Does an “Overactive to Underactive Bladder Transition” Phenomenon Exist in a Rat Lumbar Spinal Canal Stenosis Model?

Abstract

Purpose: To investigate the association between the maximum cystometric capacity (MCC) and other cystometric parameters in lumbar canal stenosis (LCS) rats. Material and Methods: One small hole was drilled at the fifth lumbar vertebral arch (Sham), and a rectangular piece of silicone rubber was then placed in the epidural space (LCS) of Wister rats. Two weeks after surgery, awake cystometry was performed. LCS rats were divided into three groups: Group A (n = 5, MCC < 0.87 mL), Group B (n = 13, MCC 0.87 -1.81 mL), and Group C (n = 14, MCC > 1.81 mL). Cystometric parameters were investigated in sham and LCS groups. Results: MCC did not significantly correlate to the frequency of non-voiding contractions (NVCs), voided volume (VV), or maximum intravesical pressure during voiding (Pmax), but significantly positively correlated to postvoid residual urine volume (PVR) and residual urine rate (RUR) (Spearman's correlation coefficients (ρ) = 0.8973 (p < 0.0001) and 0.4915 (p = 0.0068), respectively). Compared with the sham rats, LCS rats in each group revealed significantly smaller VV, larger RUR, and lower Pmax. On the other hand, among LCS rats, VV, RUR, and Pmax were not significantly different. The frequency of NVCs in each LCS group was not significantly different from that in sham-operated rats (Tukey-Kramer's HSD test). However, a Jonckheere-Terpstra trend test revealed a significant trend toward higher NVCs in the order of sham, Groups C, B, and A (p = 0.036). Conclusions: LCS rats showed the same degree of detrusor underactivity regardless of MCC. NVCs did not significantly increase in LCS rats with decreased MCC, but the trend toward higher NVCs with smaller MCC was significant.

Progressive changes in detrusor function and micturition patterns with chroinc bladder ischemia

“…These factors are thought to manifest in detrusor underactivity by disrupting neural and smooth muscle mechanisms involved in the generation of an effective voiding contraction [ 11 12 ]. Receptor modifications, interruption of afferent and efferent neural pathways secondary to systemic disorders, intrinsic changes in smooth muscle contractile apparatus, fibrosis and disruption of the afferent sensory system have been suggested as potential mechanisms [ 1 2 3 11 12 ].…”

“…However; downstream pathways underlying neuromuscular dysfunction, lack of sensation, contractile impairment and bladder progression to underactivity have not been thoroughly investigated. Animal studies support the concept of detrusor overactivity progression to detrusor underactivity [ 3 ]. It is thought that chronic untreated or treatment refractory overactive bladder may transition to dysfunctional patterns with impaired contractility and ultimately lead to detrusor underactivity.…”

“…Detrusor underactivity, characterized by prolonged emptying and/or a failure to achieve complete emptying within a normal time span, is a clinically challenging entity in terms of accurate diagnosis and effective treatment [ 1 2 3 ]. The etiology of detrusor underactivity remains essentially unknown.…”

“…The specific features of aging bladder contributing to underactivity have not been characterized or linked to a specific condition. It is thought that aging-related comorbidities influencing neurotransmission, sensation, and smooth muscle tension may hamper the bladder contractile function and impair its ability to empty [ 1 2 3 ].…”

“…Reduced strength and/or duration of bladder contractions may result from a variety of conditions including aging, bladder outlet obstruction, ischemia, diabetes mellitus, neurologic disorders, spinal cord injury, infectious neurologic problems, and pelvic surgery including radical prostatectomy. These conditions are known to engage the bladder neural system, receptors and smooth muscle cells and lead to functional deficit [ 1 2 3 ]. However; downstream pathways underlying neuromuscular dysfunction, lack of sensation, contractile impairment and bladder progression to underactivity have not been thoroughly investigated.…”