Two-Phase Concept of Function: Filling/Storage and Emptying/Voiding

Whatever disagreements exist regarding the anatomic, morphologic, physiologic, pharmacologic, and mechanical details involved in both the storage and the expulsion of urine by the lower urinary tract, the author has always taken the rather simple-minded view that the “experts” would agree on certain general points (Wein, 1981; Wein and Barrett, 1988; Wein, 2007; Wein and Moy, 2007). The first is that the micturition cycle involves two relatively discrete processes: (1) bladder filling and urine storage and (2) bladder emptying or voiding. The second is that, whatever the details involved, one can succinctly summarize these processes from a conceptual point of view as follows:

The smooth sphincter refers to the smooth musculature of the bladder neck and proximal urethra. This is a physiologic but not an anatomic sphincter and one that is not under voluntary control. The striated sphincter refers to the striated musculature that is a part of the outer wall of the proximal urethra in both the male and the female (this portion is often referred to as the intrinsic or intramural striated sphincter or rhabdosphincter) and the bulky skeletal muscle group that closely surrounds the urethra at the level of the membranous portion in the male and primarily the middle segment in the female (often referred to as the extrinsic or extramural striated sphincter). The extramural portion is the classically described external urethral sphincter and is under voluntary control (for a detailed discussion see Chapter 60; DeLancey et al, 2002; Zderic et al, 2002).

Bladder Response during Filling

The normal adult bladder response to filling at a physiologic rate is an almost imperceptible change in intravesical and detrusor pressure. During at least the initial stages of bladder filling, after unfolding of the bladder wall from its collapsed state, this high compliance (Δ volume/Δ pressure) of the bladder is due primarily to its elastic and viscoelastic properties. Elasticity allows the constituents of the bladder wall to stretch to a certain degree without any increase in tension. Viscoelasticity allows stretch to induce a rise in tension followed by a decay (“stress relaxation”) when the filling (stretch stimulus) slows or stops. The viscoelastic properties are considered to be primarily due to the characteristics of the extracellular matrix in the bladder wall. Andersson and Arner (2004) cite references demonstrating that the main extracellular components are elastic fibers and collagen fibrils present in the serosa, between muscle bundles, and between the smooth muscle cells in the muscle bundles. Brading and colleagues (1999) add that they believe that there is continuous contractile activity in the smooth muscle cells to adjust their length during filling but without the type of synchronous activity that would increase intravesical pressure, impede filling, and could cause urinary leakage. Clinically and urodynamically, therefore, the bladder seems “relaxed.” The urothelium also expands but must preserve its barrier function while doing so.

There may also be a non-neurogenic active component to the storage properties of the bladder. Hawthorn and colleagues (2000) have suggested that an as yet unidentifiable relaxing factor is released from the urothelium during filling and storage, and Andersson and Wein (2004) have suggested that urothelium-released nitric oxide may have an inhibitory effect on afferent mechanisms as well.

The viscoelastic properties of the stroma (bladder wall less smooth muscle and epithelium) and the urodynamically relaxed detrusor muscle thus account for the passive mechanical properties and normal bladder compliance seen during filling. The main components of the stroma are collagen and elastin. In the usual clinical setting, filling cystometry seems to show a slight increase in intravesical pressure, but Klevmark (1974, 1999) elegantly showed that this pressure rise is a function of the fact that cystometric filling is carried out at a greater than physiologic rate and that, at physiologic filling rates, there is essentially no rise in bladder pressure until bladder capacity is reached.

When the collagen component of the bladder wall increases, compliance decreases. This can occur with chronic inflammation, bladder outlet obstruction, neurologic decentralization, and various other types of injury. Bladder muscle hypertrophy, which can result from outlet obstruction, can also result in decreased compliance because it is said to be less elastic than normal detrusor; it also can synthesize increased amounts of collagen (Mostwin, 2006). Once decreased compliance has occurred because of a replacement by collagen of other components of the stroma, it is generally unresponsive to pharmacologic manipulation, hydraulic distention, or nerve section. Most often, under those circumstances, augmentation cystoplasty is required to achieve satisfactory reservoir function.

Does the nervous system affect the normal bladder response to filling? At a certain level of bladder filling, spinal sympathetic reflexes facilitatory to bladder filling/storage are clearly evoked in animals, a concept developed over the years by deGroat and others (deGroat et al, 1993; deGroat and Yoshimura, 2001; Chancellor and Yoshimura, 2002; Zderic et al, 2002; Yoshimura and Chancellor, 2007; see Chapter 60), who have also cited indirect evidence to support such a role in humans. This inhibitory effect is thought to be mediated primarily by sympathetic modulation of cholinergic ganglionic transmission. Through this reflex mechanism, two other possibilities exist for promoting filling/storage. One is neurally mediated stimulation of the predominantly α-adrenergic receptors (α₁) in the area of the smooth sphincter, the net result of which would be to cause an increase in resistance in that area. The second is neurally mediated stimulation of the predominantly β-adrenergic receptors (β₃ inhibitory) in the bladder body smooth musculature, which would cause a decrease in bladder wall tension. McGuire and colleagues (1983) have also proposed a direct inhibition of detrusor motor neurons in the sacral spinal cord during bladder filling related to increased afferent pudendal nerve activity generated by receptors in the striated sphincter. Good evidence also seems to exist to support an inhibitory effect of other neurotransmitters (e.g., glycine, gamma amino butyric acid [GABA], opioids, purines, the noradrenergic system) on the micturition reflex at various levels of the neural axis. Bladder filling and consequent wall distention may also result in the release of factors from the urothelium that may influence contractility (e.g., acetylcholine [Ach], adenosine triphosphate [ATP], nitric oxide, prostaglandins, other peptides, as yet unidentified inhibitory factors).

Outlet Response during Filling

There is a gradual increase in urethral pressure during bladder filling, contributed to at least by the striated sphincteric element and perhaps by the smooth sphincteric element as well. The rise in urethral pressure seen during the filling/storage phase of micturition can be correlated with an increase in efferent pudendal nerve impulse frequency and in electromyographic activity of the striated sphincter. This constitutes the efferent limb of a spinal somatic reflex, the so-called guarding reflex, which results in a gradual increase in striated sphincter activity during normal bladder filling and storage. Although it seems logical and certainly compatible with neuropharmacologic, neurophysiologic, and neuromorphologic data to assume that the muscular component of the smooth sphincter also contributes to the change in urethral response during bladder filling, probably through sympathetically induced contraction, it is extremely difficult to prove this either experimentally or clinically. The direct and circumstantial evidence in favor of such a hypothesis has been summarized by Wein and Barrett (1988), Brading (1999), and Andersson and Wein (2004).

The passive properties of the urethral wall certainly deserve mention because these undoubtedly play a role in the maintenance of continence (Zinner et al, 1983; Brading, 1999). Urethral wall tension develops within the outer layers of the urethra; however, urethral pressure is a product not only of the active characteristics of smooth and striated muscle but also of the passive characteristics of the elastic, collagenous, and vascular components of the urethral wall because this tension must be exerted on a soft or plastic inner layer capable of being compressed to a closed configuration—the “filler material” representing the submucosal portion of the urethra. The softer and more pliable this area is, the less pressure required by the tension-producing area to produce continence. Finally, whatever the compressive forces, the lumen of the urethra must be capable of being obliterated by a watertight seal. This “mucosal seal mechanism” explains why a thin-walled rubber tube requires less pressure to close an open end when the inner layer is coated with a fine layer of grease than when it is not, the latter case being much like scarred or atrophic urethral mucosa.

Voiding with a Normal Bladder Contraction

Although many factors are involved in the initiation of micturition, in adults it is intravesical pressure producing the sensation of distention that is primarily responsible for the initiation of normal voluntarily induced emptying of the lower urinary tract. Although the origin of the parasympathetic neural outflow to the bladder, the pelvic nerve, is in the sacral spinal cord, the actual coordinating center for the micturition reflex in an intact neural axis is in the rostral brainstem. The complete neural circuit for normal micturition includes the ascending and descending spinal cord pathways to and from this area and the facilitatory and inhibitory influences from other parts of the brain, particularly the cerebral cortex. The final step in voluntarily induced micturition involves inhibition of the somatic neural efferent activity to the striated sphincter and an inhibition of all aspects of any spinal sympathetic reflexes evoked during filling. Efferent parasympathetic pelvic nerve activity is ultimately what is responsible for a highly coordinated contraction of the bulk of the bladder smooth musculature.

A decrease in outlet resistance occurs with adaptive shaping or funneling of the relaxed bladder outlet. Besides the inhibition of any continence-promoting reflexes that have occurred during bladder filling, the change in outlet resistance may also involve an active relaxation of the smooth sphincter area through a noradrenergic noncholinergic (NANC) mechanism, proposed to be mediated by nitric oxide (Andersson and Arner, 2004; Andersson and Wein, 2004). The adaptive changes that occur in the outlet are probably also due at least in part to the anatomic interrelationships of the smooth muscle of the bladder base and proximal urethra. Longitudinal smooth muscle continuity (Mostwin, 2006; see Chapter 60) would promote shortening and widening of the proximal urethra during a coordinated emptying bladder contraction. Other reflexes that are elicited by bladder contraction and by the passage of urine through the urethra may reinforce and facilitate complete bladder emptying. Superimposed on these autonomic and somatic reflexes are complex, modifying supraspinal inputs from other central neuronal networks. These facilitatory and inhibitory impulses, which originate from several areas of the nervous system, allow the full conscious control of micturition in the adult.

Urinary Continence during Abdominal Pressure Increases

During voluntarily initiated micturition, the bladder pressure becomes higher than the outlet pressure and certain adaptive changes occur in the shape of the bladder outlet with consequent passage of urine into and through the proximal urethra. One could reasonably ask, why do such changes not occur with increases in intravesical pressure that are similar in magnitude but that are produced only by changes in intra-abdominal pressure such as straining or coughing? First, a coordinated bladder contraction does not occur in response to such stimuli, clearly emphasizing the fact that increases in total intravesical pressure are by no means equivalent to emptying ability. Secondly, for urine to flow into and through the proximal urethra in an individual who does not have sphincteric incontinence, there must be (1) an increase in intravesical pressure that is primarily a product of a coordinated, neurally mediated bladder contraction and that is (2) associated with characteristic tension and conformational changes in the bladder neck and proximal urethral areas.

Assuming that the bladder outlet is competent at rest, a major factor required for the prevention of urinary leakage during increases in intra-abdominal pressure is that there is at least equal pressure transmission to the proximal urethra (the midurethra, as well as in the female) during such activity. This phenomenon was first described by Enhorning (1961) and has been confirmed in virtually every urodynamic laboratory since that time. Failure of this mechanism is an invariable correlate of effort-related urinary incontinence in the female and male. The urethral closure pressure increases with increments in intra-abdominal pressure, indicating that active muscular function related to a reflex increase in striated sphincter activity or other factors that increase urethral resistance is also involved in preventing such leakage. Tanagho (1978) was the first to provide direct evidence of this. A more complete description of the factors involved in sphincteric incontinence can be found later in this chapter and in Chapters 60 and 63.

Sensory Aspects

Most of the afferent input from the bladder and urethra reaches the spinal cord through the pelvic nerve and dorsal root ganglia and some through the hypogastric nerve.

Afferent input from the striated muscle of the sphincter and pelvic floor travels in the pudendal nerve. The most important afferents for initiating and maintaining normal micturition are those in the pelvic nerve, relaying to the sacral spinal cord. These convey impulses from tension, volume, and nociceptive receptors located in the serosal, muscle, and urothelial and suburothelial layers of the bladder and urethra. In a neurologically normal adult the sensation of filling and distention, but not urgency or pain, is what develops during normal filling/storage and initiates the reflexes responsible for emptying/voiding (deGroat and Yoshimura, 2001; Chancellor and Yoshimura, 2002; Morrison et al, 2005; Birder et al, 2009; see Chapter 60). Alterations in this finely tuned pathway can be responsible for significant alterations in lower urinary tract function.

Filling/Storage Failure

Emptying/Voiding Failure

Functional System

Classification of voiding dysfunction can be formulated on a simple functional basis, describing the dysfunction in terms of whether the deficit produced is primarily one of the filling/storage or the emptying/voiding phase of micturition (Table 61–1) (Wein, 1981; Wein and Barrett, 1988). The genesis of such a system was proposed initially by F. Brantley Scott’s group (Quesada et al, 1968). This simple-minded scheme assumes only that, whatever their differences, all “experts” would agree on the two-phase concept of micturition (filling/storage and emptying/voiding), on the simple overall mechanisms underlying the normality of each phase (see previous discussion), and on the possibilities for dysfunction.

Table 61–1 Functional Classification

Storage failure results from either bladder or outlet abnormalities or a combination. The proven bladder abnormalities simply include only involuntary bladder contractions, low compliance, and heightened or altered sensation. The outlet abnormalities can include only an intermittent or continuous decrease in outlet resistance.

Emptying failure, likewise, can occur because of bladder or outlet abnormalities or a combination. The bladder side includes only inadequate or unsustained bladder contractility, and the outlet side includes only anatomic obstruction and sphincter dyssynergia or dysfunction.

There are indeed some types of voiding dysfunction that represent combinations of filling/storage and emptying voiding abnormalities. Within this scheme, however, these become readily understandable and their detection and treatment can be logically described. Various aspects of physiology and pathophysiology are always related more to one phase of micturition than another. All aspects of urodynamic and videourodynamic evaluation can be conceptualized in this functional manner as to exactly what they evaluate in terms of either bladder or outlet activity during filling/storage and emptying/voiding (Table 61–2). In addition, one can easily classify all known treatments for voiding dysfunction under the broad categories of whether they facilitate filling/storage and emptying/voiding and whether they do so by an action primarily on the bladder or on one or more of the components of the bladder outlet (Tables 61-3 and 61-4).

Table 61–2 Urodynamics Simplified

^1,2 Total bladder (Pves) and detrusor (Pdet) pressures during a filling cystometrogram (FCMG).

³ Filling cystometrogram.

⁴ Detrusor leak point pressure.

⁵ Urethral pressure profilometry.

⁶ Valsalva leak point pressure.

⁷ Fluoroscopy of outlet during filling/storage.

^8,9 Total bladder and detrusor pressures during a voiding cystometrogram (VCMG).

¹⁰ Voiding cystometrogram.

¹¹ Micturitional urethral pressure profilometry.

¹² Fluoroscopy of outlet during emptying.

¹³ Electromyography of periurethral striated musculature.

¹⁴ Flowmetry.

¹⁵ Residual urine.

Table 61–3 Therapy to Facilitate Urine Storage/Bladder Filling

Table 61–4 Therapy to Facilitate Bladder Emptying/Voiding

Failure in either category generally is not absolute but more often is relative. Such a functional system can easily be “expanded” and made more complicated to include etiologic or specific urodynamic connotations (Table 61–5). However, the simplified system is perfectly workable and avoids argument in the complex situations in which the exact etiology or urodynamic mechanism for a voiding dysfunction cannot be agreed on.

Table 61–5 Expanded Functional Classification

Proper use of the functional system for a given voiding dysfunction obviously requires a reasonably accurate notion of what the urodynamic data show. However, an exact diagnosis is not required for treatment. It should be recognized that some patients do not have only a discrete storage or emptying failure, and the existence of combination deficits must be recognized to use this system classification properly. For an example, the “classic” T10 paraplegic patient after spinal shock generally exhibits a relative failure to store because of involuntary bladder contraction and a relative failure to empty the bladder because of striated sphincter dyssynergia. With such a combination deficit, to use this classification system as a guide to treatment, one must assume that one of the deficits is primary and that significant improvement will result from its treatment alone or that the voiding dysfunction can be converted primarily to a disorder of either storage or emptying by means of nonsurgical or surgical therapy. The resultant deficit can then be treated or circumvented. Using this example, the combined deficit in a T10 paraplegic patient can be converted primarily to a storage failure by procedures directed at the dyssynergic striated sphincter; the resultant incontinence (secondary to involuntary contraction) can be circumvented (in a male) with an external collecting device. Alternatively, the deficit can be converted primarily to an emptying failure by pharmacologic or surgical measures designed to abolish or reduce the involuntary contraction, and the resultant emptying failure can then be circumvented with clean intermittent catheterization. Other examples of combination deficits include impaired bladder contractility or overactivity with sphincter dysfunction, bladder outlet obstruction with detrusor overactivity, bladder outlet obstruction with sphincter malfunction, and detrusor overactivity with impaired contractility.

One of the advantages of this functional classification is that it allows the clinician the liberty of “playing” with the system to suit his or her own preferences without an alteration in the basic concept of “keep it simple but accurate and informative.” For instance, one could easily substitute the terms overactive or oversensitive bladder and underactive outlet for because of the bladder and because of the outlet under “Failure to Store” in Table 61–1. One could choose to categorize the bladder reasons for overactivity (see Table 61–5) further in terms of neurogenic, myogenic, or anatomic causes and further subcategorize neurogenic in terms of decreased inhibitory control, increased afferent activity, increased sensitivity to efferent activity, and so on. The system is flexible.

The classification system proposed by the International Continence Society (ICS) (Table 61–6) is in essence an extension of a urodynamic classification system. The storage and voiding phases of micturition are described separately, and, within each, various designations are applied to describe bladder and urethral function (Abrams et al, 1988, 1992). Some of the definitions were changed by the standardization subcommittee of the International Continence Society in 2002, and the relevant changes are indicated here (Abrams et al, 2002, 2003). Normal bladder function during filling/storage implies no significant rises in detrusor pressure (stability). Overactive detrusor function indicates the presence of “involuntary detrusor contractions during the filling phase, which may be spontaneous or provoked.” If the condition is caused by neurologic disease, the term neurogenic detrusor overactivity (previously, detrusor hyperreflexia) is applied. If not, the term idiopathic detrusor overactivity (previously, detrusor instability) is applied. Bladder sensation can be categorized only in qualitative terms as indicated. Bladder capacity and compliance (Δ volume/Δ pressure) are cystometric measurements. Bladder capacity can refer to cystometric capacity, maximum cystometric capacity, or maximum anesthetic cystometric capacity (Abrams et al, 2002). Normal urethral function during filling/storage indicates a positive urethral closure pressure (urethral pressure minus bladder pressure) even with increases in intra-abdominal pressure, although it may be overcome by detrusor overactivity. Incompetent urethral function during filling/storage implies urine leakage in the absence of a detrusor contraction. This may be secondary to genuine stress incontinence, intrinsic sphincter dysfunction, a combination, or an involuntary fall in urethral pressure in the absence of detrusor contraction.

Table 61–6 International Continence Society Classification

During the voiding/emptying phase of micturition, normal detrusor activity implies voiding by a voluntarily initiated sustained contraction that leads to complete bladder emptying within a normal time span. An underactive detrusor defines a contraction of inadequate magnitude or duration, or both, to empty the bladder within a normal time span. An acontractile detrusor is one that cannot be demonstrated to contract during urodynamic testing. Areflexia is defined as acontractility due to an abnormality of neural control, implying the complete absence of centrally coordinated contraction. Normal urethral function during voiding indicates a urethra that opens and is continuously relaxed to allow bladder emptying at a normal pressure. Abnormal urethral function during voiding may be due to either mechanical obstruction or urethral overactivity. Dysfunctional voiding describes an intermittent or fluctuating flow rate due to involuntary intermittent contractions of the periurethral striated muscle in neurologically normal individuals. Detrusor sphincter dyssynergia defines a detrusor contraction concurrent with an involuntary contraction of the urethral or periurethral striated muscle, or both. Nonrelaxing urethral sphincter obstruction usually occurs in individuals with a neurologic lesion and is characterized by a nonrelaxing obstructing urethra resulting in reduced urine flow.

Lower urinary tract dysfunction in a classic T10-level paraplegic patient after spinal shock has passed would be classified in the ICS system as follows:

The micturition dysfunction of a stroke patient with urgency incontinence would most likely be classified during storage as overactive neurogenic detrusor function, normal sensation, low capacity, normal compliance, and normal urethral closure function. During voiding, the dysfunction would be classified as normal detrusor activity and normal urethral function, assuming that no anatomic obstruction existed.

Urodynamic Classification

As urodynamic techniques have become more accepted and sophisticated, systems of classification have evolved solely on the basis of objective urodynamic data (Table 61–7). Among the first to popularize this concept were Krane and Siroky (1984). When exact urodynamic classification is possible, such a system can provide a truly exact description of the voiding dysfunction that occurs. If a normal or hyperreflexic (overactive) detrusor exists with coordinated smooth and striated sphincter function and without anatomic obstruction, normal bladder emptying should occur. Detrusor hyperreflexia (now termed neurogenic detrusor overactivity in ICS parlance) is most commonly associated with neurologic lesions above the sacral spinal cord. Striated sphincter dyssynergia is most commonly seen after complete suprasacral spinal cord injury, following the period of spinal shock. Smooth sphincter dyssynergia is seen most classically in autonomic hyperreflexia (see Chapter 65) when it is characteristically associated with detrusor overactivity and striated sphincter dyssynergia. Detrusor areflexia (actually this category includes acontractile and areflexic bladder) may be secondary to bladder muscle decompensation or to various other conditions that produce inhibition at the level of the brainstem micturition center, the sacral spinal cord, bladder ganglia, or bladder smooth muscle. Patients with a voiding dysfunction secondary to detrusor areflexia generally attempt bladder emptying by abdominal straining, and their continence status and the efficiency of their emptying efforts are determined by the status of their smooth and striated sphincter mechanisms.

Table 61–7 Urodynamic Classification

This classification system is easiest to use when detrusor hyperreflexia (overactivity) or normoreflexia exists. Thus a typical T10-level paraplegic patient after spinal shock exhibits detrusor hyperreflexia, smooth sphincter synergia, and striated sphincter dyssynergia. When a voluntary or a hyperreflexic contraction cannot be elicited, the system is more difficult to use because it is not appropriate to speak of true sphincter dyssynergia in the absence of an opposing bladder contraction. There are obviously many variations and extensions of such a system. Such systems can work well only when total urodynamic agreement exists among classifiers. Unfortunately, there are many voiding dysfunctions that do not fit neatly into a urodynamic classification system that is agreed on by all experts. Compliance is not mentioned in this particular version, nor is sensation or the concept of deficient but not absent detrusor contractile function. As sophisticated urodynamic technology and understanding improve, this type of classification system may become more commonly used. The ICS system (see previous discussion) is in reality a logical and more complete extension of such a system.

Lapides Classification

Lapides (1970) contributed significantly to the classification and care of the patient with neuropathic voiding dysfunction by slightly modifying and popularizing a system originally proposed by McLellan in 1939 (Table 61–8). Lapides’ classification differs from that of McLellan in only one respect, and that is the division of the group of “atonic neurogenic bladder” into sensory neurogenic and motor neurogenic bladder. This remains a familiar system to urologists and nonurologists because it describes in recognizable shorthand the clinical and cystometric conditions of many types of neurogenic voiding dysfunction.

Table 61–8 Lapides Classification

A sensory neurogenic bladder results from disease that selectively interrupts the sensory fibers between the bladder and the spinal cord or the afferent tracts to the brain. Diabetes mellitus, tabes dorsalis, and pernicious anemia are the most responsible. The first clinical changes are described as those of impaired sensation of bladder distention. Unless voiding is initiated on a timed basis, varying degrees of bladder overdistention can result with resultant hypotonicity. If bladder decompensation occurs, significant amounts of residual urine result, and at that time the cystometric curve generally demonstrates a large capacity bladder with a flat, high-compliance, low-pressure filling curve.

A motor paralytic bladder results from disease processes that destroy the parasympathetic motor innervation of the bladder. Extensive pelvic surgery or trauma may produce this. Herpes zoster has been listed as a cause as well, but recent evidence suggests that the voiding dysfunction seen with herpes may be more related to a problem with afferent input (see Chapter 65). The early symptoms of a motor paralytic bladder may vary from painful urinary retention to only a relative inability to initiate and maintain normal micturition. Early cystometric filling is normal but without a voluntary bladder contraction at capacity. Chronic overdistention and decompensation may occur, resulting in a large-capacity bladder with a flat, low-pressure filling curve; a large residual urine may result.

An uninhibited neurogenic bladder was described originally as resulting from injury or disease to the “corticoregulatory tract.” The sacral spinal cord was presumed to be the micturition reflex center, and this corticoregulatory tract was believed normally to exert an inhibitory influence on the sacral micturition reflex center. A destructive lesion in this tract would then result in overfacilitation of the micturition reflex. Cerebrovascular accident, brain or spinal cord tumor, Parkinson disease, and demyelinating disease were listed as the most common causes in this category. The voiding dysfunction is most often characterized symptomatically by frequency, urgency, and urge incontinence and urodynamically by normal sensation with involuntary contraction at low filling volumes. Residual urine is characteristically low unless anatomic outlet obstruction or true smooth or striated sphincter dyssynergia occurs. The patient generally can initiate a bladder contraction voluntarily but is often unable to do so during cystometry because sufficient urine storage cannot occur before involuntary contraction is stimulated.

Reflex neurogenic bladder describes the post–spinal shock condition that exists after complete interruption of the sensory and motor pathways between the sacral spinal cord and the brainstem. Most commonly, this occurs in traumatic spinal cord injury and transverse myelitis, but it may occur with extensive demyelinating disease or any process that produces significant suprasacral (cord) spinal cord destruction. Typically, there is no bladder sensation, and there is inability to initiate voluntary micturition. Incontinence without sensation generally results from low-volume involuntary contraction. Striated sphincter dyssynergia is the rule. This type of lesion is essentially equivalent to a complete upper motor neuron (UMN) lesion in the Bors-Comarr system (see later).

An autonomous neurogenic bladder results from complete motor and sensory separation of the bladder from the sacral spinal cord. This may be caused by any disease that destroys the sacral cord or causes extensive damage to the sacral roots or pelvic nerves. There is inability to initiate micturition voluntarily, no bladder reflex activity, and no specific bladder sensation. This type of bladder is equivalent to a complete lower motor neuron (LMN) lesion in the Bors-Comarr system and is also the type of dysfunction seen in patients with spinal shock. The characteristic cystometric pattern is initially similar to the late stages of the motor or sensory paralytic bladder, with a marked shift to the right of the cystometric filling curve and a large bladder capacity at low intravesical pressure. However, decreased compliance may develop, secondary either to chronic inflammatory change or to the effects of denervation/decentralization with secondary neuromorphologic and neuropharmacologic reorganizational changes. Emptying capacity may vary widely, depending on the ability of the patient to increase intravesical pressure and on the resistance offered during this increase by the smooth and striated sphincters.

These classic categories in their usual settings are generally understood and remembered, and this is why this system provides an excellent framework for teaching some fundamentals of neurogenic voiding dysfunction to students and nonurologists. Unfortunately, many patients do not exactly fit into one or another category. Gradations of sensory, motor, and mixed lesions occur, and the patterns produced after different types of peripheral denervation/defunctionalization may vary widely from those that are classically described. The system is applicable only to neuropathic dysfunction.

Bors and Comarr (1971) made a remarkable contribution by logically deducing a classification system from clinical observation of their patients with traumatic spinal cord injury (Table 61–9). This system, primarily of historical interest at present, applies only to patients with neurologic dysfunction and considers three factors: (1) the anatomic localization of the lesion, (2) the neurologic completeness or incompleteness of the lesion, and (3) whether lower urinary tract function is balanced or unbalanced. The last terms are based solely on the percentage of residual urine relative to bladder capacity. Unbalanced signifies the presence of greater than 20% residual urine in a patient with a UMN lesion or 10% in a patient with an LMN lesion. This relative residual urine volume was ideally meant to imply coordination (synergy) or dyssynergia between the smooth and the striated sphincters of the outlet and the bladder during bladder contraction or during attempted micturition by abdominal straining or the Credé maneuver. The determination of the completeness of the lesion is made on the basis of a thorough neurologic examination.

Table 61–9 Bors-Comarr Classification

The system erroneously assumes that the sacral spinal cord is the primary reflex center for micturition. LMN implies collectively the preganglionic and postganglionic parasympathetic autonomic fibers that innervate the bladder and outlet and originate as preganglionic fibers in the sacral spinal cord. The term is used in an analogy to efferent somatic nerve fibers such as those of the pudendal nerve, which originate in the same sacral cord segment but terminate directly on pelvic floor striated musculature without the interposition of ganglia. UMN is used in a similar analogy to the somatic nervous system to describe the descending autonomic pathways above the sacral spinal cord (the origin of the motor efferent supply to the bladder).

In this system, UMN bladder refers to the pattern of micturition that results from an injury to the suprasacral spinal cord after the period of spinal shock has passed, assuming that the sacral spinal cord and the sacral nerve roots are intact and that the pelvic and pudendal nerve reflexes are intact. LMN bladder refers to the pattern resulting if the sacral spinal cord or sacral roots are damaged and the reflex pattern through the autonomic and somatic nerves that emanate from these segments is absent. This system implies that if skeletal muscle spasticity exists below the level of the lesion, the lesion is above the sacral spinal cord and is by definition a UMN lesion. This type of lesion is characterized by involuntary bladder contraction during filling. If flaccidity of the skeletal musculature below the level of a lesion exists, an LMN lesion is assumed to be present, implying that detrusor areflexia is present. Exceptions occur and are classified in a “mixed lesion group” characterized either by involuntary bladder contraction with a flaccid paralysis below the level of the lesion or by detrusor areflexia with spasticity or normal skeletal muscle tone neurologically below the lesion level.

The use of this system is illustrated as follows. A “UMN lesion, complete, imbalanced” implies a neurologically complete lesion above the level of the sacral spinal cord that results in skeletal muscle spasticity below the level of the injury. Involuntary bladder contraction occurs during filling, but a residual urine volume of greater than 20% of the bladder capacity is left after bladder contraction, implying obstruction in the area of the bladder outlet during the involuntary detrusor contraction. This obstruction is generally due to striated sphincter dyssynergia, typically occurring in patients who are paraplegic or quadriplegic with lesions between the cervical and the sacral spinal cord. Smooth sphincter dyssynergia may be seen as well in patients with lesions above the level of T6, usually associated with autonomic hyperreflexia (see Chapter 65). An “LMN lesion, complete, imbalanced” implies a neurologically complete lesion at the level of the sacral spinal cord or of the sacral roots, resulting in skeletal muscle flaccidity below that level. Detrusor areflexia results, and whatever measures the patient may use to increase intravesical pressure during attempted voiding are not sufficient to decrease residual urine to less than 10% of bladder capacity.

This classification system applies best to spinal cord injury patients with complete neurologic lesions after spinal shock has passed. It is difficult to apply to patients with multicentric neurologic disease and cannot be used at all for patients with non-neurologic disease. The system fails to reconcile the clinical and urodynamic variability exhibited by patients who, by neurologic examination alone, seem to have similar lesions. The period of spinal shock that immediately follows severe cord injury is generally associated with bladder areflexia, whatever the status of the sacral somatic reflexes. Temporary or permanent changes in bladder or outlet activity during filling/storage and emptying/voiding may occur secondary to a number of factors such as chronic overdistention, infection, and reinnervation or reorganization of neural pathways following injury or disease; such changes make it impossible to always accurately predict lower urinary tract activity solely on the basis of the level of the neurologic lesion. Finally, although the terms balanced and imbalanced are helpful, in that they describe the presence or absence of a certain relative percentage of residual urine, they do not necessarily imply the true functional significance of a lesion, which depends on the potential for damage to the lower or upper urinary tracts and also on the social and vocational disability that results.

Hald-Bradley Classification

Hald and Bradley (1982) described what they termed a simple neurotopographic classification (Table 61–10). The system is of historical interest only. A supraspinal lesion is characterized by synergy between detrusor contraction and the smooth and striated sphincters, but defective inhibition of the voiding reflex exists. Involuntary bladder contraction generally occurs, and sensation is usually preserved. However, depending on the site of the lesion, detrusor areflexia and defective sensation may be seen. A suprasacral spinal lesion is roughly equivalent to what is described as a UMN lesion in the Bors-Comarr classification. An infrasacral lesion is roughly equivalent to an LMN lesion. Peripheral autonomic neuropathy is most frequently encountered in the diabetic patient and is characterized by deficient bladder sensation, gradually increasing residual urine, and ultimate decompensation, with loss of detrusor contractility. A muscular lesion can involve the detrusor itself, the smooth sphincter, or any portion, or all, of the striated sphincter. The resultant dysfunction is dependent on which structure is affected. Detrusor dysfunction is the most common and generally results from decompensation, following long-standing bladder outlet obstruction. In my opinion, this system is as confusing as the word neurotopographic and adds little to the understanding of lower urinary tract dysfunction.

Table 61–10 Hald-Bradley Classification

Bradley Classification

Bradley’s “loop system” of classification is a primarily neurologic system based on his conceptualization of central nervous system control of the lower urinary tract that identifies four neurologic “loops” (Hald and Bradley, 1982). Dysfunctions are classified according to the loop affected. Occasional reference is made to this system, primarily by nonurologists.

Loop 1 consists of neuronal connections between the cerebral cortex and the pontine mesencephalic micturition center; this coordinates voluntary control of the detrusor reflex. Loop 1 lesions are seen in conditions such as brain tumor, cerebrovascular accident or disease, and cerebral atrophy with dementia. The final result is characteristically involuntary bladder contractions.

Loop 2 includes the intraspinal pathway of detrusor muscle afferents to the brainstem micturition center and the motor impulses from this center to the sacral spinal cord. Loop 2 is thought to coordinate and provide for a detrusor reflex of adequate temporal duration to allow complete voiding. Partial interruption by spinal cord injury results in a detrusor reflex of low threshold and in poor emptying with residual urine. Spinal cord transection of loop 2 acutely produces detrusor areflexia and urinary retention—spinal shock. After this has passed, involuntary bladder contractions result.

Loop 3 consists of the peripheral detrusor afferent axons and their pathways in the spinal cord; these terminate by synapsing on pudendal motor neurons that ultimately innervate periurethral striated muscle. Loop 3 was thought to provide a neurologic substrate for coordinated reciprocal action of the bladder and striated sphincter. Loop 3 dysfunction could be responsible for detrusor striated dyssynergia or involuntary sphincter relaxation.

Loop 4 consists of two components. Loop 4A is the suprasacral afferent and efferent innervation of the pudendal motor neurons to the periurethral striated musculature. Loop 4B consists of afferent fibers from the periurethral striated musculature that synapse on pudendal motor neurons in Onuf nucleus—the segmental innervation of the periurethral striated muscle. Bradley conceptualized that, in contrast to the stimulation of detrusor afferent fibers, which produced inhibitory postsynaptic potentials in pudendal motor neurons through loop 3, pudendal nerve afferents produced excitatory postsynaptic potentials in those motor neurons through loop 4B. These provided for contraction of the periurethral striated muscle during bladder filling and urine storage. The related sensory impulses arise from muscle spindles and tendon organs in the pelvic floor musculature. Loop 4 provides for volitional control of the striated sphincter. Abnormalities of the suprasacral portion result in abnormal responses of the pudendal motor neurons to bladder filling and emptying, manifested as detrusor striated sphincter dyssynergia or loss of the ability to contract the striated sphincter voluntarily, or both.

The Bradley system is sophisticated and reflects the ingenuity and neurophysiologic expertise of its originator, himself a neurologist. For neurologists, this method may be an excellent way to conceptualize the neurophysiology involved, assuming that there is, in fact, agreement on the existence and significance of all four loops—a big assumption. Most urologists find this system difficult to use for many types of neurogenic voiding dysfunction and not at all applicable to non-neurogenic voiding dysfunction. Urodynamically, it may be extremely difficult to test the intactness of each loop system, and multicentric and partial lesions are difficult to describe.