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Neurogenic bladder is a term used to describe lower urinary tract (LUT) dysfunction resulting from a neurologic disease or process. This is not a homogenous term, but rather encompasses any neurologic problem that can affect the bladder. The high prevalence of LUT dysfunction among individuals with neurologic disorders is representative of the complex control of the nervous system on the urinary tract. The level and severity of the neurogenic lesion can manifest as varying, but often predictable, symptoms ranging from disorders of storage to those of voiding dysfunction (Panicker et al, 2015).

Accurate diagnosis and proper management of LUT dysfunction in the neurogenic population consist of two main goals: (1) to preserve the safety of the bladder with low-pressure storage and adequate emptying and (2) to maintain a reasonable quality of life in relationship to the bladder. This chapter serves to discuss the neural control of the LUT in a healthy state, LUT dysfunction associated with various neurologic diagnoses, and the workup and treatment of these disorders.


Lower urinary tract (LUT) function represents a complex interplay of autonomic and somatic circuitry with the goal of maintaining a low-pressure bladder during filling and periodic voluntary bladder emptying. Normal neural circuitry allows an individual to voluntarily switch between storage and voiding phases, based on a perceived sense of bladder fullness and an assessment of the social appropriateness of the situation (Panicker et al, 2015).

The autonomic nervous system consists of parasympathetic and sympathetic innervation. Sympathetic nerves originate from the thoracolumbar spinal cord segments T10/11 through L2 or L3. These nerves span the lumbar sympathetic ganglion and join the presacral nerve at the superior hypogastric plexus (Figure 28–1). Sympathetic postganglionic nerves release noradrenaline, which activates (1) β-adrenergic receptors, which inhibit the detrusor muscle, causing bladder relaxation; (2) α-adrenergic receptors in the bladder and bladder neck, causing outlet contraction; and (3) β-adrenergic receptors in the bladder ganglia (Andersson and Arner, 2004).

Figure 28–1.

Neural circuitry responsible for micturition. (Reproduced with permission from Corcos J, Ginsberg D, Karsenty G: Textbook of the Neurogenic Bladder, 3rd ed. New York, NY: CRC Press; 2015.)

Parasympathetic innervation originates from spinal cord segments S2–S4 as preganglionic nerve fibers that converge into the pelvic nerve. This nerve courses deep in the pelvis on each side of the rectum and terminates at the bladder and urethra. Parasympathetic postganglionic nerves release cholinergic (acetylcholine) and nonadrenergic noncholinergic transmitters. Detrusor contraction can be initiated by release of acetylcholine binding to M2 and M3 muscarinic receptors and by noncholinergic transmission mediated by ATP action on P2X purinergic receptors in the bladder muscle. Concurrently, the parasympathetic system releases nitric oxide, which has an inhibitory impact on the urethral smooth muscle (Fowler et al, 2008), further ...

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