What happens to micturition in spinal cord injury

What happens to micturition in spinal cord injury?

Following bilateral lesions to the spinal cord, the bladder initially becomes flaccid (acute) and eventually becomes spastic (chronic).

This dysfunction occurs because with bilateral cord damage the detrusor muscle of the bladder loses its cortical inputs.

Like the deep tendon reflexes, it initially becomes flaccid, resulting in urinary retention.

As the bladder fills, overflow incontinence may develop because the bladder cannot hold any more urine.

As time passes, the detrusor muscle becomes spastic (just as the deep tendon muscles become hyperactive).

Small stretches in the detrusor muscle result in voiding.

This spastic bladder results in urinary frequency and urgency.

In a study conducted on cat with an intact neuraxis, micturition is triggered by myelinated afferent Aδ-fibers in pelvic nerve that are connected to tension receptors in the bladder wall.

Unmyelinated C-fibers innervating the bladder play a minor or undetectable role in normal micturition reflex.

However, after SCI C-fiber afferents become the main component in the newly emerged bladder spinal reflex that results in DH.

Capsaicin, the C-fiber afferent neurotoxin, administered systemically blocked the micturition reflex in chronic SCI cats, but did not block the micturition reflex mediated by Aδ-fibers in cats with an intact neuraxis 

References

Tai C, Roppolo JR, de Groat WC. Spinal reflex control of micturition after spinal cord injury. Restor Neurol Neurosci. 2006;24(2):69-78. PMID: 16720943; PMCID: PMC3119351. https://pmc.ncbi.nlm.nih.gov/articles/PMC3119351/