Neurogenic bladder is a loss of bladder control caused by damage to the nerve supply of the bladder. The damage can involve the brain, the spinal cord, peripheral nerves, or any combination thereof.
Voluntary control over the lower urinary tract is enabled by a web of interactions between autonomic and efferent nerve pathways. The autonomic pathways include sympathetic and parasympathetic nerves, and somatic control is contributed by the pudendal nerves.
Sympathetic innervation of the bladder originates from the thoracolumbar outflow of the spinal cord. On the other hand, parasympathetic innervation derives from the sacral segments of the spinal cords. Also present in these nerves are afferent axons from the lower urinary tract.
Postganglionic sympathetic nerves release norepinephrine, activating beta-adrenergic inhibitory receptors in the detrusor muscle. That signals the muscle to relax the bladder. Norepinephrine also activates the alpha-adrenergic excitatory receptors of the urethra and the neck of the bladder, as well as the alpha- and beta-adrenergic receptors in the bladder ganglia.
On the parasympathetic side, postganglionic nerves release cholinergic and non-adrenergic, non-cholinergic transmitters that cause the detrusor muscle to contract, triggering urine flow. This process is mediated by the M3 muscarinic receptor.
Somatic nerves arising in the S2-S4 motor neurons in Onuf’s nucleus supply the external urethral sphincter and connect with the pudendal nerves. Another motor nucleus at that level supplies axons innervating the pelvic floor musculature.
The spinal cord senses bladder fullness through the pelvic and hypogastric nerves, and sensory input from the neck of the bladder and urethra are carried by the pudendal and hypogastric nerves.
These nerves coordinate whether to switch urination on and off. During storage of urine, nerves organized by the spinal cord are activated to inhibit flow of urine. Voiding is triggered by reflexes controlled by the brain.
While the bladder is filling, the parasympathetic nerves inhibit contractions of the detrusor and urethral sphincter, preventing involuntary voiding. This is called the guarding reflex, and is activated through afferent nerve signals carried by pelvic nerves, organized by the spinal cord.
Bladder voiding is under conscious, voluntary control in humans, except for infants. Voiding is mediated by a pathway passing through the pontine micturition center (PMC) of the brain. Excitation of the PMC activates pathways that relax the urethra and activate sacral parasympathetic outflow. The bladder then contracts, increasing its pressure, while the urethra relaxes, decreasing its pressure. Consequently, the pressure differential allows urine to flow out of the bladder.
Urinary incontinence due to neurogenic bladder falls into three categories based on the location of the injury:
Lesions above the spinal micturition center result in urinary retention due to detrusor-sphincter dyssynergia (i.e. lack of coordination). For lesions affecting the conus medullaris or pelvic nerves, sensation of bladder fullness is lost, leading to distension of the detrusor muscle and inefficient contractions. The bladder becomes flaccid with increased capacity and large residual volumes.
Symptoms following cortical and subcortical lesions vary by the location of the lesion. Patients with acute and chronic cerebrovascular accidents have been noted to have varying symptoms such as detrusor areflexia and detrusor hyperreflexia. Mild bilateral lesions of the putamen can affect urination, but unilateral lesions have not been shown to have an effect.