Model-based analysis of the acute effects of transcutaneous magnetic spinal cord stimulation on micturition after spinal cord injury in humans
Fig 4
Simulation based on enhanced model replicates detrusor-sphincter dyssynergia after upper-level SCI (B) and hyperactive bladder activity after lower-level SCI (C). The schematic of the enhanced neural circuit of micturition with both an upper-level SCI (green dashed line) and a lower-level SCI (red dashed line) shown. B: After an upper-level SCI, supraspinal control of micturition is lost, and both voiding and storage reflexes are active, causing the detrusor-sphincter dyssynergia. The activity of Nodes 4, 8 and 9 are shown in B1. 2 and 3, respectively. Note that as the bladder is full, afferent activity from the bladder drives sympathetic (Node 4) to keep the detrusor muscle relaxed. However, there is no input from the PSC to inhibit activity of the preganglionic parasympathetic neurons (Node 8) and the detrusor receives active parasympathetic drive to contract the muscle. Simultaneously, the motor neurons driving sphincter contraction, represented by Node 9, are active. As a consequence, the bladder and external sphincter contractions occur simultaneously and the coordination of bladder sphincter activity necessary to empty the bladder is lost. C: After a lower-level SCI, sympathetic activity increases (Node 4, C1) as the bladder is filled (the time scale of filling has been accelerated), but there is no activation of detrusor contraction (Node 8, C2), and no external sphincter contraction (Node 9). As a result, the bladder leaks continuously as it is filled. This figure was created in part with BioRender.com.