Pathophysiology, Clinical Importance, and Management of Neurogenic Lower Urinary Tract Dysfunction Caused by Suprasacral Spinal Cord Injury

Abstract

Management of persistent lower urinary tract dysfunction resulting from severe thoracolumbar spinal cord injury can be challenging. Severe suprasacral spinal cord injury releases the spinal cord segmental micturition reflex from supraspinal modulation and increases nerve growth factor concentration in the bladder wall, lumbosacral spinal cord, and dorsal root ganglion, which subsequently activates hypermechanosensitive C-fiber bladder wall afferents. Hyperexcitability of bladder afferents and detrusor overactivity can cause urine leaking during the storage phase. During urine voiding, the loss of supraspinal control that normally coordinates detrusor contraction with sphincter relaxation can lead to spinal cord segmental reflex-mediated simultaneous detrusor and sphincter contractions or detrusor-sphincter dyssynergia, resulting in inefficient urine voiding and high residual volume. These disease-associated changes can impact on the quality of life and life expectancy of spinal-injured animals. Here, we discuss the pathophysiology and management considerations of lower urinary tract dysfunction as the result of severe, acute, suprasacral spinal cord injury. In addition, drawing from experimental, preclinical, and clinical medicine, we introduce some treatment options for neurogenic lower urinary tract dysfunction that are designed to: (1) prevent urine leakage arising because of detrusor overactivity during bladder filling, (2) preserve upper urinary tract integrity and function by reducing intravesical pressure and subsequent vesicoureteral reflux, and (3) prevent urinary tract and systemic complications by treating and preventing urinary tract infections.

Keywords: Cystometry; Dog; Spinal; Urinary; Urodynamics.

Figure 1

Lower urinary tract innervation and neurotransmitters. Afferents and efferents travel in paired pelvic, hypogastric, and pudendal nerves. Parasympathetic and somatic neurotransmission are mediated by cholinergic fibers; sympathetic function is mediated by adrenergic fibers.

Figure 2

Reciprocal actions during urine storage and voiding: (A) During storage, sympathetic and somatic efferents are activated to maintain urinary continence; (B) During voiding, parasympathetic efferents are activated to trigger detrusor contractions.

Figure 3

Clinical consequences of abnormal urine storage and voiding after severe upper motor neuron or suprasacral spinal cord injury.

Figure 4

Cystometry recording in pet dogs with spinal cord injury. Top panel: abnormal detrusor contractions (arrows) recorded in an 8‐year‐old French bulldog that had intervertebral disk herniation at T13–L1 1 year previously and did not recover continence or walking. Lower panel: an unremarkable cystometry recording in a 7‐year‐old Beagle that had T11–T12 intervertebral disk herniation 2 years previously.