical instillation of oxybutynin to increase the compliance and capacity of the bladder, and follow-up urodynamic studies to monitor the change were undertaken. Results: Bladder compliance was decreased in 14 (28%) patients and normal in 36 (72%) patients. There was a signi®cantly long time interval between the onset of injury and the initiation of rehabilitative treatment in the neurogenic bladder group with low compliance when compared to those of the normal compliance group (P50.05). Clean intermittent catheterization was used as the voiding method, signi®cantly less than the normal compliance group (P50.05). ADC was observed in six out of fourteen patients with low compliance neurogenic bladder, but none in the normal compliance group. Upon the completion of conservative treatment, ADC disappeared in four patients whose compliance and capacity of the bladder were normalized on follow-up urodynamic studies. Conclusion: ADC was only observed in the low compliant bladder and as ADC disappeared when compliance and capacity of the bladder was normalized; low compliance appeared to be the main cause of ADC. In addition, this study supports that the maintenance of compliance of the bladder may be the most important factor in the management of neurogenic bladder.

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“…Die sekundäre Urininkontinenz unterscheidet sich von der idiopathischen/primären Form durch das Vorliegen von zugrundeliegenden Erkrankungen (Tabelle 3) [11][12][13][14]. Zu den möglichen Ursachen der sekundären Urininkontinenz zählen:…”

Section: Ursachenunclassified

Urininkontinenz beim Mann – ein Tabuthema

Kozomara-Hocke

Hermanns

Poyet

2016

Praxis

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Male urinary incontinence is an underestimated and frequently not broached issue. The urinary incontinence is divided into stress-, urge incontinence and hybrid forms as well as overflow incontinence. The fact that there are increasingly more men over 60 means that the prevalence of the urinary incontinence is up to 40%, and urinary incontinence will increasingly gain importance in daily routine practice. Many investigations and therapies can be realized by the general practitioner. Already simple therapy approaches can lead to a considerable clinical improvement of male urinary incontinence. If the initial therapy fails or pathological results (i. e. microhaematuria, recurrent urinary tract infections, raised residual urine and so on) are found, the patient should be referred to a urologist. Si la thérapie primaire ne réussit pas à résoudre l'incontinence urinaire ou on trouve des résultats pathologique (hématurie microscopique, infection urinaire récidivé, urine résiduelle augmenté etc.) le patient doit être envoyé chez le spécialiste d'urologie.4

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The unstable bladder: towards a common mechanism

Cited by 205 publications

References 37 publications

Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

Structural and Functional Denervation of Human Detrusor after Spinal Cord Injury

Significance of low compliance bladder in cauda equina injury

Urininkontinenz beim Mann – ein Tabuthema

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