Neurogenic bladder with detrusor overactivity secondary to suprasacral spinal cord injury is often occasioned by high pressure non-voiding contractions (NVC) that may or may not precede a voiding contraction (VC). In humans with complete suprasacral spinal cord injury, a primitive spinal micturition reflex VC may be revealed, although because it is characterized by phasic striated sphincter activity and is not under conscious control, it is considered to be both detrusor-sphincter dyssynergia (Blaivas Type 2 DSD) and incontinence. In many mammalian species studied to date, phasic activity of the striated urethral sphincter may be utilized normally during the micturition reflex, and this phasic SSA appears to be generated within the lower lumbar spinal cord. Following spinal shock and return of bladder-to-bladder reflexes in the complete suprasacral spinal cord injured female rat, phasic striated urethral sphincter activity may once again be employed for voiding. However, as in all species, there may also occur numerous high pressure NVC prior to any VC, if present. These NVC have been discussed/described/treated as blocked void attempts due to tonic SSA during an attempted VC (e.g. Blaivas Type 3 DSD in humans). In other words, the very word, dyssynergia, implies a blocked void attempt. Our laboratory has long been interested in the physiological differences between NVC and VC and here report that there are differences in rates of contraction and relaxation that support different origins of the two types, supporting the assertion that DSD, as described, is an inaccurate term.

We opportunistically revisited prior experiments in 4-week post-SCI female SD rats (n=14) undergoing cystometric evaluation of drug effects on NVC. We examined the NVC and VC during the control periods in traces that demonstrated both high pressure prodromal NVC and spinal micturition center-mediated void events (as evidenced by phasic striated urethral sphincter activity). We converted intravesical pressure traces to their differential curves and measured maximum and minimum values during VC and the immediately preceding 1-3 NVC. A minimum of 2 cycles were sampled from each animal during the final stages of the treatment control period and/or after normal saline vehicle, parallel-dosing control administrations (ml/kg). NVC and VC means from each animal were used to represent that animal in the statistical analysis. Data were analyzed by 2-tailed Wilcoxon matched-pairs signed rank test for both maximal and minimal NVC vs VC values.

Rates of rise were significantly faster in VC vs NVC (medians 3.5 vs 2.1 cmH2O/sec, resp., P=0.0001), as were rates of relaxation (-3.4 vs -2.0 cmH2O/sec, resp., P=0.0001). While differences in relaxation rate may, in part, be accounted for by post-void decreased intravesical volume, this does not explain the differences seen in rise rates.

These results provide support for the involvement of different physiological mechanisms governing the contractions of NVC and VC, that, together with pharmacological data, also support the notion that NVC are primarily of myogenic while VC are of neurogenic (i.e. parasympathetic) origins via the spinal micturition center.

NVC are not simply tonic striated urethra sphincter activity-blocked (dyssynergic) VC attempts. They are of a different origin and pathophysiology unrelated to the spinal micturition center. Based on prior studies physiological and pharmacological studies, we suspect them to arise from exaggerated base-to-dome myogenic contractions, with or without a reflex parasympathetic non-voiding reflex response adding to the increased intravesical pressure, thereby producing this hallmark urodynamic observation during filling in chronic suprasacral spinal cord injured rats. The tonic striated urethral sphincter activity is simply an uninterrupted continence reflex, as there is no void intent.

Fraser MO, New insights into the pathophysiology of detrusor-sphincter dyssynergia. Current Bladder Dysfunction Reports. 2011 Jun; 6(2):93-99.