Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Neurourology and compliance abnormalities
Introduction
The primary functions of the urinary bladder are storage and emptying, which are mediated by a combination of parasympathetic, sympathetic, and autonomic signaling (see Chapter 3 ). Bladder compliance is the ability of the bladder to accommodate changes in urinary volume during the storage phase, without a significant change in bladder pressure. Changes in compliance can result in a loss of bladder distensibility during bladder filling, as well as increases in intravesical pressures and/or decreased capacity during this phase.
Bladder compliance is a urodynamic measurement that is calculated by the change in detrusor pressure ( P det ) during the change in bladder volume, and is expressed as ΔV (in mL)/Δ P det (in cm H 2 O) ( ). This can be calculated using a volume/cystometric pressure curve during urodynamic evaluation. Ultrastructural changes within the detrusor muscle, defects in the nervous system, and compromise or changes in bladder anatomy can all contribute to impaired bladder compliance through a loss of viscoelastic properties, replacement of bladder wall constituents by fibrosis, and/or changes in bladder muscle tone. Specifically, studies have demonstrated loss of bladder compliance with deposition of collagen within the extracellular matrix of the bladder as a result of chronic outlet obstruction, as well as radiation, pelvic/bladder injury, and so on ( ). This incites damage on the cellular level, including hypoxia, hypertrophy of myocytes causing thickening of the bladder wall, and decreases in neural density ( ; ). Pathologic conditions associated with impaired bladder compliance include radiation, chronic infection/inflammation including tuberculosis and schistosomiasis, outlet obstruction (urethral stricture, pelvic organ prolapse, benign prostatic hyperplasia, etc.), neurologic conditions (multiple sclerosis [MS], Shy–Drager syndrome, spinal cord injury [SCI], cauda equina), and surgical denervation (abdominoperineal resection, radical hysterectomy) ( ).
Compliance and changes in bladder neurophysiology
Normal bladder storage and emptying occur via a coordinated reflex arc involving the somatic and autonomic nervous systems. The sympathetic nervous system, through stimulation of efferent nerve fibers originating from T10 to L2 via the hypogastric nerve, allows for bladder storage (relaxation of the detrusor muscle and contraction of bladder neck/proximal urethra), while the parasympathetic nerves (S2–S4 efferents) are suppressed. In addition, the somatic efferents stimulate the contraction of the external urethral sphincter via the pudendal nerve, allowing for distensibility of the bladder at low pressures without urinary incontinence/leakage. This system, coupled with the ultrastructure of the bladder (the layers of the bladder wall, including urothelium, lamina propria, smooth muscle, and serosa), allows for bladder filling with low intraluminal pressures. See Chapter 3 for more details.
Disruption of the nervous system and/or bladder structure can result in impaired compliance ( ). SCIs, congenital disorders (i.e., spina bifida, myelomeningocele), vascular disease, diabetes, and demyelinating disorders (i.e., MS) can cause varying levels of neurologic injury, and ultimately neurogenic bladder. Injury to the various nervous systems can cause a disruption in signaling patterns between the bladder and the brain via the pontine micturition center (PMC), which plays a role in inhibition of bladder contractility. A disruption of the PMC can impair the bladder’s ability to fill at low pressures, ultimately decreasing elasticity and bladder compliance. In addition, damage to the sympathetic nerves above the level of T10 results in bladder and sphincter spasticity, increased detrusor tone, and muscle hypertrophy, and contributes to loss of bladder compliance ( ; ).
Types of neurogenic bladder
Several neurologic diseases, including SCIs, spina bifida, MS, Parkinson disease, stroke, and dementia, can result in neurogenic bladder with a variety of characteristic changes in bladder physiology and urodynamic parameters, which are summarized in Table 33.1 .
TABLE 33.1
Summary of Neuropathologies and Corresponding Bladder Patterns
| Location of Disease | Neurologic Pathology | Bladder Pattern/Dysfunction |
| Brain (pons, cortex, etc.) | Stroke a Parkinson disease Dementia Closed head injury/traumatic brain injury a Frontal lobe lesion Normal pressure hydrocephalus b Multiple sclerosis |
Detrusor overactivity ± Pseudodyssynergia ± Impaired contractility |
| Suprasacral (C1–L2) | Spinal cord injury c Tumors, infarction, infection of spinal cord Disc disease Spinal stenosis Tethered cord syndrome |
Detrusor overactivity ± Detrusor sphincter dyssynergia |
| Lower lumbar and sacral | Peripheral nerve injury Pelvic plexus injury/trauma d Cauda equina syndrome Myelomeningocele e |
Areflexic bladder Impaired contractility |
a Initial insult results in urinary retention with temporary detrusor areflexia, which is replaced with detrusor overactivity with possible impaired contractility in the stable phase.
b Triad of gait disturbances, dementia, and urinary incontinence (additionally urinary frequency, urgency, and nocturnal enuresis). Treatment with neurosurgery consultation for shunt placement.
c Initial phase/spinal shock: detrusor areflexia, flaccid paralysis. Recovery of detrusor activity often coincides with return of reflexes below the level of the lesion.
d Hypogastric nerve injury resulting in incomplete bladder neck closure, pelvic nerve injury causing impaired detrusor contractility, and pudendal nerve injury rendering external sphincter incompetent.
e Areflexic, poorly compliant bladder with high storage pressures because of external sphincter hypertonicity (failure to relax during voiding) and incompetent/open bladder neck.
Detrusor overactivity
Neurogenic detrusor overactivity (DO), sometimes called detrusor hyperreflexia, results in the inability of the bladder to store urine secondary to unsolicited bladder contractions and, over time, can lead to impaired compliance. DO has been attributed to bladder denervation supersensitivity and hypertrophy, which in turn increase the collagen content of the bladder wall, ultimately leading to decreased viscoelasticity and impaired compliance ( ). This is commonly seen in patients with MS, SCI, Parkinson disease, or stroke.
Detrusor areflexia
A bladder pattern seen in SCI, MS, peripheral nerve injury, and occasionally stroke is detrusor areflexia/acontractile and hypocontractility. During the storage/filling phase, this is often associated with a decrease in or lack of sensation/urge to void, in addition to increased storage capacity. Over time this can contribute to impaired bladder compliance, especially when associated with elevated detrusor leak point pressures (DLPPs) and/or storage pressures greater than 40 cm H 2 O.
Detrusor sphincter dyssynergia
Detrusor sphincter dyssynergia (DSD) in SCI and MS is a loss of coordination between the bladder and sphincter during the voiding phase. Normal physiology dictates sphincter relaxation before bladder contraction and micturition; DSD results in an involuntary contraction of the sphincter (periurethral striated external sphincter, and possibly smooth muscle of the internal sphincter) during an involuntary detrusor contraction. This discoordinated contraction should raise concern for risk of increased intravesical pressures causing reflux, urinary tract infection, hydronephrosis, renal failure, etc. ( ).
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here