Urinary continence requires coordination of both the somatic and autonomic nervous systems, and also involves elements of volitional control and assessments of social appropriateness. Urinary storage is primarily mediated involuntarily by the sympathetic nervous system and volitionally by the somatic neurons to the external urethral sphincter. At low bladder volumes, contraction of the internal and external urethral sphincter is maintained via α-adrenergic receptors and detrusor muscle contraction in the bladder wall is inhibited via β-adrenergic receptors. Urinary voiding is primarily mediated by the parasympathetic nervous system in conjunction with the pontine micturition center. At higher bladder volumes, descending axons from the pontine micturition center activate the parasympathetic neurons in the sacral spinal cord, which cause both detrusor muscle contraction via muscarinic acetylcholine receptors and urethral relaxation. They also inhibit the sympathetic neurons to the bladder and the somatic neurons to the external urethral sphincter. The pontine micturition center is inhibited by cortical regions so that voiding occurs in the appropriate social context.
Bladder dysfunction may signal pathology at any level from the cortex and pons to spinal cord and sacral peripheral nerve roots. However, more often it is due to a primary urologic cause affecting the bladder or urethra, and thus urologic evaluation should be performed initially, including an evaluation for urinary tract infection, prostate disease in men, and gynecologic disease in women. Urinary incontinence or retention is a frequent medication side effect. Commonly implicated medications include anticholinergics, opiates, calcium channel blockers, and diuretics.
In patients with urinary hesitancy and/or urinary retention, there is dysfunction of detrusor muscle contraction indicating a loss of parasympathetic excitation. This can be seen in focal lesions of the sacral spinal cord (conus medullaris) or sacral nerve roots (cauda equina) or in diffuse processes affecting the autonomic nervous system. An acute cervical or thoracic spinal cord injury can result in acute urinary retention (spinal shock), but patients will develop detrusor overactivity in a few weeks or months.
Due to extensive autonomic innervation, bladder dysfunction may be seen in processes that preferentially involve the autonomic system, such as polyneuropathy from diabetes or amyloidosis, idiopathic small fiber polyneuropathy, and primary autonomic failure. Multiple system atrophy (MSA) may be a unifying diagnosis when an older patient presents with isolated, prominent autonomic dysfunction without other evidence of polyneuropathy. Accompanying evidence of Parkinsonism may not be seen in the early stages of MSA. In this context, patients with bladder dysfunction should be specifically asked about other symptoms of autonomic dysfunction, such as orthostasis, dry mouth, abnormal sweating, gastroparesis, and constipation. On examination, patients should be evaluated for distal loss of pain and temperature sensation and orthostatic hypotension.
Intermittent catheterization is the main treatment for urinary retention regardless of the etiology. Intermittent catheterization overrides the internal and external urethral sphincters, obviating the need for detrusor contraction, avoids damage to the upper urinary tract from chronic retention, and minimizes the infection risk relative to chronic catheterization. Scheduled voiding may also prevent overflow incontinence episodes and promotes patient independence.
Detrusor overactivity (detrusor muscle contraction at low filling volumes) often occurs after central nervous system injury and leads to urgency, frequency, and urge incontinence. When the lesion is in the spinal cord, there may also be a loss of upper motor neuron modulation of the external urethral sphincter resulting in detrusor-sphincter dyssynergia. Thus, in addition to frequent detrusor contractions at low filling volumes, the bladder and external sphincter often contract simultaneously, resulting in ineffective voiding.
The classic triad of normal pressure hydrocephalus (NPH) includes urinary incontinence (especially urgency), gait instability (magnetic gait), and dementia. Patients need not have all three features. Brain magnetic resonance imaging or computed tomography demonstrating ventriculomegaly out of proportion to cortical atrophy is present in NPH. To more quantitatively define this finding, the ratio of the maximum width of the frontal horns of the lateral ventricles is divided by the maximum internal diameter of the skull at the same level (Evans index). A ratio of greater than 0.3 is suggestive of NPH. Ventriculoperitoneal shunting may provide relief, largely depending on the stage of illness and comorbidities.
Cortical lesions, particularly in the frontal lobe, often result in urinary urgency. Frequently cited mechanisms include interruption of conscious control of voiding or mechanisms underlying the switch from storage to evacuation of urine.
Optimal treatment of bladder dysfunction with urgency often requires a multimodal approach. Anticholinergic or β-adrenergic medications promote detrusor relaxation by inhibiting parasympathetic and activating sympathetic pathways, respectively. In patients with detrusor-sphincter dyssynergia, intermittent catheterization is usually employed as well to combat incomplete emptying, which can exacerbate detrusor overactivity, cause symptoms of urgency and frequency, and lead to infection.